Showing papers on "Epinephrine published in 1971"

Resting plasma catecholamine concentrations in patients with depression and anxiety.

Abstract: The total resting plasma catecholamine concentration from 13 drugfree, depressed patients was found to be significantly elevated over concentrations from 47 normal controls. Differential determinations of epinephrine and norepinephrine revealed that both catecholamine components were elevated in the Patients. The literature on norepinephrine concentrations in brain, spinal fluid, and urinary excretion was reviewed and indicated that rather than being decreased, norepinephrine has been found to be either unchanged or increased in depressed patients.

The role of cyclic amp in the interaction of glucagon and insulin in the control of liver metabolism

Abstract: It is now well established that insulin exerts direct effects on mammalian liver to inhibit the production of glucose and urea and to promote the uptake of potassium ions. It has been proposed that these effects of insulin may be partly due to a decrease in liver cyclic AMP.l The proposal is based on the following observations: ( 1) insulin produces a small but significant decrease in the level of cyclic AMP in the perfused rat liver; (2) depletion of insulin in vivo by treatment with insulin antiserum or alloxan results in a twofold increase in liver cyclic AMP; (3) exogenous cyclic AMP and hormones such as glucagon and epinephrine which raise the level of cyclic AMP produce effects on the liver which are opposite to those caused by insulin; (4) insulin antagonizes the actions of epinephrine, glucagon, or cyclic AMP in the perfused liver; and ( 5 ) insulin reduces the accumulation of liver cyclic AMP in the presence of glucagon. In this article we will present more recent observations on the interaction of glucagon, epinephrine, and insulin in the control of hepatic metabolism. The investigations have employed the isolated rat liver perfused by a modification of the technique of Mortimore.* The perfusion medium consisted of Krebs-Henseleit bicarbonate buffer containing 3 % bovine albumin and 20% bovine erythrocytes. Livers were from fed rats weighing 100-150 g and the perfusion flow rate was about 7 ml per minute. The perfusions were carried out in two ways. In most cases, livers were perfused for one hour with recirculating medium and hormones were infused into the portal vein at a constant rate. In these experiments, the hormone concentrations were calculated by dividing the quantity of hormone infused during the hour by the final volume of perfusate. Since this does not allow for degradation of hormone, the values are doubtlessly overestimated. In the second type of experiment livers were perfused initially for 20 minutes with recirculating media containing no additions in order to establish steady metabolic rates and levels of cyclic AMP. The perfusion system was then changed to one with nonrecirculating medium by diverting the perfusate leaving the liver into a beaker. After a six-minute control period, infusions of hormone were commenced and livers and effluent media were sampled at designated intervals. In these experi-

Effect of anterior pituitary perfusion and intraventricular injection of catecholamines on prolactin release.

Abstract: In rats, the median eminence, pituitary stalk and anterior pituitary were exposed parapharyngeally and catecholamines were injected into the third ventricle or infused into a stalk portal vessel, peduncular artery, or a tuberalis ramus of an infundibular artery. Ten min after 1.25 μg dopamine hydrochloride was injected into the third ventricle, the plasma prolactin concentration was 70% of the preinjection value; 47% at 20 min; 42% at 30 min; 57% at 60 min; 69% at 90 min; and 93% at 120 min. Similar responses occurred following the administration of 2.5 μg dopamine. Quantities of dopamine greater than 2.5 jug caused less inhibition of release, however. Intraventricular injection of 2.5 or 5 μg of epinephrine or norepinephrine bitartrate did not affect prolactin release although 100 μg did. Dopamine, epinephrine, or norepinephrine, perfused into the anterior pituitary for 30 min via a hypophysial portal vein, had no effect on prolactin release. Dopamine, infused into the stalk-median eminence complex via t...

Adrenocortical control of epinephrine synthesis

Abstract: Adrenal medulla biochemistry and morphology, discussing epinephrine synthesis control by glucocorticoid hormones

Effect of adrenergic-blocking or -stimulating agents on plasma growth hormone, immunoreactive insulin, and blood free fatty acid levels in man

Abstract: In order to determine whether an adrenergic mechanism is involved in the secretion of growth hormone and insulin, the effect of adrenergic-blocking or -stimulating agents on plasma human growth hormone (HGH), immunoreactive insulin, blood free fatty acids (FFA), and glucose levels was studied in normal human subjects. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused a rise in plasma HGH, a transient decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was inhibited either by the combined administration of isoproterenol, a beta adrenergic-stimulating agent, along with propranolol or by oral glucose loading immediately before the start of propranolol infusion. The concomitant administration of epinephrine and propranolol brought about a rise in plasma HGH comparable with that produced by propranolol alone, without any significant change in blood FFA. Alpha adrenergic blockade by the intravenous infusion of phenotolamine significantly suppressed plasma HGH responses to insulin-induced hypoglycemia and to arginine infusion, and enhanced plasma insulin response to arginine infusion. It also stimulated lipid mobilization significantly. The intravenous infusion of alpha adrenergic-stimulating agents, phenylephrine and methoxamine, caused an increase in plasma HGH, a slight decrease in blood FFA, and no significant change in plasma insulin. This increase in plasma HGH was significantly inhibited by the simultaneous administration of phentolamine along with methoxamine. On the contrary, a beta adrenergic stimulant, isoproterenol, raised plasma insulin and blood FFA, and abolished the plasma HGH response to propranolol. Another beta stimulator, isoxsuprine, raised blood FFA but not plasma insulin. It is concluded that either beta adrenergic blockade or alpha stimulation enhances HGH secretion and inhibits insulin secretion and fat mobilization, whereas either alpha blockade or beta stimulation stimulates insulin secretion and fat mobilization and inhibits HGH secretion.

Adrenal function and alcoholism. II. Catecholamines.

Abstract: Urinary excretion of catecholamines and their metabolites were determined in alcoholic subjects during chronic ethanol ingestion and after alcohol withdrawal. A dose response relationship was found between magnitude of blood alcohol levels and increased excretion of epinephrine, metanephrine, norepi

Effects of Catecholamines and Renal Nerve Stimulation on Renin Release in the Nonfilterlng Kidney

Abstract: The mechanisms whereby catecholamines and renal nerve stimulation increase renin secretion were studied in dogs with nonfiltering kidneys. In six dogs, epinephrine was infused into the renal artery at a rate that decreased renal blood flow to half of the control value. Papaverine was then infused into the renal artery to block the decrease in renal blood flow produced by the catecholamine, and the epinephrine infusion was resumed while the papaverine infusion was continued. In this experiment, renin release increased during infusion of epinephrine alone, but no change occurred with epinephrine during papaverine infusion. The protocol for the experiment on six other dogs was similar except that the infused catecholamine was norepinephrine. In this experiment, norepinephrine increased renin release both prior to and during papaverine infusion. In seven dogs, the effect of electrical stimulation of the renal nerves on renin secretion was studied both before and during the infusion of papaverine into the renal artery; renin release increased strikingly both before and during papaverine infusion. It is suggested that epinephrine increased renin secretion in the nonfiltering kidney by an action on the renal arterioles. In contrast, norepinephrine and renal nerve stimulation apparently increased renin secretion in the nonfiltering kidney by a direct effect on the juxtaglomerular cells. These data provide evidence for specific mechanisms of action of epinephrine, norepinephrine, and the renal nerves in renin release.

Human Red Blood Cells: Prostaglandin E2, Epinephrine, and Isoproterenol Alter Deformability

Abstract: The human red blood cell responds to prostaglandin E(2), epinephrine, and isoproterenol with a decrease in deformability. The maximum decrease is brought about by 10(-10)M prostaglandin E(2), 10(-9)M epinephrine, or 10(-7)M isoproterenol. The dose response curve is biphasic. The sensitivity of the red cell to prostaglandin suggests that this cell may be a primary target for prostaglandin action. These changes in response to vasoactive substances indicate that the red cell must be considered an active element in circulatory control.

Stimulation by epinephrine of adenyl cyclase activity, cyclic AMP formation, DNA synthesis and cell proliferation in populations of rat thymic lymphocytes†

Abstract: : During the first ten minutes after the beginning of a continuous exposure of rat thymocyte populations (maintained in vitro) to epinephrine, there is an increase in the cellular concentration of cyclic AMP. The hormone also increases the activity of a crude preparation of the thymocyte's cyclic AMP-forming enzyme, adenyl cyclase. Between 30 and 45 minutes after the beginning of exposure to epinephrine, an additional part of the cell population begins to synthesize deoxyribonucleic acid (DNA). These changes are finally followed two to four hours later by an increase of the flow of cells into mitosis. Since cyclic AMP itself is known to stimulate both the initiation of DNA synthesis and thymocyte proliferation, and since the mitogenic action of epinephrine is shown to be potentiated by caffeine and inhibited by imidazole, it is concluded that the mitogenic action of this hormone is mediated by the cyclic nucleotide. (Author)

Responses of coronary vessels to adrenergic stimuli

Abstract: Experiments were done on anesthetized dogs (chloralose-urethane) to characterize the pattern of responsisveness to adrenergic stimuli. The left circumfles coronary artery was perfused with blood at constant rate. Changes in perfusion pressure of the coronary vessels reflected changes in coronary vascular resistance. Responses to direct electrical nerve stimulation of the cardiac sympathetic nerves, to intra-coronary injections of norepinephrine, isoproterenol, epinephrine; to electrical stimulation of carotid sinus nerves; and to stimulation of carotid chemoreceptors with nicotine and cyanide were tested. The intravenous administration of Practolol (1–2 mg/kg) eliminated changes in contractility which could result from these interventions and thus minimized or eliminated changes in coronary vascular resistance in response to changes in myocardial metabolism. The results indicated that 1) there is a paucity of alpha adrenergic vasoconstrictor receptors in the coronary vessels as compared to other vascular beds; 2) the coronary vascular beta receptors are not homologous to the cardiac beta receptors and are responsive to isoproterenol and epinephrine but not to norepinephrine nor to mose sympathetic nerve stimulation; 3) most of the dilator effect of isoproterenol represents activation of coronary and not cardiac beta receptors; 4) stimulation of baroreceptor nerves causes withdrawal of the sympathetic vasoconstrictor influence and minimal activation of cholinergic vagal vasodilator fibers; and 5) stimulation of chemoreceptors caused significant activation of cholinergic vagal vasodilator fibers.

Emotional and adrenal reactions to stress in bronchial asthma.

Abstract: Urinary epinephrine (E), norepinephrine (NE) and vanylmandelic acid (VMA), plasma cortisol and free fatty acids (FFA), respiratory and cardiovascular indices, and subjectively reported emotion were measured on successive days under conditions of stress and relaxation in 6 healthy males and 6 matched young males with perennial, mild-to-moderate bronchial asthma in remission. They had taken no medication for at least a week and no steroids for 6 months. Asthmatics, as compared to control Ss, had significantly lower urinary E values, during both stress and control periods. Initial levels of NE and VMA excretion in urine were normal; NE levels responded to stress as expected, but did not discriminate between groups. Plasma cortisol did not differ between groups in this small sample. These findings argue against a global sympathetic nervous system or adrenal cortical defect, and are consistent with the hypothesis of a specific hypothalamicadrenal medullary defect in bronchial asthma. Respiratory indices (unlike heart rate and blood pressure) differentiated between the groups: asthmatics had lower airway conductance and respiratory rate and an opposite direction of change in these indices under stress. Psychologically, asthmatic Ss exhibited a marked field independence and, although as emotionally aroused by stressors as were controls, gave evidence of inhibition of aggressive impulses.

Role of glucose in arginine-induced insulin release in man

Abstract: In five healthy subjects the plasma insulin response to intravenous arginine was markedly diminished when the amino acid was administered during insulin-induced hypoglycemia. This inhibition of insulin release was not due to the catecholamine secretion during hypoglycemia since, in separate experiments, infusion of a large dose of epinephrine was unable to suppress significantly the insulin response to arginine. It is concluded that the insulinogenic effect of arginine, for its expression, requires a normal blood glucose concentration. The close interrelationship between arginine and glucose regarding insulin secretion was further illustrated by the finding that the insulin response to intravenous glucose infusion was markedly enhanced by the prior administration of arginine. In experiments where hyperglycemia was achieved through epinephrine infusion, no synergism could be observed between arginine and hyperglycemia on insulin secretion. Immediately on cessation of epinephrine infusion, a prompt and marked insulin peak was obtained. These findings indicate that synergism between arginine and glucose appears only when glucose itself is able to elicit insulin release. We suggest that arginine stimulates insulin release by modulating the insulinogenic signal evoked by glucose in the β-cell, and not by its own primary action on the insulin-releasing machinery.

A Fraction of the Ventricular Myocardium That Has the Specificity of the Cardiac Beta-Adrenergic Receptor

Abstract: The 78,000 × g microsomal fraction of canine ventricular myocardium effected a 20-fold concentration of [3H]norepinephrine from a 10-9 M solution. The [3H]norepinephrine bound was displaced by physiologic concentrations of the beta-adrenergic catecholamines isoproterenol, epinephrine, and norepinephrine, in that order, which is the order of effectiveness of their actions on the force and rate of cardiac contraction. Alpha-adrenergic compounds did not displace [3H]norepinephrine until concentrations four orders of magnitude greater were reached. The beta-adrenergic blocker propranolol displaced at 10-6 M, whereas the alpha-adrenergic blocker phentolamine was inactive. Metabolites of the catecholamines did not compete for this binding site. It is concluded that, on the basis of specificity and affinity of binding, these microsomal particles are likely to contain the beta-adrenergic receptor.

Propranolol-insensitive effects of epinephrine on action potential repolarization in electrically driven atria of the guinea pig

Abstract: Transmeinbrane action potentials were recorded from cells in the electrically driven left atrial appendage of the guinea-pig heart bathed in Tyrode's solution at 30°C. Epinephrine, isoproterenol and norepinephrine produced modifications in the plateau and the phase of rapid repolarization without changing the resting potential. All of the catecholamines increased the duration of the plateau phase of the action potential. Modest concentrations ( 10-6 M) tended to decrease the 80% duration. At all concentrations examined. isoproterenol did not appreciably change the 80% duration. Characteristically, the actions of isoproterenol on the action potential were associated with an increase in developed tension and propranolol completely prevented the changes in electrical and mechanical activity caused by this agent. Large concentrations of epinephrine also increased developed tension whereas modest concentrations of this agent were usually ineffective in this regard. Moreover, the ability of modest concentrations of epinephrine to increase the 80% duration was insensitive to blockade by propranolol and was antagonized by phentolamine and dihydroergotamine. It is concluded that atrial muscle cells in the guinea pig display two pharmacologically distinct adrenoceptive sites.

Epinephrine: selective inhibition of the acute insulin response to glucose

Abstract: An epinephrine infusion of 6 mug/min decreased the rapid insulin response to a 5 g glucose pulse by 96% (P < 0.001) compared with the preinfusion control. In contrast when an identical epinephrine infusion was superimposed on a prolonged glucose infusion, elevated steady-state insulin levels did not decrease, but increased from 26.9 +/-6 (mean +/-SD, muU/ml) to 56.8 +/-15 muU/ml (P < 0.05) in parallel with the epinephrine-induced hyperglycemia. Thus epinephrine inhibition of insulin secretion was observed during acute but not chronic glucose stimulation. To evaluate further the insulin responses during a prolonged glucose infusion, a 5 g glucose pulse was given before and 60 min later during a concomitant epinephrine infusion. Although the acute insulin response to the first glucose pulse was observed during the elevated steady-state glucose and insulin levels associated with the glucose infusion, epinephrine again inhibited the acute insulin response to the subsequent 5 g glucose pulse by 91% (P < 0.01). Thus epinephrine appears to inhibit selectively the rapid insulin response to glucose but not to influence insulin output stimulated by prolonged hyperglycemia. These observations provide further evidence for a model of insulin secretion which includes a small storage pool available for immediate release to a glucose challenge and a more slowly responding pool regulating insulin secretion in the basal and steady state.

Synergistic effect of cortisol and growth hormone on hepatic ornithine decarboxylase activity.

Abstract: SummaryLiver ornithine decarboxylase activity is stimulated by hydrocortisone as well as by growth hormone. Hypophysectomy lowers basal levels but adrenalectomy does not. Simultaneous administration of both growth hormone and hydrocortisone increases the activity more than the sum of the increase due to each hormone alone. Pharmacological dosages of testosterone, epinephrine, insulin, l-thyroxine, estradiol, and glucagon produced only minor alterations in hepatic ODC levels.

Synthesis of Adrenal Catecholamines in Rats During and After Immobilization Stress

Abstract: Repeated intervals of immobilization previously have been found to cause elevation of levels of tyrosine hydroxylase in the adrenals of rats. In the present study it was found that the increased levels of enzymes result in enhanced synthesis of epinephrine-14C from tyrosine-14C but not from dopa-3H. During immobilization, conversion of tyrosine-14C to catecholamines is further increased and may exceed the capacity of even the elevated levels of dopa- mine-β-hydroxylase to convert dopamine to nor-epinephrine. Thus, while tyrosine hydroxylase is normally rate limiting, dopamine-β-hydroxylation may become rate limiting when dopamine formation is markedly accelerated. (Endocrinology 89: 46, 1971)