Role Of Beta-adrenergic Receptors Research Articles

Delayed arousal from anesthesia: A further similarity between stress and beta-1 adrenoceptor blockade

The present studies investigated the role of beta adrenergic receptors in mediating arousal from anesthesia and the effects of stress on this process. In support of previous findings by others, it was found that blockade of beta-1 and beta-2 receptors by propranolol delayed arousal from halothane anesthesia and that this effect was attributable to blockade of beta-1 receptors because it was duplicated by betaxolol but not by ICI 118,551. Restraint stress also produced a delay in arousal from both halothane and hexobarbital anesthesia. This effect, which was observed at 0.5 but not 24 h after the stress, could not be explained by a stress-induced alteration in the metabolism of the anesthetic, as no difference in brain concentration of hexobarbital was found between stressed and control mice. The parallel effects of beta-1 blockade and stress further supports the hypothesis that stress produces an impairment in function at either the beta-1 receptor or some process coupled to this receptor.

Effects of beta adrenergic receptor blockade on hemodynamic changes associated with obstructive sleep apnea

To study the effects of airway obstruction (AWO) and arousal on coronary blood flow, mean arterial pressure (MAP) and heart rate (HR), pigs were chronically instrumented with arterial catheters, Doppler flow probes on the left circumflex coronary artery, and electrodes for determination of sleep stages. A modified balloon catheter was placed in the trachea to obstruct the upper airway during sleep. Following control studies, the role of beta adrenergic receptors in hemodynamic responses to AWO was assessed by administering propranolol, a beta adrenoreceptor blocking agent. In control studies, during nonrapid eye movement sleep (NREM), MAP was 85 ± 2 mmHg before AWO and increased by 8 ± 2 mmHg upon arousal. Mean arterial pressure was lower during rapid eye movement (REM) sleep (64 ± 2 mmHg) and the increase upon arousal was threefold greater (22 ± 2 mmHg). Heart rate was similar in both sleep stages (NREM 123 ± 5 bpm; REM 125 ± 6 bpm) and increased significantly upon arousal (NREM, 11 ± 2 bpm; REM, 18 ± 3 bpm increase.) Coronary blood flow was similar during both stages (NREM 44 ± 5 ml/min; REM 44 ± 6 ml/min) and increased by 13% (NREM) and 22% (REM) during arousal. Coronary vascular resistance increased significantly by 17% during arousal from AWO during REM sleep. All changes were significant at p < 0.05. Following beta adrenergic receptor blockade studies using propranolol, baseline HR was reduced in NREM sleep and HR and coronary blood flow increases during arousal from apnea were eliminated. Adrenoreceptor blockade studies suggest that these effects were mediated by the beta adrenergic component of the sympathetic nervous system.

The effect of acidosis on beta-adrenergic receptors in ferret cardiac muscle.

Acidosis decreases the force of contraction of cardiac muscle in response to noradrenaline. The role of beta-adrenergic receptors in this response to acidosis was investigated. Radioligand techniques were used to determine beta-adrenergic receptor number and the degree of G-protein coupling, and to see whether these were altered in tissues subject to acidosis. The effect of pH on agonist and antagonist binding to these receptors was also investigated. Tissue pre-exposure to acidic conditions had no effect on numbers of beta-adrenergic receptors and no effect on the affinity of [125I]iodocyanopindolol (ICYP) for the receptors. Agonist competition experiments indicated that there was no change in the affinity of isoprenaline for these receptors, and there was no change in the relative proportions of high and low affinity binding sites. When radioligand experiments were performed under acidic conditions, however, the total number of beta-adrenergic receptors increased, and the affinity of these receptors for isoprenaline increased. This increase in agonist affinity might, therefore, minimize the shift to the right seen in the dose-response curve to noradrenaline during acidosis.

In Vivo Stimulation of Rat Pineal Type II Thyroxine 5'-Deiodinase Activity by Either Norepinephrine or Isoproterenol

Herein we show, for the first time, a very marked increase in thyroxine 5'-deiodinase (5'-D) activity in rats injected with norepinephrine (NE) and desmethylimipramine, a drug which inhibits NE uptake by nerve terminals. The response to NE was greater in pineals collected from hypothyroid animals than in glands from euthyroid animals. NE was more effective in stimulating pineal 5'-D than was isoproterenol, suggesting that, in addition to beta-adrenergic receptors, alpha-adrenergic receptors might be involved in the 5'-D activation. However, phenylephrine, an alpha-adrenergic agonist, did not potentiate the effect of isoproterenol on pineal 5'-D activity. The nocturnal increase in pineal 5'-D activity was completely abolished by propranolol, a beta-adrenergic receptor blocker, while prazosin, an alpha-adrenergic receptor blocker, had minimal effect. These results show that the role of alpha-receptors in promoting the NE-mediated rise in rat pineal 5'-D activity is minor in contrast to the role of beta-adrenergic receptors.

An update to silent myocardial ischemia: Pathophysiological, diagnostic, and therapeutic approaches

Silent myocardial ischemia (SMI) is a common ischemia process which can be defined as objective evidence of myocardial ischemia without chest pain or other equivalent indications. SMI can occur in totally asymptomatic patients, as well as in patients who have documented coronary artery disease (CAD) and who, on exercise and/or during Holter monitoring, may show ischemic changes. The precise mechanism for pathogenesis and pathophysiology of SMI remains to be clarified. A great deal has been learned about the role of beta-adrenergic receptors, adenylyl cyclase, and guanine nucleotide binding proteins (G proteins) in the myocardial ischemic process of SMI. Moreover, standard exercise test and long-term ECG recordings have proved to be of great value, especially when performed jointly, however, in this field there is still room for expanded knowledge. Pharmacological interventions to date have demonstrated the beneficial effects of beta-adrenergic receptor antagonists and/or calcium antagonists as contributing substantially to reducing both frequency and duration of SMI episodes. However, therapeutic options to improve the prognosis of SMI appear to be limited.

Beta-adrenergic receptors on canine coronary collateral vessels: characterization and function

The present studies were performed to examine the role of beta-adrenergic receptors in modulating smooth muscle tone in mature coronary collaterals. To examine the beta-adrenergic receptor population present, radioligand binding-cover slip autoradiographic studies were performed on sections of native canine coronary vessels and sections of coronary collaterals developed after placement of Ameroid constrictors. Specific binding of the nonselective beta-adrenergic antagonist [125I]iodopindolol to vascular smooth muscle in segments of both collaterals and native coronary arteries was saturable and stereospecific. Maximal binding and the potency of beta-adrenergic subtype-selective antagonists were similar in all segments. Beta-adrenergic relaxation of native coronary vessels and collateral vessels were studied in isolated organ chambers after preconstriction with prostaglandin F2 alpha. Both native coronary arteries and collateral segments demonstrated beta-adrenergic-mediated relaxation with affinities for both agonists and antagonists compatible with a mixed population of beta 1- and beta 2-adrenergic receptors. These studies indicate that during development, the new collateral vascular smooth muscle expresses a functional population of beta-adrenergic receptors, comparable to that in native vessels.

The role of beta-adrenergic receptors in the cardiac output response during carbon monoxide hypoxia.

Cardiac output increases during carbon monoxide hypoxia (COH) in anesthetized dogs when the level of carboxyhemoglobin exceeds 40% (Einzig et al., 1980; King et al., 1984; King et al., 1985; Sylvester et al., 1979). This compensatory response partially offsets the decrease in whole body oxygen delivery which results from the reduced oxygen content; oxygen uptake is maintained in spontaneously breathing anesthetized dogs at both 50 and 65% carboxyhemoglobin (King et al., 1984). The mechanisms underlying the cardiac output response during COH are not fully understood. It has been shown that nonselective β1 and β2-adrenergic blockade with propranolol resulted in lower values for cardiac output at 30 minutes of COH than in unblocked animals (King et al., 1985; Villeneuve et al., 1985). The effect of propranolol could have resulted from blockade of β1, β2 or a combination of the β1 and β2-adrenergic receptor sub-types. In the present study, the effects of the selective β2 blocker ICI 118,551 on cardiac output and whole body oxygen uptake responses were observed during severe COH (62% decrease in arterial oxygen concentration) in anesthetized, spontaneously breathing dogs. The data were compared to our earlier results obtained during COH in dogs treated with propranolol.KeywordsCardiac OutputUntreated GroupTotal Peripheral ResistanceBody OxygenArterial Oxygen ContentThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Antagonism by dopamine, but not noradrenaline receptor blockers of the anti-immobility activity of desipramine after different treatment schedules in the rat

The effect of antidopaminergic and antiadrenergic agents on the anti-immobility activity of desipramine after different schedules of treatment was studied in rats. 0.5 mg/kg i.p. haloperidol and 100 mg/kg i.p. sulpiride antagonized the anti-immobility effect of three injections of 10 mg/kg desipramine. Similar results were obtained after 7 or 21 daily doses of 10 mg/kg desipramine. Neither 5 mg/kg i.p. propranolol nor 3 mg/kg s.c. prazosin had any effect on desipramine after the various treatment schedules. It is suggested that DA mechanisms are involved in the anti-immobility effect of repeated desipramine in the rat. A possible role of beta-adrenergic receptors in the development of this effect is discussed.

A possible role for beta-adrenergic receptors in the expression of audiogenic seizures

DBA/2 mice are genetically prone to audiogenic seizures and, when compared with seizure resistant C57BL/6 mice, were found to have an increased density of β-adrenergic receptors in their midbrain at the age of peak seizure susceptibility. Propranolol, a β-receptor blocking agent, attenuated all stages of the seizure syndrome. However, a comparison of the effects of its d- and l-isomers suggested that propranolol's anticonvulsant activity was due to its local anesthetic-liked action. Pindolol, a more potent beta blocker that is at least 100 times less potent than propranolol with respect to local anesthetic-like activity, produced anticonvulsant effects in approximately the same systematic dose range as propranolol. This indicates that pindolol's anticonvulsant activity could be due to beta blockade and, taken together, these data suggest that β-adrenergic receptors may play a role in the expression of audiogenic seizures in these animals.

Interaction of beta-adrenergic agonists and antagonists with the stimulation of growth hormone release induced by clonidine or by morphine in the rat.

The beta-adrenergic agonist, isoprenaline, and antagonist, propranolol, had no effect on the delayed basal secretion of GH consistently observed in rats treated with the narco-analgesic gamma-hydroxybutyrate. Under the same experimental conditions, GH release was distinctly stimulated by infusion of the alpha-adrenergic agonist, clonidine, and by morphine; both responses were dose-dependent. The effects of beta-adrenergic agonists and antagonists on these GH responses were as follows: in rats pretreated with isoprenaline -the GH release induced by clonidine and morphine was abolished whereas it was enhanced in rats pretreated with propranolol. These data confirmed and extended previous reports from this laboratory on the inhibitory role of beta-adrenergic receptors on GH regulation.

Beta-adrenergic influence on cardiac dynamics during shock-avoidance in dogs

The role of beta-adrenergic receptors in the mediation of the cardiodynamic effects of a shock-avoidance task was evaluated in conscious dogs with the cardioselective beta-adrenergic antagonist practolol. The animals were chronically instrumented for the measurement of peak rate of change of left ventricular pressure (LV dP/dt), heart rate (HR), cardiac output (CO), systolic (SBP) and diastolic (DBP) blood pressure and total peripheral resistance (TPR), and were each subjected to brief bouts of shock-avoidance with and without practolol pretreatment (2–4 mg/kg). Shock-avoidance evoked reliable increases of LV dP/dt, HR, CO, SBP and DBP, and decreases of TPR. Beta-adrenergic blockade virtually eliminated LV dP/dt increases, attenuated HR and CO increases as well as the vasodilatation, diminished SBP increases in certain animals but did not affect DBP increases. Stable interindividual differences in the magnitude of LV dP/dt and HR increases during shock-avoidance were demonstrated; these differences were abolished by beta blockade. These findings indicate that a beta-adrenergic mechanism accounted for most of the rise of LV dP/dt during avoidance but contributed proportionally less to the elevations of HR and CO. Inter-individual differences in myocardial reactivity were however completely ascribable to beta-adrenergic factors.

Role of beta-adrenergic receptors in mobilization of energy sources in exercising dogs

ARTICLESRole of beta-adrenergic receptors in mobilization of energy sources in exercising dogsB. Issekutz JrB. Issekutz JrPublished Online:01 Jun 1978https://doi.org/10.1152/jappl.1978.44.6.869MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe Combined Effect of Short Term Green Tea Extract and a Single Bout of Cycle Ergometer on Glycerol and Free Fat Acid of Trained Males31 October 2017 | Jentashapir Journal of Health Research, Vol. 8, No. 5Green Tea, Intermittent Sprinting Exercise, and Fat Oxidation13 July 2015 | Nutrients, Vol. 7, No. 7Role of the sympathoadrenergic system in adipose tissue metabolism during exercise in humans1 October 2001 | The Journal of Physiology, Vol. 536, No. 1β-Adrenergic blockade augments glucose utilization in horses during graded exerciseRaymond J. Geor, Kenneth W. Hinchcliff, and Richard A. Sams1 September 2000 | Journal of Applied Physiology, Vol. 89, No. 3Epinephrine inhibits exogenous glucose utilization in exercising horsesRaymond J. Geor, Kenneth W. Hinchcliff, Laura Jill McCutcheon, and Richard A. Sams1 May 2000 | Journal of Applied Physiology, Vol. 88, No. 5Role of hepatic α- and β-adrenergic receptor stimulation on hepatic glucose production during heavy exerciseRobert H. Coker, Mahesh G. Krishna, D. Brooks Lacy, Deanna P. Bracy, and David H. Wasserman1 November 1997 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 273, No. 5Acclimatization to 4,300-m altitude decreases reliance on fat as a substrateA. C. Roberts, G. E. Butterfield, A. Cymerman, J. T. Reeves, E. E. Wolfel, and G. A. Brooks1 October 1996 | Journal of Applied Physiology, Vol. 81, No. 4Catecholamines in prevention of hypoglycemia during exercise in humansJ. C. Marker, I. B. Hirsch, L. J. Smith, C. A. Parvin, J. O. Holloszy, and P. E. Cryer1 May 1991 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 260, No. 5Abnormal glucoregulation during exercise in type II (non-insulin-dependent) diabetesMetabolism, Vol. 36, No. 12Carbohydrate dynamics in the hypermetabolic septic ratMetabolism, Vol. 33, No. 10Muscle glycogenolysis during exercise: dual control by epinephrine and contractionsE. A. Richter, N. B. Ruderman, H. Gavras, E. R. Belur, and H. Galbo1 January 1982 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 242, No. 1Effects of glucose infusion on hepatic and muscle glycogenolysis in exercising dogsB. Issekutz1 May 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 240, No. 5Role of epinephrine for muscular glycogenolysis and pancreatic hormonal secretion in running ratsE. A. Richter, B. Sonne, N. J. Christensen, and H. Galbo1 May 1981 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 240, No. 5 More from this issue > Volume 44Issue 6June 1978Pages 869-876 Copyright & PermissionsCopyright © 1978 the American Physiological Societyhttps://doi.org/10.1152/jappl.1978.44.6.869PubMed209004History Published online 1 June 1978 Published in print 1 June 1978 Metrics

Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors

Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors

Role of beta-adrenergic receptors in catecholamine-induced desensitization of adenylate cyclase in human astrocytoma cells.

Role of beta-adrenergic receptors in catecholamine-induced desensitization of adenylate cyclase in human astrocytoma cells.

Changes in left ventricular internal diameter with increasing pericardial pressure.

Changes in left ventricular internal diameter resulting from increasing intrapericardial pressure induced by increasing the pericardial fluid volume were studied in closed chest, anaesthetized dogs. Left ventricular internal diameters were measured by placing an ultrasonic dimension catheter in the left ventricle at the time of the experiments. With increasing pericardial pressure, significant increases occurred in heart rate and mean left atrial pressure. Left ventricular end-diastolic and end-systolic diameter progressively decreased as the pericardial pressure was elevated. After beta adrenergic blockade with propranolol (1 mg/kg), the decline in end-systolic diameter during pericardial tamponade was significantly reduced. These observations indicate the importance of the systolic reserve and the role of beta adrenergic receptors in the adaptation of the left ventricle to increases in pericardial tamponade.

Role of beta-adrenergic receptors in the circulatory response to hypoxia.

Role of beta-adrenergic receptors in the circulatory response to hypoxia.

Role of beta-adrenergic receptors in counterregulation to insulin-induced hypoglycemia.

Since beta-adrenergic blockade dampens the rebound of plasma glucose after insulin-induced hypoglycemia in man but does not affect epinephrine-stimulated hepatic glycogenolysis, studies were undertaken to define further the metabolic role of beta-adrenergic stimulation, particularly its participation in the induction of peripheral insulin resistance by epinephrine. In in vitro studies, propranolol, a specific beta-adrenergic blocker, was shown to prevent both epinephrine and isoproterenol from inducing inhibition of insulin-stimulated glucose uptake by rat hemidiaphragm. Methoxamine, an alpha-adrenergic stimulator, did not alter insulin-stimulated glucose uptake. In man, propranolol blocked the late rise of blood lactate levels which occurs during insulin tolerance tests, indicating that muscle glycogenolysis was prevented and suggesting that propranolol prevents epinephrine from inducing peripheral insulin resistance. This might in part account for the prolonged hypoglycemia observed in propranolol-insulin tolerance tests.