Showing papers on "Vasopressin published in 1972"
TL;DR: Treatment with lysine vasopressin increased resistance to extinction, irrespective of the time of treatment, and nonshocked control animals showed no increase in response latencies on successive trials.
Abstract: On a single conditioning trial, a 1-sec electric shock (.125 or.250 mA) was administered when rats entered a darkened chamber from a lighted elevated runway. Latency to enter the chamber was recorded on retention trials given 24 and 48 h later. Animals received subcutaneous injections of varying doses of lysine vasopressin or a placebo solution immediately after the training trial or immediately before the first retention trial. Nonshocked control animals showed no increase in response latencies on successive trials, nor was there a difference between the placebo and vasopressin groups under the “no-shock” condition. Treatment with lysine vasopressin increased resistance to extinction, irrespective of the time of treatment.
151 citations
TL;DR: Male rats were trained in an active avoidance and/or a “step-through” type of passive avoidance situation and resistance to extinction of active avoidance behavior was obtained when lysine vasopressin was injected 1 hr prior to the first retention trial on Day 3 of training.
141 citations
TL;DR: It is concluded that active Na transport is augmented by vasopressin in the collecting tubule, similar to the effect previously observed in anuran membranes.
117 citations
TL;DR: This is the first demonstration of in vitro biosynthesis of vasopressin by a tumor from a patient with SIADH, and the bronchogenic carcinoma was composed of small undifferentiated and granulated cells.
Abstract: Tumors from patients with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) have been found to contain large amounts of the antidiuretic hormone vasopressin. A lung tumor from a patient with hyponatremia most likely due to SIADH was removed at surgery and found to contain 23.5 mU vasopressin/g wet weight by radioimmunoassay Slices of this tumor were incubated with phenylalanine-(3)H. Arginine vasopressin-(3)H was purified from the incubate by Sephadex G-25 column chromatography in two different systems, performic acid oxidation, and gradient elution column chromatography with diethylaminoethyl Sephadex. As oxidation of vasopressin results in drastic conformational change with breaking of the ring of the cyclic polypeptide and addition of two cysteic acid residues per molecule, the radioactive material which eluted coincident with vasopressin both before and after this procedure was considered to be arginine vasopressin-(3)H. To our knowledge this is the first demonstration of in vitro biosynthesis of vasopressin by a tumor from a patient with SIADH.Ultrastructurally, the bronchogenic carcinoma was composed of small undifferentiated and granulated cells. The granulated neoplastic cells had well developed organelles (endoplasmic reticulum, free ribosomes) concerned with protein synthesis. Secretion granules present in the tumor cells were small, surrounded by a limiting membrane, and resembled those reported in polypeptide hormone-secreting cells.
113 citations
TL;DR: The effect of vasopressin on blood platelets resembled its action on smooth muscle and was almost inactive in citrated platelet-rich plasma but caused aggregation in recalcified citrated or native material.
Abstract: Synthetic [8-arginine]-vasopressin [8-lysine]-vasopressin [8-ornithine]-vasopressin or [2-phenylalanine 8-lysine]-vasopressin aggregated human platelets in heparinized platelet-rich plasma. The lowest effective concentrations (1-4mU/ml) caused a primary transient aggregation while higher concentrations also caused a secondary irreversible aggregation. Vasopressin was almost inactive in citrated platelet-rich plasma but caused aggregation in recalcified citrated or native material. Vasopressin also aggregated washed human platelets suspended in buffered saline if fibrinogen and either Ca2+ or Mg2+ ions were present. Ethylene glycol-bis (beta-aminoethyl ether)-NN-tetraacetic acid inhibited aggregation completely but only after preincubation with the platelets suggesting that platelet-bound calcium was also required. Phosphocreatine with creatine phosphokinase partially inhibited primary aggregation of platelets by vasopressin and prevented secondary aggregation which suggests that release of platelet ADP contributed to these processes. Concentrations of vasopressin causing irreversible aggregation released small amounts of 14C from platelets containing serotonin-14C. Platelet aggregation induced by vasopressin was inhibited by adenosine prostaglandin E1 N62-0-dibutyryl cyclic 35-AMP caffeine imipramine or N-ethylmaleimide. Adenosine and prostaglandin E each inhibited the action of vasopressin much more powerfully than that of ADP and therefore cannot act solely by inhibiting the effects of the ADP released. In several respects the effect of vasopressin on blood platelets resembled its action on smooth muscle. (Authors modified)
111 citations
TL;DR: It appears that pressorpeptides are more potent protective agents than corticotropin when administered subcutaneously, and that vasopressin contamination of the commercial preparation was probably responsible for the protective effects previously reported.
Abstract: The puromycin-induced blockade of expression of maze learning in mice can be prevented by subcutaneous administration of “Purified Cortrophin Gel” up to 3 days prior to training. A similar protective effect was not found when highly purified corticotropin was tested, but was observed after administration of desglycinamide9-lysine vasopressin. It appears that pressorpeptides are more potent protective agents than corticotropin when administered subcutaneously, and that vasopressin contamination of the commercial preparation was probably responsible for the protective effects previously reported. These experiments suggest that vasopressin and its congeners modify memory consolidation in such a way that the “expression” of memory becomes insensitive to puromycin.
102 citations
TL;DR: Oxytocin excited the majority of PV units which could be activated antidromically by stimulation of the neural lobe but failed to excite PV neurons which could not be identified in this way and cells in the SO nucleus, cortex, and thalamus.
99 citations
TL;DR: Although these studies suggest that vasopressin is effective therapy, prospective controlled clinical trials are needed to establish the efficacy and safety of this new therapeutic tool in stopping hemorrhage and in improving survival.
91 citations
TL;DR: Preliminary experiments suggest that noradrenaline is the transmitter released by the postganglionic nerves to the human spleen, which provides direct evidence that the normal humanSpleen, unlike that of the dog, does not have a reservoir function.
Abstract: 1. The responses of the smooth muscle of the capsule and blood vessels of the isolated, perfused human spleen to sympathetic nerve stimulation, adrenaline, noradrenaline, angiotensin, oxytocin, vasopressin, isoprenaline and acetylcholine have been investigated and compared with those of dog spleen.2. Stimulation of the postganglionic sympathetic nerves to the human spleen at frequencies of 3-10 Hz evoked graded vasoconstriction but very small changes in spleen volume.3. The injection of adrenaline and noradrenaline in doses of 0.25-25 mug to the human spleen produced graded increases in splenic vascular resistance with very small decreases in spleen volume.4. Administration of the alpha-adrenoceptor blocking drug phenoxybenzamine completely abolished or considerably reduced the vascular responses of the human spleen to sympathetic nerve stimulation or the injection of noradrenaline.5. The vascular action of adrenaline was often reversed to elicit a vasodilatation after phenoxybenzamine suggesting the presence of beta-adrenoceptors in the vascular bed. This was confirmed by the administration of isoprenaline which induced a marked reduction in vascular resistance of the human spleen.6. The polypeptides angiotensin and vasopressin induced a marked vasoconstriction in the human spleen without changes in the spleen volume. These effects were uninfluenced by the administration of phenoxybenzamine.7. The polypeptide oxytocin caused a slight vasodilatation in the human spleen, an effect almost exactly mimicked by the preservative chlorobutanol.8. Preliminary experiments suggest that noradrenaline is the transmitter released by the postganglionic nerves to the human spleen.9. These results provide direct evidence that the normal human spleen, unlike that of the dog, does not have a reservoir function. It is suggested that contractions of the enlarged human spleen may occur in various pathological conditions.
84 citations
TL;DR: The iv injection of crude methanol or acid extracts of porcine hypothalamic fragments (SME) induces at ten min a significant rise in radioimmunoassayable prolactin levels in male rats treated with 50 μg estradiol benzoate, and 25 mg progesterone daily for three days prior to assay.
Abstract: The iv injection of crude methanol or acid extracts of porcine hypothalamic fragments (SME) induces at ten min a significant rise in radioimmunoassayable prolactin levels in male rats treated with 50 μg estradiol benzoate, and 25 mg progesterone daily for three days prior to assay. The response is log-dose dependent over the range of 2–25 SME equivalents. Although vasopressin in large doses also induces prolactin release, the effects of SME extract cannot be accounted for solely by the relatively small amounts of this hormone present in the extract; moreover, vasopressin can be separated from prolactin releasing activity (PRA) by thin-layer chromatography. Thyrotrophin-releasing hormone (TRH) in amounts far in excess of those found in SME extracts with PRA does not release prolactin, and by Sephadex G-10 chromatography a distinct fraction that exhibits PRA can be separated from TRH. As judged by the distribution on Sephadex G-10, PRA is distinct from luteinizing hormone-releasing factor (LRF). The sensiti...
79 citations
TL;DR: Results support the hypothesis that the diuretic effect of alpha adrenergic stimulation is mediated by inhibition of the effect of vasopressin to increase cyclic AMP generation.
Abstract: Catecholamines have several physiological effects on the kidney. These include: (a) stimulation of renin synthesis in the cortex: (b) antidiuresis by beta adrenergic agents; and (c) diuresis by alpha adrenergic stimulation. The role of cyclic 3',5'-adenosine monophosphate (cyclic AMP) in the renal actions of catecholamines was evaluated by measuring the effects of several adrenergic agents on cyclic AMP concentration in the dog kidney. Beta adrenergic activity increased cyclic AMP concentration in the renal cortex, a finding consistent with the hypothesis that beta-adrenergic stimulation augments renin synthesis by increasing cyclic AMP generation. Beta adrenergic stimulation, like vasopressin, increased cyclic AMP concentration in the renal medulla. This suggests that beta adrenergic stimulation causes antidiuresis by augmenting cyclic AMP generation in the renal medulla. Alpha adrenergic activity inhibited the effect of vasopressin to stimulate cyclic AMP generation. These results support the hypothesis that the diuretic effect of alpha adrenergic stimulation is mediated by inhibition of the effect of vasopressin to increase cyclic AMP generation.
TL;DR: The responses of pituitary hormones to insulin-induced hypoglycemia, lysine-8-vasopressin infusion and arginine infusion were examined in patients with Cushing's syndrome and plasma ACTH was not detectable at any time during all of the studies.
Abstract: The responses of pituitary hormones to insulin-induced hypoglycemia, lysine-8-vasopressin infusion and arginine infusion were examined in patients with Cushing's syndrome. In patients with adrenal hyperplasia, basal levels of plasma ACTH were slightly elevated and responses were preserved to both insulin-induced hypoglycemia and lysine-8-vasopressin infusion, though the magnitude of response was variable. All of the patients had an increase of plasma 11-hydroxycorticosteroids following lysine-8-vasopressin. After insulin-induced hypoglycemia, 11-hydroxycorticosteroids increased in only half of the patients. In patients with adrenal adenomas, plasma 11-hydroxycorticosteroid concentrations did not increase after insulin-induced hypoglycemia but there was a rise observed after lysine-8-vasopressin infusion. However, in patients with adrenal adenomas plasma ACTH was not detectable at any time during all of the studies. There was usually no increase of plasma GH concentration in response to any of the stimuli....
TL;DR: It is concluded that the antidiuretic effect associated with cervical vagotomy is initiated by interruption of parasympathetic afferent pathways and is mediated by increased endogenous release of vasopressin.
Abstract: The present experiments were undertaken to investigate the mechanism whereby the parasympathetic nervous system may be involved in the renal regulation of solute-free water excretion. The effects of interruption of parasympathetic pathways by bilateral cervical vagotomy were examined in eight normal and seven hypophysectomized anesthetized dogs undergoing a water diuresis. In the normal animals cervical vagotomy decreased free-water clearance (C(H2O)) from 2.59+/-0.4 se to -0.26+/-0.1 ml/min (P < 0.001), and urinary osmolality (U(osm)) increased from 86+/-7 to 396+/-60 mOsm/kg (P < 0.001). This antidiuretic effect was not associated with changes in cardiac output, renal perfusion pressure, glomerular filtration rate, renal vascular resistance, or filtration fraction and was not affected by renal denervation. A small but significant increase in urinary sodium and potassium excretion was observed after vagotomy in these normal animals. Pharmacological blockade of parasympathetic efferent pathways with atropine, curare, or both was not associated with an alteration in either renal hemodynamics or renal diluting capacity. In contrast to the results in normal animals, cervical vagotomy was not associated with an antidiuretic effect in hypophysectomized animals. C(H2O) was 2.29+/-0.26 ml/min before and 2.41+/-0.3 ml/min after vagotomy, and U(osm) was 88+/-9.5 mOsm/kg before vagotomy and 78+/-8.6 mOsm/kg after vagotomy in the hypophysectomized animals. Changes in systemic or renal hemodynamics or electrolyte excretion were also not observed after vagotomy in these hypophysectomized animals. On the basis of these results, we conclude that the antidiuretic effect associated with cervical vagotomy is initiated by interruption of parasympathetic afferent pathways and is mediated by increased endogenous release of vasopressin. This antidiuresis was also demonstrated to occur in the absence of renal nerves and alterations in systemic and renal hemodynamics.
TL;DR: Lithium has a similar effect on the antidiuretic activity of oxytocin and choline on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.
Abstract: 1. The effect of intravenous infusions of various ions on the antidiuretic action of antidiuretic hormone has been studied in rats.
2. Lithium (13 mmol/l.) reversibly inhibits the antidiuretic responses. Similar concentrations of potassium, rubidium, strontium, magnesium, choline and calcium do not. Lithium has a similar effect on the antidiuretic activity of oxytocin.
3. The inhibition is not simply related to blood nor whole body lithium concentrations.
4. Lithium (2 mmol/l.) in contact with the serosal surface also inhibits the transport of water facilitated by either 0·5 U/l. antidiuretic hormone or 1·1 mmol/l. cyclic adenosine monophosphate in the isolated toad bladder.
5. Choline (2 mmol/l.) on the serosal surface also inhibits the transport of water facilitated by vasopressin in the toad bladder.
TL;DR: The specific radioactivities of isotopically pure oxytocin and vasopressin prepared from the neural lobe of the pituitary gland have been measured at various times after an intracisternal injection of [3H]tyrosine.
Abstract: 1. The specific radioactivities of isotopically pure oxytocin and vasopressin prepared from the neural lobe of the pituitary gland have been measured at various times after an intracisternal injection of [3H]tyrosine.
2. Radioactive hormone began to appear in the gland 1-2 hr after the injection which suggests an intra-axonal transport velocity of 1-2 mm/hr.
3. From 7 days onwards the specific radioactivity of each hormone declined exponentially with the same rate constant and a half-life of about 13 days.
4. If the decline in radioactivity can be equated with the release of the hormones, the rates of secretion for the male rat in water balance are 18·7 m-u./day for oxytocin and 28·9 m-u./day for vasopressin.
5. Calculation from the secretion rates gave steady-state plasma concentrations of about 3 μu./ml. for each hormone.
TL;DR: It is suggested that neurological dysfunction associated with the syndrome of inappropriate secretion of ADH is unlikely to be due to cerebral edema but may be related to the decreased potassium content of brain tissue.
Abstract: Administration of fluid and vasopressin injection to rats induced within 24 to 48 hours a condition which can be considered as an experimental model of the syndrome of inappropriate secretion of antidiuretic hormone (ADH). Concurrently with hyponatremia and hypoosmolarity in serum, the changes in muscle consisted of a fall in sodium content and a decrease in percentage dry weight equivalent to 12% swelling. There was no loss of potassium from muscle. In contrast, in brain the decrease in sodium content was smaller, the tissue percentage dry weight decreased only slightly, indicating minimal swelling, and there was a significant net loss of potassium. It is suggested that neurological dysfunction associated with the syndrome of inappropriate secretion of ADH is unlikely to be due to cerebral edema but may be related to the decreased potassium content of brain tissue.
Journal Article•
TL;DR: The results are in agreement with the contention that the specific association of neurophysin I with oxytocin and of Neurophysin II with vasopressin in neurosecretory granules is a result of compartmentalization during the biosynthesis of the neurohypophysial hormones and neurophysIn proteins.
Abstract: Native bovine neurophysin II has one binding site per monomer for lysine-vasopressin at physiological pH (pH 7.38), as revealed by equilibrium dialysis. Oxytocin is bound to neurophysin II with the same or slightly greater affinity than vasopressin, but binding of the two hormones is competitive. The affinities of vasopressin and oxytocin for neurophysins I and II are essentially the same. Substitution of the asparagine (position 5) and glycinamide (position 9) residues in oxytocin by valine and glycine, respectively, has no substantial effect on binding of the resulting analogues to neurophysin; substitution of the glutamine residue by ornithine in position 4 of oxytocin slightly increases the affinity of the analogue for neurophysin II. The results are in agreement with the contention that the specific association of neurophysin I with oxytocin and of neurophysin II with vasopressin in neurosecretory granules is a result of compartmentalization during the biosynthesis of the neurohypophysial hormones and neurophysin proteins. The relatively low binding constants of neurohypophysial hormones to neurophysin proteins at physiological pH assure complete dissociation of the hormone-protein complexes after their release into the blood. Our observations also show that the specificity of the hormone-binding site of neurophysin proteins for the neurohypophysial hormones differs from that of the hormone receptors.
TL;DR: The secretion of vasopressin in response to haemorrhagic shock has been investigated in anaesthetized dogs and the results confirmed the role of EMT in this response.
Abstract: 1 The secretion of vasopressin in response to haemorrhagic shock has been investigated in anaesthetized dogs
2 The changes in the plasma concentrations of vasopressin were followed over a period of 5 hr, during which the arterial blood pressure was kept constant at 40 mm Hg It was found that vasopressin concentration in plasma rose to a high peak shortly after the onset of shock and gradually declined thereafter Five hours later, it was still 3·5 times higher than control Re-transfusion of blood was followed by a return to control levels
3 The clearance of vasopressin was calculated before and during shock in normal dogs and in dogs with experimental diabetes insipidus Soon after the onset of shock, the clearance rate dropped to one quarter of its normal level but slowly recovered, returning to near control values at the fifth hour of shock Clearance rates did not vary as a function of infusion rates, suggesting that there is no maximal transport rate for the removal of the hormone over the entire secretory range found in normal and hypotensive dogs
4 From the clearance rates and from the plasma concentrations of endogenously secreted vasopressin it has been possible to calculate the approximate secretory rates of the hormone in response to shock Secretion rose to a very high level, some 40 times greater than control, at the onset of shock This was followed by a fairly constant secretory plateau At the fifth hour of shock secretion was 3·5 times higher than control
5 The half-life of vasopressin was measured in normal and hypotensive dogs Control measurements confirm the generally accepted value of approximately 5 min The half-life was significantly higher in the early stage of shock, but returned to control values in the later stage
6 Haemorrhage experiments performed in normal and diabetic dogs suggest that vasopressin may play a part in the development of irreversible haemorrhagic shock: all normal animals died within a few hours of retransfusion, whereas four out of eight diabetic dogs similarly treated survived a 24 hr observation period In a separate set of experiments, eight diabetic dogs were subjected to the haemorrhage procedure while receiving a constant infusion of vasopressin: only two of these survived Surviving dogs showed none of the characteristic lesions of irreversible haemorrhagic shock
TL;DR: The hypothesis that prostaglandins may play a role in the regulation of hormonal effects in the kidney is supported by the enhanced release by vasopressin.
TL;DR: Dose‐response curves were obtained for intravenous infusions of adrenaline, noradrenaline, angiotensin, vasopressin and histamine in cats anaesthetized with pentobarbitone and there was no evidence that these agents caused net transsinusoidal fluid movements.
Abstract: 1. Hepatic volume was recorded by a plethysmographic technique in cats anaesthetized with pentobarbitone; the hepatic artery and portal vein remained intact. Dose-response curves were obtained for intravenous infusions of adrenaline, noradrenaline, angiotensin, vasopressin and histamine.2. Adrenaline and noradrenaline decreased hepatic blood volume and did not differ significantly in potency. Up to 40% of the hepatic blood volume was expelled by doses within the range secreted by the adrenal medullae.3. Isoprenaline, infused into the hepatic artery, had no significant effect on hepatic blood volume in doses which caused maximal vasodilatation of the hepatic arterial bed. Relaxation of hepatic capacitance vessels mediated by beta-adrenoceptors did not occur.4. Angiotensin infusions in doses previously shown to cause intestinal and splenic vasoconstriction, decreased hepatic blood volume and on a molar or microgramme basis, angiotensin was the most potent of the agents tested. Doses within the probable physiological range of endogenous production decreased hepatic blood volume by up to 20%. The responses were not significantly different when the hepatic nerves were intact or sectioned.5. Vasopressin infusions produced only small decreases in hepatic blood volume. Doses within the range secreted by the posterior pituitary which constrict the intestinal and splenic resistance vessels, did not decrease hepatic blood volume by more than 10%.6. Histamine produced no change in hepatic blood volume in doses which readily produce outflow block in dogs. Either the specific hepatic venous smooth muscle involved in outflow block is absent in the cat or it has no histamine receptors.7. After the rapid change in hepatic blood volume at the onset of the infusion, hepatic volume remained steady for the duration of each infusion. There was no evidence that these agents caused net transsinusoidal fluid movements.
TL;DR: Exsanguinating esophageal varices which could not be stopped by a Sengstaken-Blakemore tube were controlled by the constant infusion of vasopressin into the superior mesenteric artery.
Abstract: Exsanguinating esophageal varices which could not be stopped by a Sengstaken-Blakemore tube were controlled by the constant infusion of vasopressin into the superior mesenteric artery. At autopsy, the varices and small mesenteric veins were thrombosed, and there was segmental infarction of the small intestine. Intermittent infusion of vasopressin, portal pressure monitoring, and serial serum lactic acid determinations might be helpful in preventing this complication of an extremely valuable procedure.
TL;DR: The results are interpreted as indicating that the foregoing permissive effects of aldosterone on the permeability responses to vasopressin and theophylline are mediated by a steroid-dependent increase in the accumulation of cAMP in the pertinent epithelial cells, probably as a consequence of a diminution in the rate of degradation of the intracellular nucleotide.
Abstract: Vasopressin and theophylline both increase the content of adenosine 3′:5′-cyclic monophosphate (cAMP) in epithelial cells of the urinary bladder of toads (Bufo marinus). Incubation of the tissue with 0.2 μM aldosterone markedly increases this response to the two agents; incubation for a similar time without steroid reduces the response. The permeability responses (sodium transport and water flow) of the intact tissue to vasopressin, theophylline, and exogenous cAMP are also considerably greater in bladders incubated with aldosterone than without. The results are interpreted as indicating that the foregoing permissive effects of aldosterone on the permeability responses to vasopressin and theophylline are mediated by a steroid-dependent increase in the accumulation of cAMP in the pertinent epithelial cells, probably as a consequence of a diminution in the rate of degradation of the intracellular nucleotide.
TL;DR: The infusion of angiotensin II in hydrated dogs anesthetized with either pentobarbital, or sedated with morphine and anesthenized with urethane and chloralose produced no effect on the plasma levels of vasopressin in the present investigation.
Abstract: The relationship between iv infusions of angiotensin II and vasopressin release has been investigated in the anesthetized dog. In dogs sedated with morphine and anesthetized with a mixture of chloralose and urethane, a 40-min iv infusion of angiotensin II ranging from 10-60 ng/ kg/min failed to stimulate the release of vasopressin. This was observed when the control plasma levels of vasopressin were moderately elevated due to anesthesia and surgical trauma, approximately 15 M*U/ml, or when suppressed by hydration to approximately 3 nU/ml. In hydrated dogs anesthetized with pentobarbital and subjected to less surgery, the starting levels of vasopressin were 1.2 H-U/ml. In these dogs a 75-min infusion of 10 ng/kg/min of angiotensin II into a common carotid artery also failed to stimulate the release of vasopressin. {Endocrinology 90: 1647, 1972) T T HAS BEEN reported that the administra•*• tion of angiotensin directly into the ventricles of the brain in the anesthetized dog (1), the hydrated conscious goat (2), and the conscious rat (3) results in an increased release of vasopressin from the posterior pituitary. It has also been claimed that the circulating levels of vasopressin are elevated following the infusion of angiotensin II via a peripheral vein in the conscious dog (4) and a common carotid artery in the dog anesthetized with pentobarbital (1). However, the changes in the plasma vasopressin concentration in these experiments in which the angiotensin was injected into the circulation were quite small, and the results of only three experiments were reported by Mouw et al. (1). In addition, one wonders to what extent the findings in the conscious dogs (4) were influenced by emotional reactions to the experimental procedure and to the increase in blood pressure induced by the angiotensin. In view of these considerations and reports of several situations in which plasma levels of renin and vasopressin fail to change in a parallel fashion (5,6), it seemed advisable to reinvestigate the effect of the systemic infusion of angiotensin Received October 28, 1971. This work has been supported by grants HL-12990 from the National Heart Institute, USPHS, and HL-14242 (Specialized Center of Research in Hypertension). Computer assistance was supported by grant HL-09495 from the National Heart Institute, USPHS. The authors express their gratitude for the able technical assistance of Miss J. T. Crofton and Mr. S. E. Pienaar. II on the plasma concentration of vasopressin. Because of the cardiovascular effects of angiotensin, some of these studies were accompanied by measurements of arterial mean and pulse pressures and left atrial pressure, factors which play an important role in the control of vasopressin release. The infusion of angiotensin II in hydrated dogs anesthetized with either pentobarbital, or sedated with morphine and anesthetized with urethane and chloralose produced no effect on the plasma levels of vasopressin in the present investigation. Similar observations are obtained in normally hydrated dogs under morphine-urethane-chloralose anesthesia. Materials and Methods All experiments were performed on male mongrel dogs weighing 14.5-26.0 kg. Some dogs were sedated with a sc injection of 0.1 ml/kg of 2.0% morphine and anesthetized with an iv infusion of a mixture of urethane (6.0%) and chlorolose (0.6%) in 0.9% saline, approximately 9.0 ml/kg. Others were anesthetized with iv infusions of approximately 1.0 ml/ kg of 3.0% sodium pentobarbital. Surgery. The trachea and right and left femoral arteries and veins were cannulated in all dogs. In the dogs receiving morphine, urethane and chloralose anesthesia, the chest was opened in the fourth intercostal space on the left side, so that the left atrium could be catheterized via the atrial appendage. During this procedure the dog's respiration was maintained by positive pressure ventilation. The intercostal incision was then closed and a catheter was left in the pleural cavity. The chest was evacuated, arti-
TL;DR: By coupling purification on silicagel column and thin-layer chromatography with quantitation on gas-liquid chromatography, the concentrations of progesterone, 5β-pregnane- 3,20-dione and 3β-hydroxy-5 β-pregnan-20-one in the ovarian venous plasma of proestrous rats were determined with good accuracy and reproducibility.
Abstract: By coupling purification on silicagel column and thin-layer chromatography with quantitation on gas-liquid chromatography 5apregnane- 3,20-dione, progesterone, 3β-hydroxy-5apregnan- 20-one, 20β-hydroxy-5β-pregnan-3-one, 20βx-hydroxypregn-4-en-3-one and Sa-pregnane- 3β,20β-diol were specifically determined in the rat plasma with good accuracy and reproducibility. This method permitted measurement of as little as 0.2 μg of each steroid with average recovery rates within a range of 80-109%. A single iv injection of LH, FSH, TSH, HCG, and PMS resulted in a prompt and remarkable increase in the concentrations of progesterone, 5β-pregnane- 3,20-dione and 3β-hydroxy-5β-pregnan-20-one in the ovarian venous plasma of proestrous rats. The stimulation by FSH seems to be due to its LH content. Prolactin, ACTH, oxytocin, and vasopressin were ineffective. (Endocrinology 90: 1356, 1972)
TL;DR: It is suggested that the responsiveness of the toad bladder to antidiuretic hormones diminishes as the effective osmotic pressure of the interstitial fluids declines.
Abstract: The effect of dilution of the interstitial fluids on the responsiveness of the toad urinary bladder to antidiuretic hormones has been examined in vivo and in vitro. Toads were given periodic injections with vasopressin while in water so that their plasma osmolality fell below 190 mosmoles/kg H2O. The hydraulic conductivity of bladders which had been removed from the animal and fixed with 1% glutaraldehyde was 10-fold less in overhydrated toads than in normally hydrated controls. A similar inhibitory phenomenon was observed in in vitro studies, when the tonicity of Ringer's fluid in which the bladders were suspended was lowered from its isotonic value. Mannitol, but not urea, could be effectively substituted for one-half of the NaCl content of Ringer's fluid. In other experiments it has been shown that the responsiveness of the bladder to vasotocin is depressed during bulk water movement across the tissue. This "flux inhibition" was found to depend upon the velocity and the duration of water flow from mucosa to the serosa. It is suggested that the responsiveness of the toad bladder to antidiuretic hormones diminishes as the effective osmotic pressure of the interstitial fluids declines.
TL;DR: Chlorpropamide and acetaminophen are effective antidiuretic agents in diabetes insipidus and appear to act by sensitizing the kidney to the low levels of vasopressin that may continue to circulate in many patients with this disease.
Abstract: Chlorpropamide and acetaminophen are effective antidiuretic agents in diabetes insipidus. They appear to act by sensitizing the kidney to the low levels of vasopressin that may continue to circulate in many patients with this disease. To determine the mechanism of action of these agents, a series of studies of their effects on water flow was carried out in the isolated urinary bladder of the toad. The patterns of action of chlorpropamide and the phenylacetamides (phenacetin, acetaminophen and structurally related compounds) were compared to that of theophylline, a potent phosphodiesterase inhibitor. Theophylline enhanced the effect of low and saturating concentrations of vasopressin, enhanced the effect of cyclic AMP, had no effect on the inhibitory action of prostaglandin E1 (PGE1) and (at 3 × 10−3m) greatly increased water flow in the absence of vasopressin. Chlorpropamide differed from theophylline in all major respects, enhancing only low concentrations of vasopressin, inhibiting the effect of cyclic ...
TL;DR: The increase of short-circuit current seen in the presence of vasopressin is reduced by Li+.
TL;DR: Preliminary studies in the vole demonstrated that COH occurred and was significantly blocked by melatonin and Altschule's aqueous pineal extract, demonstrating the anti-FSH action by pineal principles in induced ovulators similar to that described above in spontaneous ovulators (mice).
TL;DR: The administration of estradiol benzoate and progesterone daily for three days has been found to “sensitize” rats to the growth hormone (GH) releasing activity of hypothalamic extracts to cause significant elevations of RIA-GH and had no depleting effect on pituitary GH concentration.
Abstract: The administration of estradiol benzoate, 50 μg, and progesterone, 25 mg, daily for three days has been found to “sensitize” rats to the growth hormone (GH) releasing activity of hypothalamic extracts. At ten minutes following the injection of 90% methanol extracts of 10 porcine hypothalamic fragments, a significant rise in radioimmunoassayable GH was detected (mean increase in pentobarbital anesthetized rats was 28.5 ng/ml ± 12.3 (SE) VS control of 1.6 ng/ml ± 7.9, p < 0.05). The equivalent of 25 hypothalamic fragments gave a significantly larger response. In a series of animals anesthetized with either pentobarbital or ether, 25 or 10-20 hypothalamic equivalents caused significant elevations of RIA-GH and had no depleting effect on pituitary GH concentration. Without steroid pretreatment, significant effects on plasma GH were not observed even with twenty-five hypothalamic equivalents. In steroid pretreated animals, large doses of vasopressin (5 U) and oxytocin (2 U) also induced GH discharge. TRH at a ...