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At least 937 records · Page 52Linked to original sources
PubMed1976

Coronary vascular sympathetic beta-receptor innervation.

Recent studies indicate that coronary vessels have alpha- and beta-2-adrenergic receptors and that the alpha receptors are functionally innervated. We studied whether the beta-2-vasodilator receptors are functionally innervated, using a dog in situ modified Langendorff preparation with constant coronary perfusion pressure. The beating, nonworking heart and systemic circulation were supported with a pump oxygenator. Stimulation of the left stellate ganglion increased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values. After beta-1-receptor blockade (practolol, 10 mg/kg), stellate stimulation decreased coronary blood flow and decreased coronary sinus oxygen tension from prestimulation control values, revealing alpha-receptor vasoconstriction. After the addition of alpha-receptor blockade (Dibozane, 5 mg/kg), stellate stimulation increased coronary blood flow and coronary sinus oxygen tension a small amount from prestimulation values. Finally, after the addition of beta-2-receptor blockade (propranolol, 2 mg/kg), stellate stimulation increased flow and coronary sinus oxygen tension slightly from prestimulation control values. Direct intracoronary injections of isoproterenol, norepinephrine, and epinephrine gave results consistent with the presence of beta-1 myocardial receptors and alpha and beta-2 coronary receptors. We conclude that there is little functional innervation of coronary vascular beta-2 receptors. Intracoronary injections of isoproterenol and epinephrine activated beta-2-receptor coronary vasodilation after beta-1-receptor blockade, but norepinephrine did not.

Adrenergic alpha-Antagonists↗
PubMed1977

Pharmacological analysis of sympathetic function in the embryonic chick heart.

Sympathetic nerve cells enter the embryonic chick heart on the fifth day in ovo, but it is uncertain when these nerves become functional. Using pharmacological probes known to affect the embryonic circulation, sympathetic nerve function was examined at various stages of development. Exogenous norepinephrine elicited cardioacceleration in the hearts of embryos with intact extraembryonic circulation both before (stage 20-24) and after (stage 28-32) sympathetic innervation of the heart, and this acceleration could be inhibited by propranolol and practolol. In contrast, ganglionic stimulation with 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) elicited cardioacceleration only after stages 27-28 (i.e., after sympathetic innervation), producing a 25-30% increase in heart rate over the predrug levels of 148.7 +/- 1.8 beats/min. DMPP-elicited positive chronotropy was reduced by beta-receptor antagonists, hexamethonium, guanethidine (GuE), and tetrodotoxin. In preparations of the embryonic thorax in which the innervated heart was separated from brain and adrenal influences, DMPP elicited a GuE-sensitive cardioacceleration. It is concluded that during chick embryonic development, no more than a 1-day interval exists between the appearance of sympathetic nerves in the heart and the onset of neuronal function in that organ.

Animals↗
PubMed1975

Effects of arterial hypoxemia and splenic nerve stimulation on myocardial adenosine 3',5'-Monophosphate in dogs.

Epinephrine infusion, 5-percent oxygen breathing, and splenic nerve stimulation were employed to increase cardiac output by 50-100% in anesthetized dogs. Epinephrine infusion as expected, increased plasma and myocardial cyclic AMP concentrations. Arterial hypoxemia increased cyclic AMP concentration in plasma but not in the heart. Practolol pretreatment abolished the increase in plasma cyclic AMP concentration and reduced the rise in cardiac output during hypoxemia. Splenic nerve stimulation was not associated with increases in either plasma or myocardial cyclic AMP. Adenylate cyclase activity was increased by addition of plasma into the incubation medium. However, splenic venous plasma obtained during splenic nerve stimulation did not increase adenylate cyclase activity more than control plasma obtained before stimulation. We conclude that the positive inotropic action of arterial hypoxemia and splenic nerve stimulation does not depend on the adenylate cyclase-cyclic AMP system.

Adenylyl Cyclases↗
PubMed1977

Effects of sympathetic blockade and splenectomy on cardiac output response to muscular work in dogs.

The effects of splenectomy and sympathetic blockade on cardiac output (Q) response to mild to moderate exercise were studied in chloralose-anesthetized vagotomized dogs during electrically-induced muscular work, which increased oxygen consumption (VO2) 4- to 5-fold. Splenectomy reduced the exercise factor (deltaQ/deltaVO2 ratio) from 5.86 +/- 0.43 (SE) to 3.30 +/- 0.34 (p less than 0.001), while left nephrectomy had no effect. The exercise factor was not affected by beta-adrenoceptor blockade produced by propranolol or practolol, but was reduced by mecamylamine. The spleen did not increase cardiac output by displacing blood into the general circulation because pulmonary artery wedge pressure did not change during exercise in normal dogs. Furthermore, cardiac output was increased 35 +/- 6% after intraportal infusion of splenic venous blood obtained during exercise, whereas arterial blood infusion increased cardiac output only 10%. We conclude that the cardiac output rise during exercise in part is caused by the inotropic action of a splenic noncatecholamine substance, which is released by sympathetic stimulation.

Animals↗
PubMed1976

Effect of catecholamines and sympatholytics on survival and circulatory parameters in protracted anaphylactic shock of guinea pigs.

Protracted anaphylactic shock of guinea pigs led to death in over 90% of the animals, and good protection was obtained with an infusion of adrenaline after dibenamine pretreatment. Adrenaline alone, in doses which prevented the anaphylactic fall of arterial blood pressure, had no beneficial effect. Practolol abolished the therapeutic action of the combination of dibenamine/adrenaline. Stimulation of beta-receptors by isoproterenol did not increase the survival rate. With dopamine, however, a significant prolongation of the survival times was obtained.

Anaphylaxis↗
PubMed1979

Effect of norepinephrine on in vitro histamine release from rat mast cells.

The effect of norepinephrine on compound 48/80-induced histamine release from rat peritoneal mast cells, was studied in an in vitro system. It was found that norepinephrine, within the concentration range 10(-5)--10(-3) M, exerts a significant, dose-related, repressive effect. This effect is greatly potentiated by the beta-antagonist practolol (10(-3) M), throughout the concentration range of 10(-11)--10(-3) M norepinephrine. Methoxyamine, a selective alpha-adrenergic agonist, also represses histamine release in a dose-dependent manner; however, it is not as potent as norepinephrine. The present results would seem to suggest that the repressive effect on histamine release, observed within a low concentration range of norepinephrine, may be due to alpha-adrenoceptor mechanisms.

Animals↗
PubMed1974

Comparison of the effects on renin release of beta adrenergic antagonists with differing properties.

Continuous 6-h infusions of the beta adrenergic blockers d,l-propranolol or oxprenolol significantly reduced plasma renin activity (PRA) and mean blood pressure in the resting rabbit and prevented the stimulatory effects of isoproterenol on renin release and heart rate. These actions were due to blockade of beta receptors, for the inactive isomer, d-propranolol, had no effect. Despite sustained high plasma concentrations of d,l-propranolol (0.2 mug/ml) in the unstimulated animal, PRA did not fall below 36% of control values, suggesting that basal renin secretion is maintained partly by factors other than beta adrenergic mechanisms.Prindolol, another beta blocker, also abolished the effects of isoproterenol on renin and on the heart, and reduced blood pressure in the resting animal. However, prindolol increased resting PRA and heart rate, and in animals already receiving d,l-propranolol, it raised PRA and heart rate without further altering blood pressure. This suggests that the effect on PRA of prindolol was due to its intrinsic sympathomimetic activity and not hypotension-mediated mechanisms. The observation that the blood pressure-lowering effect of prindolol was associated with a rise in PRA, while another beta antagonist, H 35/25, lowered PRA but had no effect on blood pressure, indicates that the hypotensive action of beta blockers is unrelated to their effects on renin release. In both unstimulated and isoproterenol-challenged animals, only blockers possessing beta-1 receptor affinity (d,l-propranolol, oxprenolol, prindolol, practolol, and metoprolol) affected heart rate, while effects on PRA were more prominent with agents possessing beta-2 activity (d,l-propranolol, oxprenolol, prindolol, and H 35/25). Thus, the changes in PRA caused by the beta adrenergic blockers appear to be dependent upon the summation of their direct effects, antagonistic or sympathomimetic, on beta-2 adrenergic receptors regulating renin release.

Adrenergic beta-Agonists↗
PubMed1988

Autoradiographic localization of beta-adrenoreceptors in rat uterus.

The inhibitory effects of catecholamines on uterine smooth muscle are known to be mediated through beta-adrenergic receptors. To investigate further the distribution of these receptors in the rat uterus, we utilized in vitro autoradiography using [125I]-cyanopindolol [CYP], a specific beta-receptor ligand that has equal activity for both beta 1- and beta 2-receptor subtypes. The specificity of the labeling and the characterization of receptor subtypes in different cell types were achieved by displacement of radioligand with increasing concentrations of zinterol, a beta-adrenergic agonist with preferential affinity for the beta 2-adrenoreceptor subtype, and practolol, a beta-adrenergic antagonist that binds preferentially to the beta 1-subtype. Quantitative estimation of ligand binding was performed by densitometry. It was shown that the vast majority of beta-adrenoreceptors were of the beta 2-subtype and were found in high concentration not only in the myometrium but also in the endometrial and serosal epithelia. Specific labeling was also observed in glandular elements. These results suggest that beta-adrenoreceptors might be involved in different functions in the uterus.

Animals↗
PubMed1983

Noradrenergic regulation of growth hormone secretion in the baboon.

We have investigated the effects of iv administered noradrenergic agonists and antagonists on plasma GH concentration in the adolescent baboon, Papio papio, with the aim of defining the relative roles of adrenergic receptor subtypes (alpha 1, alpha 2, beta 1, and beta 2) in the regulation of GH release. Clonidine (0.02 mg/kg) or UK-14,304 (0.02 mg/kg), potent centrally acting alpha 2 noradrenergic agonists, were infused into 24 animals pretreated with either saline, or selective alpha 1 and alpha 2 noradrenergic antagonists. Both agonists potently augment plasma GH, producing peak levels of 30-60 ng/ml 15 min post infusion. These responses can be prevented by the prior infusion of the alpha 2 antagonist, piperoxane (1.0 mg/kg), but not by the alpha 1 antagonist, prazosin (2.0 mg/kg). Log dose response curves of the 2 agonists demonstrate a greater potency for UK-14,304 vs. clonidine on a molar basis. In animals pretreated with monoamine depleting agents (reserpine and alpha-methyl paratyrosine) the plasma GH response to an infusion of clonidine (0.02 mg/kg) is significantly enhanced (P less than 0.001). Beta-Adrenoreceptor antagonism by propranolol (0.02 or 1.0 mg/kg) or the more selective beta 2-adrenoreceptor antagonist, ICI 118,551 (0.02-1.0 mg/kg), results in a rapid and significant (P less than 0.01) increase in plasma GH. The beta 1-antagonist, practolol (0.2-2.0 mg/kg), does not alter plasma GH levels. It is proposed that in the baboon, noradrenaline acts on alpha 2-noradrenergic receptors to stimulate GH release and on beta 2-noradrenergic receptors to inhibit GH release.

Albuterol↗
PubMed1975

Studies on inhibition of TSH stimulation of adenyl cyclase activity in thyroid plasma membrane preparations by propranolol.

Propranolol (1 mM) was found to inhibit TSH stimulation of adenyl cyclase activity in a subcellular fraction from bovine thyroid enriched in plasma membranes. However, stimulation due to PGE1 or NaF was not similarly inhibited. Since (i) and inhibition was observed at concentrations of propranolol between 10-minus 4 and 10- minus 3M, and appeared to be noncompetitive (ii) the optical isomers of propranolol were equipotent, (iii) inhibition was specific for propranolol since it was not observed with the closely related drug practolol (1 mM), and (iv) quinidine (1 mM) and the local anaesthetics lignocaine and aptocaine also proved inhibitory, we concluded that propranolol inhibition of TSH stimulation was due to its "quinidine-like" properties (i.e., relatively specific and characteristic membrane-active properties) and not to its action as a beta-adrenergic antagonist.

Adenosine Triphosphatases↗
PubMed1996

Potentiation by higenamine of the aconitine-induced positive chronotropic effect in isolated right atria of mice: the effects of cholera toxin, forskolin and pertussis toxin.

Aconitine and higenamine are the major cardioactive compounds obtained from processed aconite. The chronotropic interaction between these two compounds was investigated in isolated right atria of mice. Both aconitine and higenamine potentiated the action of the other. Practolol (1 nM), a selective beta 1-adrenergic antagonist, but not butoxamine (1 microM), a beta 2-adrenergic antagonist, blocked the potentiation by higenamine (5 nM) of the aconitine-induced positive chronotropic effect and, at high concentrations (30 and 300 nM) also shifted the aconitine concentration-response curves to the right. The potentiating interaction between aconitine and higenamine was reversed by pretreating with cholera toxin (CTX) and forskolin. In CTX (100 nM, 1 h)- and forskolin (30 and 100 nM)-treated atria, higenamine significantly depressed the aconitine-induced response, which was abolished by pertussis toxin (PTX, 150 micrograms/kg, i.p., 3 d). Neither CTX (50 and 100 nM) nor forskolin (15-100 nM) significantly affected the aconitine-induced positive chronotropic effect, while PTX (150 micrograms/kg) depressed it. These results suggest that the potentiating interaction between aconitine and higenamine involves "cross-talk" between the beta 1-adrenergic signalling pathway and Gi-protein.

Aconitine↗
PubMed1978

Inhibition of gastric acid secretion in dogs by a new sympathomimetic drug.

The effect of salmefamol, a new beta 2-agonist, on pentagastrin-induced gastric acid secretion was studied in conscious gastric fistula dogs. Salmefamol inhibited the acid secretion, an effect which was dose dependent. The volume as well as the acidity was inhibited. Salmefamol caused an increase in the pulse rate. Propranolol prevented the inhibition of acid output as well as the increase in pulse rate. Practolol, a beta 1-adrenoceptor blocker, had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with 6 doses of pentagastrin and 1 dose of salmefamol showed a decrease in calculated maximal response (CMR) and an unchanged D50. It is concluded that salmefamol strongly inhibits pentagastrin-induced acid output in the dog, and the inhibition follows a non-competitive kinetic. The mechanism of gastric secretion probably involves a beta 2-receptor.

Animals↗
PubMed1979

Effects of beta2-sympathomimetic on histamine-stimulated gastric acid secretion in dogs.

The effect of a selective beta2-adrenoceptor agonist on histamine-stimulated gastric acid secretion was studied in conscious gastric-fistula dogs. A dose-dependent inhibition was found, most pronounced for the lowest doses of histamine. The inhibition was on the volume, whereas the acidity was unchanged. The pulse rate was increased by the beta2-agonist and by histamine. Propranolol prevented the inhibition of acid secretion as well as the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but reduced the increase in pulse rate. Dose-response experiments with six doses of histamine and two doses of the beta2-agonist showed unchanged calculated maximal response and an increase in D50. It is concluded that the beta2-agonist inhibits histamine-induced acid secretion in the dog, but to a lesser degree that pentagastrin-induced acid secretion, as found in earlier experiments. The inhibition follows competitive kinetics, and beta2-receptors are probably involved. The influence of beta2-sympathomimetics on the mechanism of gastric acid secretion is discussed.

Animals↗
PubMed1981

Effect of isoprenaline on pentagastrin-stimulated gastric acid secretion in dogs with gastric fistula.

The purpose of this study was to elucidate the effect of a beta 1-adrenoceptor agonist on gastric acid secretion in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist was used alone and in conjunction with selective blockade of beta 2- and beta 1-receptors. Isoprenaline dose-dependently inhibited the secretory volume and the acidity. The antisecretory effect of isoprenaline was significantly blocked by the beta 1-adrenoceptor blocker practolol and by the beta 1 + beta 2-adrenoceptor blocker propranolol but not by H 35/25, a beta 2-adrenoceptor blocker. This indicates that isoprenaline acts on the acid secretion exclusively through beta 1-receptors. Dose-response experiments with five logarithmically increased doses of pentagastrin and one dose of isoprenaline showed unchanged calculated maximum response and an increase in half-maximum acid response. It is concluded that the inhibitory effect of isoprenaline on gastric acid secretion is of competitive or uncompetitive type.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of isoprenaline on bethanechol-stimulated gastric acid secrtion and mucosal blood flow in dogs with gastric fistula.

The prupose of this study was to elucidate the effect of the beta-adrenoceptor stimulation by isoprenaline on cholinergic-stimulated gastric acid secretion and mucosal blood flow in conscious dogs with gastric fistula. Isoprenaline, a beta 1- and beta 2-agonist, was used alone and in conjunction with selective blockade of beta 2 and beta 1 receptors. A low dose of isoprenaline had no significant effect, whereas higher doses had a significant antisecretory effect. The antisecretory effect was significantly blocked by the beta 1-adrenoceptor blocker practolol but not by H 35/25, a beta 2-adrenoceptor blocker. The dose-response curve with five doses of bethanechol with and without isoprenaline was in accordance with a non-competitive inhibition. There was no significant effect on gastric mucosal blood flow, indicating that the acid inhibition was not secondary to changes in blood flow. The inhibitory effect of isoprenaline seems to be mediated by the beta 1 receptors and with an action primarily on the 'gastrinergic receptors'.

Adrenergic beta-Antagonists↗
PubMed1983

Adrenergic control of rat gastric somatostatin and gastrin release.

The effect of adrenergic agonists and antagonists on the secretion of gastric somatostatin-like immunoreactivity (SLI) and gastrin was investigated in an isolated, vascularly perfused rat stomach preparation. Two- to six-fold increases in SLI secretion induced by isoproterenol, epinephrine, and norepinephrine were completely abolished by propranolol but were not influenced by phentolamine. Propranolol did not alter glucagon- and DB-cAMP-induced stimulation of SLI release. Experiments in which the beta 2-agonist salbutamol and the beta 1- and beta 2-blockers practolol and H35/25 were used showed that both subtypes of beta receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2 X 10(-8) to 1.5 X 10(-4) M). The results obtained in this study suggest that in rats 1) the SLI response to adrenergic agonism is predominantly mediated by beta receptors; 2) both beta 1- and beta 2-adrenergic receptors are involved; 3) under in vitro conditions, adrenergic agonism is a weak stimulus for gastrin secretion.

Adrenergic beta-Agonists↗
PubMed1985

Influence of adrenergic antagonist and naloxone on the anti-allergic shock effect of electro-acupuncture in mice.

Our recent studies indicated that there was a good therapeutic effect selecting acupoints "Renzhong (Du26 =G.V. 26)" "Chengjiang (Ren. 24=C.V.24) of electro-acupuncture (E-A) in the treatment of allergic shock induced by bovine serum in mice. Phentolamine or propranolol injection before needling could partially reverse this anti-allergic shock effect, while practolol had no influence on the effect of E-A in the treatment. Another series of experiments showed that the E-A anti-allergic shock effect could not be blocked by Naloxone or previous exhaustion of pituitary endorphins, thus suggesting that there might be a difference between mechanisms underlying the analgesic effect and those underlying the anti-allergic shock effect of acupuncture.

Acupuncture Therapy↗
PubMed1975

Intracardiac conduction defects following overdose of tricyclic antidepressant drugs.

Atrioventricular and intraventricular conduction were assessed in 4 patients with tricyclic antidepressant overdosage. The proximal or A-V nodal conduction (A-H) was normal, but 3 patients showed a drug-related increase in the QRS duration and His-Purkinje (H-V) conduction time. One patient with a normal H-V interval had a normal width QRS. The findings were independent of the heart rate and suggested a "quinidine-like effect" of the tricyclic drugs when ingested in suicidal doses. All 4 patients had normal intracardic conduction when restudied 8 days later. Procainamide and quinidine have similar effects on the intracardiac conduction and would appear undesirable in the treatment of cardiac arrhythmias in patients with tricyclic overdosage. Practolol in a dose of 20 mg by intravenous injection reduced the heart rate and caused a relative increase in the A-H interval but did not affect either the distal atrioventricular or intraventricular conduction. Although there was a slight drop in blood pressure, it may be a safer drug to use.

Aged↗