Showing papers on "Vasopressin published in 1971"
TL;DR: To determine whether vasopressin affects the sensitivity of the anterior pituitary to corticotropin-releasing factor, vasopressingin was administered intravenously in doses subthreshold with respect to ACTH release to rats pretreated with dexamethasone (dex), Nembutal (Nem), and, sometimes, also morphine (morph).
Abstract: To determine whether vasopressin affects the sensitivity of the anterior pituitary to corticotropin-releasing factor, vasopressin was administered intravenously in doses subthreshold with respect to ACTH release to rats pretreated with dexamethasone (dex), Nembutal (Nem), and, sometimes, also morphine (morph). Crude ovine CRF was given intravenously immediately following the vasopressin. The adrenocortical response to CRF was increased at least 100% by the prior administration of subthreshold doses of vasopressin. When 1/20 of the intravenous dose of vasopressin was placed into both lobes of the anterior pituitary it again failed to release ACTH itself, but increased 2.5 times the response to CRF given intravenously. This potentiation of CRF-induced ACTH release by vasopressin at the adenohypophysis was not observed if the vasopressin was administered into one lobe only of the anterior pituitary. In rats pretreated with dex +Nem the potentiation was the same as in those pretreated with dex + Nem+morph. Ox...
242 citations
TL;DR: In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested, finding that these substances did not cause the rat to drink water.
Abstract: 1. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.
2. Injection of 0·001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.
3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.
4. β-aspartic acid1-valine5-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.
5. The (2–8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1–7) heptapeptide results in an inactive compound.
6. The (3–8) hexapeptide and the (4–8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1–4) and (5–8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.
7. Kallikrein, bradykinin, adenosine-3′5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.
8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
221 citations
TL;DR: OXYTOCIN, a potent stimulant of myometrial activity, is used extensively in clinical practice for the induction of labour and the role of endogenous oxytocin, however, has been disputed.
Abstract: OXYTOCIN, a potent stimulant of myometrial activity, is used extensively in clinical practice for the induction of labour. The fact that in animals circulating concentrations of this peptide are increased during labour and maximal at the time of delivery1,2 suggests that oxytocin released by the maternal posterior pituitary may play an important part in spontaneous labour. The role of endogenous oxytocin, however, has been disputed. Bioassays suggest that the circulating concentrations are increased to 100 µU/ml. or more3,4, while indirect evidence suggests that there is no more than 10 µU/ml., and perhaps much less5.
218 citations
TL;DR: Of 48 patients given selective mesenteric arterial infusion of vasopressin for the control of gastrointestinal hemorrhage, 28 were actively bleeding from varices secondary to portal hypertension, 14 were infused electively at the time of portosystemic shunt surgery, and 6 were infused because of hemorrhage from an arterial or capillary source demonstrated on prior selective arteriography.
Abstract: Of 48 patients given selective mesenteric arterial infusion of vasopressin for the control of gastrointestinal hemorrhage, 28 were actively bleeding from varices secondary to portal hypertension, 14 were infused electively at the time of portosystemic shunt surgery, and 6 were infused because of hemorrhage from an arterial or capillary source demonstrated on prior selective arteriography. The indications, technique, and results of the vasopressin infusions are described.
180 citations
TL;DR: Assays in hypophysectomized rats demonstrated that these peptides were devoid of direct adrenal-stimulating activity, and Amino acid content indicates that these products are peptide in nature and different in composition from conventional corticotropin-releasing-factor-like products.
Abstract: Evidence was found for the existence of four tumor peptides with corticotropin-releasing-factor-like (CRF) activity, two isolated from a pancreatic tumor (P-CRF-1, P-CRF-2) and two from the primary tumor and metastases of an oat-cell carcinoma (L-CRF-1, L-CRF-2). Tumor tissue was extracted for ACTH, and both tumors were demonstrated to certain ectopic ACTH. A peptide similar in size to ACTH and another, smaller than vasopressin, were isolated from each tumor. All four fractions appeared to be homogeneous on high-voltage electrophoresis at pH 6.5. Assays in hypophysectomized rats demonstrated that these peptides were devoid of direct adrenal-stimulating activity. CRF assays in the rat treated with chlorpromazine-morphine-pentobarbital showed ACTH-releasing activity comparable to the ACTH-releasing ability of 20 to 40 mU pressor activity of standard lysine vasopressin but no antidiuretice activity. Amino acid content indicates that these products are peptide in nature and different in composition f...
156 citations
TL;DR: It is inferred that vasopressin directly increases active ion transport in the cortical collecting tubule with much higher resistance than that previously reported for rat proximal convoluted tubules and is consistent with the much lower ionic permeability of the collecting tubules.
Abstract: HELMAN, S. I., J. J. GRANTHAM, AND M. B. BURG. Eject of vasopressin on electrical resistance of renal cortical collecting tubules. Am. J. Physiol. 220(6) : 1825-1832. 197 1 .-A method is reported for measuring the transepithelial potential difference and electrical resistance in isolated rabbit renal cortical collecting tubules. The mean resistance with isotonic perfusion fluid was 13.8 X lo4 ohm cm (tubule length) or 867 ohm cm2 (tubule luminal area). This resistance is much higher than that previously reported for rat proximal convoluted tubules and is consistent with the much lower ionic permeability of the collecting tubule. Vasopressin caused a transient increase in potential difference (PD) without any change in electrical resistance. It is inferred that vasopressin directly increases active ion transport in the cortical collecting tubule. Increasing the tubule diameter by elevation of perfusion pressure reduced the PI> without any change in electrical resistance.
126 citations
TL;DR: The dissociation of TSH and LH into two subunits raises a number of biological questions—for example, those concerning the control of biosynthesis of individual chains and the possible effects of releasing factors.
Abstract: Publisher Summary
This chapter describes the structure of thyrotropin and its relationship to luteinizing hormone (LH). The pituitary peptide hormones were among the first compounds to yield evidence for probable evolutionary relationships among proteins and peptides with different functions—that is, oxytocin and vasopressin; the corticotropins, melanotropins, and β-lipotropin; and more recently prolactin and growth hormone. The likelihood that follicle-stimulating hormone (FSH) contains subunits was recognized by Gray, and Papkoff and Ekblad reported that the FSH chain of LH may have common properties with a subunit of FSH. The dissociation of TSH and LH into two subunits raises a number of biological questions—for example, those concerning the control of biosynthesis of individual chains and the possible effects of releasing factors.
123 citations
TL;DR: It is proposed that Ca(++) inhibits the core enzyme directly since at the minimally inhibitory concentration (0.1 mm), CaCl(2) reduced to an equivalent extent basal activity, the response to graded doses of vasopressin and theresponse to maximal stimulatory concentrations of NaF.
Abstract: Adenyl cyclase activity was assayed in crude homogenates of the renal cortex, medulla, and papilla of the golden hamster. The specific activity (moles C-AMP/unit of time per mg protein of tissue) of the enzyme under basal conditions, was greatest in papilla, somewhat lower in medulla, and least in cortex. On an absolute scale, the sensitivity to vasopressin was greater in the medullary and papillary than in the cortical homogenates. In addition, at concentrations of 0.1-1.0 mm, CaCl(2) inhibited the enzyme in the order papilla > medulla > cortex. These results imply the existence of distinct differences in the composition of the adenyl cyclase-receptor complex in various parts of the kidney. We proposed that Ca(++) inhibits the core enzyme directly since at the minimally inhibitory concentration (0.1 mm), CaCl(2) reduced to an equivalent extent (a) basal activity, (b) the response to graded doses of vasopressin (0.5 to 50.0 mU/ml) and (c) the response to maximal stimulatory concentrations of NaF (10 mm). Prostaglandin E(1) (PGE(1) = 10(-7)m) had no effect on either basal adenyl-cyclase activity or the response to 10 mm NaF in medullary and papillary homogenates. 7-Oxa-13-prostynoic acid (10(-4)m) similarly had no effect under basal conditions or on stimulation with NaF in medullary homogenates. Both fatty acids, however, inhibited the enzymic response to vasopressin, particularly at low concentrations of the peptide. The straight-chain fatty acid, 11-eicosanoic acid (10(-7)m), was inactive on basal activity or on the response to vasopressin. The possibility that PGE(1) modifies the coupling mechanism between the core enzyme and the hormone-specific receptor is discussed.
118 citations
TL;DR: The cyclase of the tumor as well as of the adrenals was stimulated by adrenocorticotropic hormone (ACTH) over similar concentration ranges, and the tumor enzyme was also stimulated by epinephrine, norepinephrine, and thyroid-stimulating hormone (TSH).
Abstract: Properties of adenyl cyclase of normal adrenals and of a corticosterone-producing adrenal cancer of the rat have been compared. Enzyme activity was found in all particulate fractions of both tissues. The cyclase of the tumor as well as of the adrenals was stimulated by adrenocorticotropic hormone (ACTH) over similar concentration ranges. Unexpectedly, the tumor enzyme was also stimulated by epinephrine, norepinephrine, and thyroid-stimulating hormone (TSH). These hormones produced a dose-related effect over a concentration span that was comparable with that for ACTH. The tumor cyclase was not responsive to angiotensin Il, vasopressin, glucagon, insulin, growth hormone, parathyroid hormone, and thyrocalcitonin. ACTH was the only hormonal preparation that stimulated normal adrenal cyclase. These findings are compatible either with the possibility that the adenyl cyclase receptor of the tumor has undergone structural alteration with a consequent loss of specificity for ACTH or with the possibility that the tumor possesses several cyclase regulatory receptors.
111 citations
TL;DR: Results in the inner medulla are consistent with the hypothesis that PGE(1) can compete with vasopressin for adenyl cyclase-binding sites, but the findings in the outer medulla suggest the situation is more complex.
Abstract: A B S T R A C T Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3',5'-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E1 (PGE1), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE1 can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10 M PGE1 had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE1 increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.
107 citations
TL;DR: Electrical recordings were made from antidromically identified supraoptic and paraventricular units during intracarotid injections of hypertonic and isotonic sodium chloride solutions in rats to study the effects of these injections onopsis and EMT.
Abstract: 1. Electrical recordings were made from antidromically identified supraoptic and paraventricular units during intracarotid injections of hypertonic and isotonic sodium chloride solutions in rats.
2. The blood concentrations of vasopressin and oxytocin were estimated by bio-assay before and at different intervals after similar injections.
3. Although a significant change in the action potential activity of the supraoptic nucleus was associated with hormone release, the results were not entirely consistent with a simple relationship between action potential activity and hormone secretion. Firstly, although some units were excited by the stimulus a substantial number were inhibited. Secondly, the blood concentration of the hormones, particularly ADH, remained elevated for longer than might have been expected if additional hormone had ceased to be secreted as soon as firing rates had returned to control values.
4. There were substantial differences between the initial blood concentrations of vasopressin and oxytocin but the firing rates of units in the supraoptic and paraventricular nuclei appeared to be the same.
5. Although significantly less paraventricular than supraoptic units were affected by hypertonic injections the blood concentration of oxytocin was increased by a factor of 8 whereas that of vasopressin was increased by a factor of 2·7.
TL;DR: A sensitive double-antibody radioimmunoassay for the measurement of arginine vasopressin (AVP) in plasma is described and shows a good correlation with plasma osmolality.
Abstract: A sensitive double-antibody radioimmunoassay for the measurement of arginine vasopressin (AVP) in plasma is described. Vasopressin has been extracted from plasma by adsorption to Florisil followed by elution with acidacetone. Assay of serial dilutions of such extracts shows that they behave in the assay system in the same way as synthetic AVP standards. Recovery of added vasopressin from plasma averaged 45.7±8.1 % (sd). Plasma AVP concentration (uncorrected for recovery) in mildly dehydrated subjects ranged from less than 1 to 4.3 pg/ml, and showed a good correlation with plasma osmolality. After nicotine, concentrations up to 21.8 pg/ml were found, and in 4 subjects with the syndrome of inappropriate ADH secretion levels ranged from 24.0 to 102.1 pg/ml.
TL;DR: It is concluded that vasopressin constitutes a probe for the rapid reproducible determination ofENa under a wide variety of physiological conditions.
Abstract: Vasopressin stimulates Na(+) transport across toad bladder largely or entirely by decreasing the resistance to Na(+) entry into the transporting epithelial cells. Therefore, the hormone should induce proportional changes in short circuit current (I S ) and tissue conductance; the ratio of these changes should equal the driving force (E Na) of the Na(+) pump.Administration of vasopressin provided a rapid, reversible and reproducible technique for the measurement ofE Na. Values calculated forE Na ranged from 74 to 186 mV, in agreement with previously published estimates. The results were not dependent on the vasopressin concentration over a wide range of concentrations.Ouabain, an agent thought to inhibit specifically the Na(+) pump, decreased bothI S andE Na. On the other hand, amiloride, a diuretic thought to block specifically Na(+) entry, markedly reducedI S , without reducingE Na.It is concluded that vasopressin constitutes a probe for the rapid reproducible determination ofE Na under a wide variety of physiological conditions.
TL;DR: It is suggested that two proteins present in the gland in the same ratio as the hormones vasopressin and oxytocin-neurophysin of theRat neurohypophysial extracts are the vasoppressin-Neurophys in the rat.
Abstract: 1. Rat neurohypophysial extracts have been examined by polyacrylamide-gel electrophoresis. 2. Three of the proteins were tentatively identified as neurophysins by their acidic nature and their disappearance after dehydration of the animals. 3. These proteins were radioactive 24h after intracisternal injection of [(35)S]cysteine. 4. Two of the proteins were present in much greater quantities than the third, and these two were present in the gland in the same ratio as the hormones vasopressin and oxytocin. 5. One of these proteins was absent from glands of rats homozygous for diabetes insipidus but present in heterozygous animals. 6. It is suggested that these two proteins are the vasopressin-neurophysin and oxytocin-neurophysin of the rat.
TL;DR: Oxytocin and vasopressin content of the neurohypophysis was determined by means of bioassays in pregnant rats before, during, and after spontaneous as well as Oxytocin- induced parturition, indicating that no neurophypophysial accumulation of oxytocin was found.
Abstract: Oxytocin and vasopressin content of the neurohypophysis was determined by means of bioassays in pregnant rats before, during, and after spontaneous as well as oxytocin- induced parturition. Before parturition the levels of oxytocin and vasopressin in the neural lobe were equal on Days 21 and 22 of gestation. Immediately after spontaneous parturition the content of both hormones was about 60% of the prelabor values. At the delivery of the first fetus the oxytocin level had decreased by only about 10%, which is not a significant difference, while the vasopressin content of the posterior lobe was almost as low as at the end of parturition. When parturition was induced by oxytocin or combined oxytocin-arginine-vasopressin infusions, the pituitary oxytocin level was unchanged but the level of vasopressin was as low as after spontaneous delivery. Infusions of exogenous hormone to pregnant rats before term did not alter the endogenous hormone levels, indicating that no neurophypophysial accumulation of oxytocin ...
TL;DR: The data are interpreted as indicating impairment of the osmoreceptor mechanism as the primary cause of the hyperosmolar syndrome and that vasopressin secretion was regulated primarily by changes in effective blood volume.
Abstract: A physiological explanation for sustained hyperosmolality was sought in a patient with histiocytosis. During 23 days of observation with only sodium intake regulated at 100 mEq daily, elevation (mean 310 mOsm/kg of water) and fluctuation (range 298-323) of the fasting plasma osmolality were recorded. The presence of endogenous vasopressin was indicated by the patient's ability to concentrate the urine to as high as 710 mOsm/kg of water with a creatinine clearance of 84 cc/min, and by dilution of the urine in response to alcohol. The failure of increasing fluid intake to as high as 6.2 liters daily to lower the plasma osmolality indicated that deficient fluid intake was not solely responsible for the elevated plasma osmolality. Hypertonic saline infusion during water diuresis resulted in the excretion of an increased volume of dilute urine. The water diuresis continued despite a rise in plasma osmolality from 287 to 339. An isotonic saline infusion initiated during hydropenia resulted in a water diuresis which continued despite a rise in the plasma osmolality from 303 to 320. Stable water diuresis induced during recumbency by either oral ingestion of water or intravenous infusion of normal saline was terminated by orthostasis and resumed with the return to the recumbent position. Antecedent alcohol ingestion blocked the antidiuresis of orthostasis. The data are interpreted as indicating impairment of the osmoreceptor mechanism as the primary cause of the hyperosmolar syndrome. They also indicate that vasopressin secretion was regulated primarily by changes in effective blood volume. Chlorpropamide was found to be an effective treatment for the syndrome.
TL;DR: The data suggest that inappropriately elevated levels of ADH play a major role in the defect in water excretion of anterior hypopituitarism, and that Glucocorticoids appear to be necessary for a normal neurohypophyseal response to inhibitory stimuli.
Abstract: To evaluate the role of antidiuretic hormone (ADH) in the defect in water excretion which is characteristic of glucocorticoid deficiency, the effects of hydrocortisone and ethanol upon urinary dilution during a sustained water load were studied in patients with anterior hypopituitarism. A spectrum of defects in urinary dilution was found in the seven patients with anterior hypopituitarism, and the subjects were separable into two groups. Four patients were unable to excrete a urine hypotonic to plasma (group I) while three diluted the urine (group II). In two of the group II patients, despite maintenance of hydration, urinary osmolality later rose to hypertonicity. Physiological doses of hydrocortisone improved urinary dilution in all patients. Submaximal doses of oral hydrocortisone, when given to the group I patients, converted their response to hydration to one characteristic of the group II patients, i.e., an initial hypotonic urine followed by a secondary rise to hypertonicity. Ethanol, a known inhibitor of ADH secretion, had no effect in the group I patients. When two of these patients were pretreated with sub-maximal doses of hydrocortisone, however, so that they were able to transiently dilute the urine, ethanol prevented the secondary rise in urine osmolality. Similarly, the administration of ethanol to the untreated group II patients, when the urine was hypotonic, improved diluting ability as characterized by a lowering of urinary osmolality and an increased excretion of solute-free water in all three patients. Hydrocortisone did not improve urinary dilution in three patients with complete hypophyseal diabetes insipidus and one with both anterior and posterior insufficiency receiving constant infusions of vasopressin. These data suggest, therefore, that inappropriately elevated levels of ADH play a major role in the defect in water excretion of anterior hypopituitarism. Glucocorticoids appear to be necessary for a normal neurohypophyseal response to inhibitory stimuli.
TL;DR: An examination of fractions from extracts of porcine pituitary has revealed the presence of a number of peptide components active in restoring the ability of hypophysectomized rats to acquire a conditioned avoidance response.
TL;DR: In anaesthetized dogs urinary bladder distension caused variable changes of mean blood pressure; these were unaffected by vagotomy and cervical vagotomy did not abolish the antidiuresis.
Abstract: 1. In anaesthetized dogs urinary bladder distension caused variable changes of mean blood pressure; these were unaffected by vagotomy. 2. Catecholamines were detected in the circulation during bladder distension in fourteen of seventeen dogs. The catecholamine concentration during bladder distension was greater after cervical vagotomy. 3. Vasopressin could not be detected in the blood during urinary bladder distension before or after section of the cervical vagus nerves. Cervical vagotomy itself resulted in a. transient release of vasopressin. 4. A prostaglandin-like material was sometimes detected in the circulation during or immediately after urinary bladder distension. The origin of this material was not determined; it was detected in arterial and venous blood. 5. Urine flow consistently decreased during urinary bladder distension. This decrease was due neither to circulating catecholamines nor to vasopressin; it was probably caused by renal sympathetic activity. Cervical vagotomy did not abolish the antidiuresis.
TL;DR: The complete amino acid sequence of bovine neurophysin II, a 97 amino acid protein which specifically binds the posterior pituitary hormones oxytocin and arginine vasopressin, is proposed.
TL;DR: The influence of alterations in blood volume on osmotically-induced vasopressin release has been determined in normal subjects and the plasma osmolality at which vasoppressin release was initiated is determined.
Abstract: The influence of alterations in blood volume on osmotically-induced vasopressin release has been determined in normal subjects. The plasma osmolality at which vasopressin release was initiated (osmoti
TL;DR: It was found that, in hemibladders mounted in chambers and bathed on their mucosal surface by sodium Ringer's with24Na, the gains of chemical sodium and24Na after vasopressin were equivalent.
Abstract: Isolated sheets of epithelial cells as well as epithelial cells scraped from paired hemibladders mounted in chambers both showed significant increases in water, sodium and chloride contents after exposure to vasopressin (100 mU/ml), without any change in potassium content. In the isolated cells these changes were prevented by amiloride (10−5m), suggesting that the gain of sodium after vasopressin occurs across the mucosal membrane. This hypothesis was confirmed in experiments in which it was found that, in hemibladders mounted in chambers and bathed on their mucosal surface by sodium Ringer's with24Na, the gains of chemical sodium and24Na after vasopressin were equivalent.
TL;DR: Sensitive and specific immunofluorescence techniques have been used to show that the hormonebinding protein for lysine vasopressin (porcine neurophysin-n) occurs throughout the hypothalamoneurohypophysial system of the adult and neonatal pig and is localized principally in the neurosecretory neurons arising from the supraoptic nucleus.
Abstract: Sensitive and specific immunofluorescence techniques have been used to show that the hormonebinding protein for lysine vasopressin (porcine neurophysin-n) occurs throughout the hypothalamoneurohypophysial system of the adult and neonatal pig and is localized principally in the neurosecretory neurons arising from the supraoptic nucleus. The results are discussed with reference to the hypothesis that the supraoptic and paraventricular nuclei are concerned with the elaboration of vasopressin and oxytocin respectively.
TL;DR: The activation energy for the diffusion of water across the epithelial cell layer of the toad bladder was determined in the absence and presence of vasopressin and results are consistent with an increase in the number rather than the size of aqueous channels in the cell membrane, which differs from the generally held view that the hormone increases the radius of pores in the membrane.
Abstract: The activation energy (E(A)) for the diffusion of water across the epithelial cell layer of the toad bladder was determined in the absence and presence of vasopressin. An experimental approach was employed which minimized the effects of unstirred layers and the thick supporting layer of the bladder on the measurement of water diffusion. E(A) in the absence of vasopressin was 11.7 +/-1.4 kcal.mole(-1); after vasopressin it was 10.6+/-1.1 kcal.mole(-1). The difference between the two values was not significant. The results are consistent with an increase in the number rather than the size of aqueous channels in the cell membrane, a finding which differs from the generally held view that the hormone increases the radius of pores in the membrane.
TL;DR: The cultured hypothalamic tissues of the guinea pig that were pulsed with [(3)H]uridine incorporated label into the RNA of neurosecretory neurons, as determined by radioautography and chemical analysis.
Abstract: Fragments of the anterior hypothalamus that contain supraoptic nuclei and short axonal segments from adult guinea pigs have been kept in organ culture for up to 15 days. Electron micrographs displayed intact nuclei, Nissl substance, Golgi bodies, and an ultrastructure characteristic of viable neurosecretory cells; by contrast, the surrounding neurophil showed extensive degeneration. The cultured hypothalamic tissues of the guinea pig that were pulsed with [3H]uridine incorporated label into the RNA of neurosecretory neurons, as determined by radioautography and chemical analysis. Furthermore, and most important, these cells retained a complement of hormones and the ability to incorporate 3H- and 35S-labeled amino acids into vasopressin, neurophysin, and other polypeptides. This incorporation was inhibited by either puromycin or cycloheximide.
TL;DR: It is shown that the effect of the hormone on the sodium pump is not dependent on the presence of sodium in the serosal medium, and it is presented that under control conditions, the pump rate coefficient is a decreasing function of the pool size, a characteristic feature of a saturating system.
Abstract: In the accompanying paper, a compartmental model for the toad bladder sodium transport system was developed. In the present paper, the model is tested by determining the effects of antidiuretic hormone on the pools and fluxes. It is shown that this hormone affects only that sodium pool previously designated as the transport pool, and that the effects are on two separate sites. In the first place, the hormone stimulates entry at the mucosal side of the transport compartment, and by this means brings about an increase in the amount of sodium contained in the compartment. Second, the hormone has a distinct stimulatory effect on the rate coefficient for efflux across the serosal boundary, the pump rate coefficient. Evidence is presented that under control conditions, the pump rate coefficient is a decreasing function of the pool size, a characteristic feature of a saturating system. Therefore, the effect of vasopressin in increasing both the pool size and the pump rate coefficient must be construed as a direct effect on the pump, and not one which is secondary to the increase in the pool size. Furthermore, it is shown that the effect of the hormone on the sodium pump is not dependent on the presence of sodium in the serosal medium.
TL;DR: The concentration of neurophysin increased progressively from the hypothalamus along thepituitary stalk to the posterior pituitary lobe, where the concentration was 1000 times that found in the hypothalamic lobe.
Abstract: Neurophysin is a generic term for neurohypophysial proteins that bind vasopressin and oxytocin. Two such substances, peptides II and III, were isolated from porcine posterior pituitary glands. Antiserum against either peptide II or III cross-reacted with both polypeptides. The antisera formed lines of identity in Ouchterlony plates with posterior pituitary extracts of rat, rabbit, guinea pig, dog, lamb, cattle, monkey and human. A radioimmunoassay with a sensitivity of 1 ng/ml of neurophysin was utilized for measuring neurophysin in the neurohypophysis and in serum. The concentration of neurophysin increased progressively from the hypothalamus along the pituitary stalk to the posterior pituitary lobe, where the concentration was 1000 times that found in the hypothalamus. Neurophysin in several species had the same molecular weight; however, its electrophoretic mobility varied considerably in different species. In pigs, serum neurophysin appeared similar in molecular weight, electrophoretic mobility and im...