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1

DiCarlo, S. E., R. W. Blair, V. S. Bishop, and H. L. Stone. "Role of beta 2-adrenergic receptors on coronary resistance during exercise." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2287–93. http://dx.doi.org/10.1152/jappl.1988.64.6.2287.

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The effects of regional alpha- and specific beta 2-adrenergic receptor blockade on measurements of late diastolic coronary resistance (LDCR) and mean coronary blood flow velocity (CBFV) during exercise were examined in 14 conscious adult mongrel dogs. Specific beta 2-adrenergic receptor blockade (ICI 118.551) significantly decreased CBFV and increased LDCR by blockade of beta 2-vasodilator tone independent of alpha-adrenergic receptor-mediated tone and independent of altering myocardial metabolism. alpha-Adrenergic receptor blockade (phentolamine, 1 mg) significantly increased CBFV and decreas
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2

Awad, E. W., and M. Anctil. "IDENTIFICATION OF beta-LIKE ADRENOCEPTORS ASSOCIATED WITH BIOLUMINESCENCE IN THE SEA PANSY RENILLA KOELLIKERI." Journal of Experimental Biology 177, no. 1 (April 1, 1993): 181–200. http://dx.doi.org/10.1242/jeb.177.1.181.

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Previous studies have reported pharmacological and biochemical evidence for the involvement of adrenergic substances in the regulation of neuroeffector activities in the bioluminescent cnidarian Renilla koellikeri (Cnidaria, Anthozoa). Therefore, direct radiobinding assays were developed to identify and characterize beta-adrenergic binding in membrane preparations from this species, using the two beta-antagonists [3H]dihydroalprenolol and [3H]CGP12177 as tracers. In addition, the effect of various beta-adrenergic agents on luminescence was examined. Binding of the radioligands at 25°C was rapi
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3

Jasper, J. R., H. J. Motulsky, L. C. Mahan, and P. A. Insel. "Beta-adrenoceptor metabolism in wild-type, Gs, and protein kinase A-variant S49 cells." American Journal of Physiology-Cell Physiology 259, no. 1 (July 1, 1990): C41—C46. http://dx.doi.org/10.1152/ajpcell.1990.259.1.c41.

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To determine the role of the stimulatory guanine nucleotide-binding protein, Gs, and adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase in the basal metabolism of beta-adrenergic receptors in S49 lymphoma cells, we measured the return of receptor number and function after irreversible blockade of receptors. After inactivation of receptors with the irreversible ligand N8-(bromoacetyl)-N'-[3-(4-indolyoxy)-2-hydroxypropyl]-(2)-1,8-diam ino-p- methane (BIM), beta-adrenergic receptors (defined as [125I]iodocyanopindolol binding sites) reappeared in a biphasic manner, the faster ph
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4

Vatner, S. F., D. R. Knight, and T. H. Hintze. "Norepinephrine-induced beta 1-adrenergic peripheral vasodilation in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 1 (July 1, 1985): H49—H56. http://dx.doi.org/10.1152/ajpheart.1985.249.1.h49.

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Norepinephrine (NE) elicits alpha-adrenergic vasoconstriction and beta 1-adrenergic increases in heart rate and myocardial contractility. To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery from instrumentation for the measurement of cardiac output, arterial pressure, and left ventricular (LV) pressure and calculations of LV dP/dt and total peripheral resistance (TPR). NE, after pretreatment with hexamethonium and phentolamine, reduced mean arterial pressure 40 +/- 5% from 117 +/- 9 mmHg and TPR 60 +/- 5% from 0.058 +/-
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5

Kagiya, T., M. Hori, K. Iwakura, K. Iwai, Y. Watanabe, S. Uchida, H. Yoshida, A. Kitabatake, M. Inoue, and T. Kamada. "Role of increased alpha 1-adrenergic activity in cardiomyopathic Syrian hamster." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 1 (January 1, 1991): H80—H88. http://dx.doi.org/10.1152/ajpheart.1991.260.1.h80.

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We investigated serial changes in myocardial norepinephrine content and myocardial adrenergic receptors during the development of cardiomyopathy in Syrian hamsters (Bio 14.6) and their age-matched healthy controls. We also examined phosphatidylinositide hydrolysis after alpha 1-adrenergic stimulation and the effects of alpha 1-blockade. We found that in the prehypertrophic stage, myocardial norepinephrine content and densities of alpha 1- and beta-adrenergic receptors were significantly higher in the cardiomyopathic hamsters than in the controls. However, in the early heart failure stage, beta
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6

Borst, M. M., R. Marquetant, W. Kubler, and R. H. Strasser. "Beta-blockade reduces effects of adenosine and carbachol by transregulation of inhibitory receptors and Gi proteins." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 4 (April 1, 1997): H1672—H1679. http://dx.doi.org/10.1152/ajpheart.1997.272.4.h1672.

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Chronic blockade of stimulatory beta-adrenergic receptors may decrease inhibitory receptors of the adrenergic signal transduction system. This transregulation process might reduce the negative inotropic response of the myocardium to inhibitory receptor stimulation. Rats were treated for 6 days with the beta-blocker atenolol (2 mg/day). beta-Adrenergic receptors in cardiac plasma membranes increased from 49 +/- 6 to 75 +/- 9 fmol/mg protein (means +/- SE; P = 0.053), whereas muscarinic M2 receptors decreased (155 +/- 15 vs. 105 +/- 10 fmol/mg protein; P < or = 0.05). Moreover, inhibitory G a
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7

Kaufman, Beth D., and Robert E. Shaddy. "Beta-adrenergic receptor blockade and pediatric dilated cardiomyopathy." Progress in Pediatric Cardiology 24, no. 1 (November 2007): 51–57. http://dx.doi.org/10.1016/j.ppedcard.2007.08.004.

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8

Laughlin, M. H., and R. B. Armstrong. "Adrenoreceptor effects on rat muscle blood flow during treadmill exercise." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1465–72. http://dx.doi.org/10.1152/jappl.1987.62.4.1465.

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The purpose of this study was to examine the effects of the adrenergic receptors on the distribution of blood flow within and among skeletal muscles in rats. Blood flow was measured with the radiolabeled microsphere technique before exercise and during treadmill exercise at 15 or 60 m/min. Alpha- (phentolamine) or beta- (propranolol) adrenergic blocking drugs were administered, and then blood flow was measured and results compared with those from saline-treated rats. Before exercise, alpha-blockade caused increases in total muscle blood flow and in all fast-twitch muscles, whereas muscles comp
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9

Kuleshova, E. V., N. V. Kuzmenko, M. G. Pliss, and V. A. Tsyrlin. "Mechanisms of beta-blockers antihypertensive action." "Arterial’naya Gipertenziya" ("Arterial Hypertension") 27, no. 3 (August 4, 2021): 291–99. http://dx.doi.org/10.18705/1607-419x-2021-27-3-291-299.

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This article presents an analysis of data on the mechanisms of antihypertensive effect of β-adrenergic receptor blockers. The article describes the effectiveness of cardiotropic action of drugs to reduce high blood pressure (BP) with short-term and long-term action of compounds, the effect of blockers on the activity of plasma renin. The influence of β-blockers on the central mechanisms of blood circulation regulation is considered. Information on the effect of β-blockers on myogenic mechanisms of vascular tone regulation is presented. The possibilities of blockade of β-adrenergic receptors of
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10

Ferrara, L. Aldo, Teodoro Marotta, Paolo Rubba, Biagio De Simone, Giovanni Leccia, Stefano Soro, and Mario Mancini. "Effects of alpha-adrenergic and beta-adrenergic receptor blockade on lipid metabolism." American Journal of Medicine 80, no. 2 (February 1986): 104–8. http://dx.doi.org/10.1016/0002-9343(86)90168-3.

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11

Stonestreet, B. S., E. Le, and D. J. Berard. "Circulatory and metabolic effects of beta-adrenergic blockade in the hyperinsulinemic ovine fetus." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1098—H1106. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1098.

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Offspring of women with poorly controlled diabetes exhibit hypoxemia, elevated catecholamine concentration at birth, and an increased incidence of fetal death. Experimental fetal hyperinsulinemia results in increased catecholamine concentration and hemodynamic changes including increased combined ventricular output and vasodilation of select fetal organs. We hypothesized that insulin-induced catecholamine-mediated beta-adrenergic stimulation supports some of these hemodynamic changes in the hyperinsulinemic ovine fetus. To study this, 24 chronically instrumented fetal sheep receiving insulin f
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12

Knight, D. R., and S. F. Vatner. "Calcium channel blockers induce preferential coronary vasodilation by an alpha 1-mechanism." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 3 (September 1, 1987): H604—H613. http://dx.doi.org/10.1152/ajpheart.1987.253.3.h604.

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The effects of nitrendipine were evaluated on coronary and systemic dynamics in conscious dogs. Nitrendipine (8 micrograms X kg-1 X min-1) decreased late diastolic left circumflex coronary resistance (62 +/- 1.3%) significantly more (P less than 0.01) than total peripheral resistance (54 +/- 1.8%). After propranolol (1 mg/kg) and atropine methyl bromide (0.1 mg/kg) to eliminate reflex increases in myocardial metabolic demand, nitrendipine still reduced late diastolic coronary resistance (56 +/- 1.5%) significantly more (P less than 0.01) than total peripheral resistance (46 +/- 1.4%). However,
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13

Claustre, J., S. Brechet, P. Plaisancie, JA Chayvialle, and JC Cuber. "Stimulatory effect of beta-adrenergic agonists on ileal L cell secretion and modulation by alpha-adrenergic activation." Journal of Endocrinology 162, no. 2 (August 1, 1999): 271–78. http://dx.doi.org/10.1677/joe.0.1620271.

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Postprandial release of peptide YY (PYY) and glucagon-like peptide-1 (GLP-1) from L cells results from both nutrient transit in the ileal lumen and neural drive of endocrine cells. The adrenosympathetic system and its effectors have been shown to induce secretion of L cells in vivo or in vitro. Because these transmitters act through three receptors, beta, alpha1, alpha2, coupled to different intracellular pathways, we evaluated the responses of L cells to specific agonists, using the model of isolated vascularly perfused rat ileum. General stimulation of adrenergic receptors with epinephrine (
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14

McIntyre, R. C., A. Banerjee, D. D. Bensard, E. C. Brew, A. R. Hahn, and D. A. Fullerton. "Adenosine A1-receptor mechanisms antagonize beta-adrenergic pulmonary vasodilation in hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 6 (December 1, 1994): H2179—H2185. http://dx.doi.org/10.1152/ajpheart.1994.267.6.h2179.

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Hypoxic pulmonary vasoconstriction is refractory to beta-adrenergic receptor (beta-AR)-mediated pulmonary vasodilation. We hypothesized that hypoxic pulmonary arteries release adenosine (Ado) that antagonizes beta-AR-mediated pulmonary vasodilation. Using isolated rat pulmonary artery rings, we investigated 1) the effect of hypoxia and exogenous Ado on beta-AR-mediated pulmonary vasodilation, 2) the intracellular site of dysfunctional beta-AR-mediated pulmonary vasodilation in hypoxia, and 3) the Ado receptor subtype responsible for dysfunction of beta-AR-mediated pulmonary vasodilation. Hypox
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15

Inderwies, Tyra, Johannes Riedl, Evangelos Kiossis та Rupert M. Bruckmaier. "Effects of α- and β-adrenergic receptor stimulation and oxytocin receptor blockade on milking characteristics in dairy cows before and after removal of the teat sphincter". Journal of Dairy Research 70, № 3 (21 липня 2003): 289–92. http://dx.doi.org/10.1017/s0022029903006289.

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Alpha (α)- and beta (β)-adrenergic receptors in the bovine mammary gland are mainly present in the teat muscles and in the region where large milk ducts reach the cisternal cavities. The aim of the study was to test the hypothesis that the region of the large mammary ducts is the most important location of α- and β-adrenergic receptor stimulation affecting milk ejection and milk removal. Effects of α- and β-adrenergic receptor stimulation and of oxytocin (OT) receptor blockade on milking characteristics were tested in six cows. Milk flow was measured before and after the distal part of one tea
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16

Stagner, J. I., and E. Samols. "Role of intrapancreatic ganglia in regulation of periodic insular secretions." American Journal of Physiology-Endocrinology and Metabolism 248, no. 5 (May 1, 1985): E522—E530. http://dx.doi.org/10.1152/ajpendo.1985.248.5.e522.

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The regulatory system responsible for insulin oscillations from the in vitro pancreas is unknown. To test the hypothesis that intrapancreatic ganglia are the pacemaker or driver of the oscillations, combined nicotinic, muscarinic, and adrenergic antagonists were infused. Combined muscarinic, alpha- and beta-adrenergic, and presynaptic nicotinic receptor blockade (beta-bungarotoxin) was without effect on oscillations. The infusion of the postsynaptic nicotinic receptor antagonists, hexamethonium, alpha-bungarotoxin (ATX), or curarine, significantly altered the preinfusion oscillatory pattern of
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17

McDonald, J. V., L. W. Gonzales, P. L. Ballard, J. Pitha, and J. M. Roberts. "Lung beta-adrenoreceptor blockade affects perinatal surfactant release but not lung water." Journal of Applied Physiology 60, no. 5 (May 1, 1986): 1727–33. http://dx.doi.org/10.1152/jappl.1986.60.5.1727.

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We induced beta-adrenergic receptor blockade at 28 days gestation in the fetal rabbit with an irreversible beta-antagonist, bromace-tylalprenolomenthane (BrAlp). There was a marked decrease in concentration of available receptors in lung with increasing doses of BrAlp. BrAlp treatment decreased isoproterenol, but not prostaglandin, stimulated adenosine 3′,5′-cyclic monophosphate (cAMP) generation in lung minces, and had no effect on activation of adenylate cyclase through non-beta-receptor-mediated components of the cyclase system in particulate preparations. Phospholipid recovery via lung lav
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18

Granneman, J. G., and K. N. Lahners. "Regulation of mouse beta 3-adrenergic receptor gene expression and mRNA splice variants in adipocytes." American Journal of Physiology-Cell Physiology 268, no. 4 (April 1, 1995): C1040—C1044. http://dx.doi.org/10.1152/ajpcell.1995.268.4.c1040.

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This study examined the regulation of murine beta 3-receptor mRNA and determined whether the recently described mRNA splice variants are differentially regulated by agents that alter total beta 3-receptor mRNA levels. In vivo treatment of mice with the beta 3-receptor agonist BRL-26830 reduced total beta 3-transcripts by 64% in white adipose tissue but did not alter the mRNA splicing pattern. Further analysis in cultured 3T3-F442A adipocytes showed that isoproterenol, dexamethasone, or phorbol 12-myristate 13-acetate also greatly reduced beta 3-receptor mRNA levels without selectively altering
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19

Maman, Stephan R., Alvaro F. Vargas, Tariq Ali Ahmad, Amanda J. Miller, Zhaohui Gao, Urs A. Leuenberger, David N. Proctor, and Matthew D. Muller. "Beta-1 vs. beta-2 adrenergic control of coronary blood flow during isometric handgrip exercise in humans." Journal of Applied Physiology 123, no. 2 (August 1, 2017): 337–43. http://dx.doi.org/10.1152/japplphysiol.00106.2017.

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During exercise, β-adrenergic receptors are activated throughout the body. In healthy humans, the net effect of β-adrenergic stimulation is an increase in coronary blood flow. However, the role of vascular β1 vs. β2 receptors in coronary exercise hyperemia is not clear. In this study, we simultaneously measured noninvasive indexes of myocardial oxygen supply (i.e., blood velocity in the left anterior descending coronary artery; Doppler echocardiography) and demand [i.e., rate pressure product (RPP) = heart rate × systolic blood pressure) and tested the hypothesis that β1 blockade with esmolol
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20

Philipsen, E. K., J. Myhre, S. Larsen, M. Damkjær Nielsen, J. J. Holst, and J. Hilsted. "The relationship between some beta-adrenergic mediated responses and plasma concentrations of adrenaline and cyclic AMP in man." Acta Endocrinologica 122, no. 1 (January 1990): 115–20. http://dx.doi.org/10.1530/acta.0.1220115.

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Abstract To test the hypothesis that increments in plasma cyclic AMP during beta-adrenergic stimulation reflect integrated second messenger function of the tissues activated by the angonist, graded adrenaline infusion resulting in plasma adrenaline concentrations within the physiological range was performed in 8 healthy subjects with and without concomitant beta-adrenoceptor blockade by iv propranolol. A significant correlation was found between increments in plasma adrenaline and plasma cyclic AMP in the experiments without beta-blockade; during concomitant beta-blockade the increase in plasm
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21

Shen, Y. T., D. E. Vatner, H. E. Gagnon, and S. F. Vatner. "Species differences in regulation of alpha-adrenergic receptor function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1110—R1116. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1110.

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The effects of alpha-adrenergic receptor stimulation with norepinephrine and phenylephrine after beta-adrenergic and muscarinic receptor blockades were compared in conscious baboons, calves, dogs, and rats in which left ventricular (LV) pressure. LV maximum rate of pressure development (dP/dt), and heart rate were measured. Autonomic receptor density was examined in crude sarcolemmal preparations from the hearts. The major physiological differences were observed in rats, where alpha 1-adrenergic receptor stimulation resulted in the greatest (P less than 0.05) increases in LV dP/dt (29 +/- 2%)
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22

Hamdad, N., Z. Ming, R. Parent, and M. Lavallee. "Beta 2-adrenergic dilation of conductance coronary arteries involves flow-dependent NO formation in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 5 (November 1, 1996): H1926—H1937. http://dx.doi.org/10.1152/ajpheart.1996.271.5.h1926.

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The contribution of nitric oxide (NO) formation to the dilation of large epicardial coronary arteries to beta 1- and beta 2-adrenergic receptor stimulation was investigated in conscious dogs. After beta 1-adrenergic blockade (atenolol, 1.0 mg/kg iv), selective beta 2-adrenergic receptor activation with intracoronary bolus injections of pirbuterol (50 ng/kg) increased coronary blood flow (CBF) by 95 +/- 19% from 48.5 +/- 8.4 ml/min and external epicardial coronary diameter (CD) by 0.14 +/- 0.03 from 3.23 +/- 0.31 mm. After intracoronary N omega-nitro-L-arginine methyl ester (L-NAME, 50 microgra
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23

laccarino, G., V. Trimarco, F. Lanni, E. Cipolletta, R. Izzo, G. F. Di Renzo, L. Annunziato, and B. Trimarco. "BETA ADRENERGIC RECEPTOR POLYMORPHISMS AND METABOLIC ADVERSE EVENTS TO ANTIHYPERTENSIVE BETA BLOCKADE TREATMENT." Journal of Hypertension 22, Suppl. 2 (June 2004): S291—S292. http://dx.doi.org/10.1097/00004872-200406002-01011.

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24

Tucker, B. J., C. A. Mundy, and R. C. Blantz. "Effects of beta 1-adrenergic blockade on glomerular dynamics and angiotensin II response." American Journal of Physiology-Renal Physiology 257, no. 2 (August 1, 1989): F225—F230. http://dx.doi.org/10.1152/ajprenal.1989.257.2.f225.

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Adrenergic activity regulates renal function by several mechanisms. Renal nerves not only exert vasoconstrictor functions but also may influence glomerular hemodynamics by beta-adrenergic activity, especially via the effects on renin angiotensin activity. Little is known of the specific glomerular hemodynamic alterations resulting from beta 1-adrenergic blockade. Current studies examined the effects of 4-6 days of treatment with atenolol (50 mg/kg), a beta 1-selective adrenergic antagonist, on glomerular hemodynamics in plasma volume-expanded Munich-Wistar rats. Atenolol treatment reduced bloo
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25

Friedman, D. B., G. A. Ordway, and R. S. Williams. "Exercise-induced functional desensitization of canine cardiac beta-adrenergic receptors." Journal of Applied Physiology 62, no. 4 (April 1, 1987): 1721–23. http://dx.doi.org/10.1152/jappl.1987.62.4.1721.

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To test the hypothesis that the high levels of endogenous catecholamines associated with strenuous exercise produce functional desensitization of cardiac beta-adrenergic receptors, we measured the bolus chronotropic dose of isoproterenol necessary to produce a 25-beats/min increase in heart rate (CD25) in the resting state and after the return of heart rate to resting levels after 60 min of treadmill running in 13 normal dogs. Immediately after exercise, 12 of 13 dogs were less sensitive to the chronotropic effects of beta-adrenergic receptor stimulation: mean CD25 increased from 1.16 +/- 0.17
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26

Bonham, A. C., D. D. Gutterman, J. M. Arthur, M. L. Marcus, G. F. Gebhart, and M. J. Brody. "Electrical stimulation in perifornical lateral hypothalamus decreases coronary blood flow in cats." American Journal of Physiology-Heart and Circulatory Physiology 252, no. 3 (March 1, 1987): H474—H484. http://dx.doi.org/10.1152/ajpheart.1987.252.3.h474.

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Based on evidence implicating the central nervous system in the regulation of coronary vascular resistance and the knowledge that the hypothalamus is a central site for integration of cardiovascular control, studies were undertaken to determine if electrical stimulation in the hypothalamus produced coronary vasoconstriction. In anesthetized cats, following beta-adrenergic receptor blockade, stimulation in perifornical lateral hypothalamus produced a transient decrease in coronary blood flow velocity (30 +/- 5%), a small pressor effect (7 +/- 2 mmHg), and an initial decrease in hindquarter bloo
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27

Hatton, D. C., K. E. Scrogin, D. Levine, D. Feller, and D. A. McCarron. "Dietary calcium modulates blood pressure through alpha 1-adrenergic receptors." American Journal of Physiology-Renal Physiology 264, no. 2 (February 1, 1993): F234—F238. http://dx.doi.org/10.1152/ajprenal.1993.264.2.f234.

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To investigate the role of adrenergic receptor activity in dietary calcium-induced alterations in blood pressure, weanling spontaneously hypertensive rats (SHR) were placed on either high-calcium (2.0%) or low-calcium (0.1%) diets for 1-2 wk. Baseline blood pressure was higher and pressor responses to exogenous norepinephrine (NE) were greater in the SHR on low-calcium diets than high-calcium diets. There was no difference between diet groups in circulating NE or in the pressor response to angiotensin II. The difference in basal blood pressure was eliminated by the alpha 1-adrenergic receptor
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28

Cooper, G., R. L. Kent, P. McGonigle, and A. M. Watanabe. "Beta adrenergic receptor blockade of feline myocardium. Cardiac mechanics, energetics, and beta adrenoceptor regulation." Journal of Clinical Investigation 77, no. 2 (February 1, 1986): 441–55. http://dx.doi.org/10.1172/jci112323.

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29

Naden, R. P., and C. R. Rosenfeld. "Role of alpha-receptors in estrogen-induced vasodilation in nonpregnant sheep." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 3 (March 1, 1985): H339—H344. http://dx.doi.org/10.1152/ajpheart.1985.248.3.h339.

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Estradiol-17 beta (E2) produces vasodilation in several systemic vascular beds, but most extensively in the nonpregnant uterus. It has been postulated that E2 induces this vasodilation via blockade of vascular alpha-adrenergic receptors. This hypothesis was tested in six chronically instrumented, nonpregnant sheep by comparing the systemic and uterine hemodynamic responses to intravenous E2, to an alpha-adrenergic receptor blocker, phentolamine, and to both agents given together. Uterine blood flow (UBF) increased significantly after E2 administration, from 20 +/- 7 to 233 +/- 37 (SE) ml/min.
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30

van Wylen, D. G., and L. G. D'Alecy. "Regional blood flow distribution during the Cushing response: alterations with adrenergic blockade." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (January 1, 1985): H98—H108. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h98.

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Regional blood flow distribution (microspheres) and cardiac output (CO, thermal dilution) were measured during the Cushing response in unblocked (UB), beta-receptor-blocked (BB, 2 mg/kg propranolol iv), or alpha-receptor blocked (AB, 0.5 mg/kg + 0.5 mg X kg-1 X min-1 phentolamine iv) chloralose-anesthetized dogs. Intracranial pressure was increased to 150 mmHg by infusion of temperature-controlled artificial cerebrospinal fluid into the cisterna magna. Similar increases in mean arterial pressure were seen in UB and BB, but in AB a Cushing response could not be sustained. In UB, cerebral blood
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31

Deschamps, A., and S. Magder. "Effects of heat stress on vascular capacitance." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 5 (May 1, 1994): H2122—H2129. http://dx.doi.org/10.1152/ajpheart.1994.266.5.h2122.

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In dogs and humans, heat stress is associated with an increase in cardiac output that sustains blood flow to heat-dissipating organs. Because cardiac output and venous return are equal in the steady state, the circulation must also adjust in heat stress to allow the venous return to increase. To analyze these adjustments, we measured blood volumes, unstressed volumes, blood flow distribution, venous compliance, venous resistance, and the time constant of venous drainage of the splanchnic and extrasplanchnic vascular beds in dogs anesthetized with alpha-chloralose at normal and at high core tem
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Lee, H. T., C. I. Thompson, J. Linden, and F. L. Belloni. "Differential sensitization of cardiac actions of adenosine in rats after chronic theophylline treatment." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (May 1, 1993): H1634—H1643. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1634.

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To determine the effect of chronic adenosine receptor blockade on atrial responsiveness, we administered theophylline to rats in their drinking water (0.6 mg/ml) for 2 wk. Inotropic and chronotropic responses to the adenosine receptor agonists N6-cyclopentyladenosine (CPA) and 5'-(N-ethylcarboxamido)-adenosine (NECA) were then measured in isolated atria from treated and control animals. The indirect (antiadrenergic) actions of CPA and NECA on force and rate, measured during beta-adrenergic receptor stimulation by isoproterenol, were markedly sensitized (2- to 10-fold reductions in the agonist
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33

Porcelli, R. J., and M. V. Cutaia. "Pulmonary vascular reactivity to biogenic amines during acute hypoxia." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 2 (August 1, 1988): H329—H334. http://dx.doi.org/10.1152/ajpheart.1988.255.2.h329.

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The effects of acute hypoxia on the pressor responses to five biogenic amines were studied in isolated blood-perfused cat lungs. Hypoxia (Po2 = 46 +/- 2 Torr) reduced the pressor responses to phenylephrine while changing the pressor responses to epinephrine and norepinephrine to vasodilation. Hypoxia reduced the pressor responses to histamine, and these reductions were preceded by small but significant vasodilations. Hypoxia had no effect on the pressor responses to serotonin. These changes in pulmonary vasoactivity were reversed on reoxygenation, independent of changes in base-line tone and n
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Hooper, S. B., and R. Harding. "Effect of beta-adrenergic blockade on lung liquid secretion during fetal asphyxia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 4 (October 1, 1989): R705—R710. http://dx.doi.org/10.1152/ajpregu.1989.257.4.r705.

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The hypothesis tested in this study was that beta-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the beta-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 +/- 1.0 to 1
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35

Hargrove, D. M., G. J. Bagby, C. H. Lang, and J. J. Spitzer. "Adrenergic blockade prevents endotoxin-induced increases in glucose metabolism." American Journal of Physiology-Endocrinology and Metabolism 255, no. 5 (November 1, 1988): E629—E635. http://dx.doi.org/10.1152/ajpendo.1988.255.5.e629.

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Combined alpha- and beta-adrenergic blockade was used to investigate the role of catecholamines in endotoxin-induced elevations in glucose kinetics. Glucose kinetics were measured before and for 4 h after the injection of endotoxin [100 micrograms/100 g body wt iv, 30% lethal dose (LD30) at 24 h]. Adrenergic blockade was achieved by the bolus injection of phentolamine and propranolol followed by their continuous infusion. Endotoxin-treated rats exhibited a transient hyperglycemia and sustained (greater than 4 h) increase in plasma lactate concentration, as well as elevated rates of glucose app
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Takahashi, Toshiyuki, Toshihisa Anzai, Tsutomu Yoshikawa, Yuichiro Maekawa, Keitaro Mahara, Michikado Iwata, H. Kirk Hammond, and Satoshi Ogawa. "Angiotensin receptor blockade improves myocardial beta-adrenergic receptor signaling in postinfarction left ventricular remodeling." Journal of the American College of Cardiology 43, no. 1 (January 2004): 125–32. http://dx.doi.org/10.1016/j.jacc.2003.07.036.

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37

Cogswell, T. L., G. A. Bernath, H. Raff, R. G. Hoffmann, and H. S. Klopfenstein. "Total peripheral resistance during cardiac tamponade: adrenergic and angiotensin roles." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 251, no. 5 (November 1, 1986): R916—R922. http://dx.doi.org/10.1152/ajpregu.1986.251.5.r916.

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During progressive cardiac tamponade in conscious dogs, cardiac output falls continuously while arterial blood pressure is maintained until cardiovascular decompensation by increases in total peripheral resistance (TPR). Plasma renin activity (PRA) is known to increase at decompensation. We hypothesized that the increase in TPR during cardiac tamponade was mediated by alpha-adrenergic and renin-angiotensin mechanisms. Twelve adult dogs were instrumented to measure cardiac output (electromagnetic flow probe), aortic and right atrial blood pressures, and intrapericardial pressure (IPP). TPR was
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Sato, N., Y. T. Shen, K. Kiuchi, R. P. Shannon, and S. F. Vatner. "Splenic contraction-induced increases in arterial O2 reduce requirement for CBF in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (August 1, 1995): H491—H503. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h491.

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We investigated the extent to which sympathomimetic amines induced splenic contraction and associated increases in arterial O2 content (CaO2) and how these mechanisms affected control of the coronary circulation by sympathomimetic amines in conscious dogs. Blood hemoglobin (Hb) and CaO2 increased by 16 +/- 2 and 18 +/- 2%, respectively, during norepinephrine (NE, 0.8 micrograms.kg-1.min-1 iv) in the intact, conscious state after splenic contraction. Phenylephrine (PE) induced similar effects. After either alpha 1-adrenergic-receptor blockade or splenectomy, these effects were abolished. Isopro
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Hryniewicz, Katarzyna, Aleksandr Yasskiy, Jeffrey R. Bender, Lynn O'Donnell, and Stuart D. Katz. "Vascular endothelial effects of chronic beta-adrenergic receptor blockade in heart failure." Journal of Cardiac Failure 10, no. 4 (August 2004): S46. http://dx.doi.org/10.1016/j.cardfail.2004.06.099.

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40

Zeman, R. J., Y. Zhang, and J. D. Etlinger. "Clenbuterol, a beta 2-agonist, retards wasting and loss of contractility in irradiated dystrophic mdx muscle." American Journal of Physiology-Cell Physiology 267, no. 3 (September 1, 1994): C865—C868. http://dx.doi.org/10.1152/ajpcell.1994.267.3.c865.

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Treatment with the adrenergic beta 2-receptor agonist clenbuterol prevented, in dystrophic muscle from mdx mice, a pronounced loss of contractile strength that is observed after blockade of muscle regeneration with gamma irradiation. In addition, muscle mass and myosin content were greater (62-109%) in irradiated hindlimbs from clenbuterol-treated mdx mice, whereas the effects of the beta 2-agonist were relatively smaller (12-21%) in the nonirradiated hindlimbs. Together, these results suggest that beta 2-agonists can antagonize degenerative processes occurring in muscle fibers lacking dystrop
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Arici, Aylin, Sule Kalkan, Omer Demir, Nil Hocaoglu Aksay, Sedef Gidener, and Yesim Tuncok. "Does adenosine A1 receptor stimulation causes beta adrenergic receptor blockade in amitriptyline-induced QRS prolongation?" Toxicology Letters 180 (October 2008): S126. http://dx.doi.org/10.1016/j.toxlet.2008.06.737.

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42

Ririe, Douglas G., John F. IV Butterworth, Roger L. Royster, Drew A. MacGregor та Gary P. Zaloga. "Triiodothyronine Increases Contractility Independent of β-Adrenergic Receptors or Stimulation of Cyclic-3',5'-Adenosine Monophosphate". Anesthesiology 82, № 4 (1 квітня 1995): 1004–12. http://dx.doi.org/10.1097/00000542-199504000-00025.

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Background Triiodothyronine regulates cardiac contractility; however, the mechanisms by which it produces its acute contractile effects remains unknown. We compared the acute effects of thyroid hormones (triiodothyronine [T3] and thyroxine [T4]) and of isoproterenol on the contractility of isolated rat hearts. In addition, we sought to determine whether the acute inotropic effects of thyroid hormones were mediated by beta-adrenergic receptors or by increased production of cyclic-3',5'-adenosine monophosphate (cAMP). Methods A Langendorff heart preparation harvested from euthyroid male Sprague-
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Lang, C. H. "Beta-adrenergic blockade attenuates insulin resistance induced by tumor necrosis factor." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 5 (May 1, 1993): R984—R991. http://dx.doi.org/10.1152/ajpregu.1993.264.5.r984.

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The macrophage secretory product tumor necrosis factor (TNF) impairs insulin action on peripheral glucose uptake and hepatic glucose output. Because circulating catecholamines are also elevated by TNF, the present study was performed to determine the role of the adrenergic system in eliciting the insulin resistance. Human recombinant TNF (1 microgram.h-1.kg-1) was infused intravenously into chronically catheterized fasted rats for approximately 18 h. Before TNF, an infusion of either saline, propranolol (nonselective beta-antagonist), atenolol (selective beta 1-antagonist), or phentolamine (al
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Badgett, Robert G., Valerie A. Lawrence та Steven L. Cohn. "Variations in Pharmacology of β-Blockers May Contribute to Heterogeneous Results in Trials of Perioperative β-Blockade". Anesthesiology 113, № 3 (1 вересня 2010): 585–92. http://dx.doi.org/10.1097/aln.0b013e3181e73eea.

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Background Randomized controlled trials and meta-analyses provide conflicting guidance on the role of beta-adrenergic receptor blockers (beta-blockers) in reducing perioperative complications. We hypothesize that variability in trial results may be due in part to heterogeneous properties of beta-blockers. First, we propose that the extent of beta-blocker metabolism by cytochrome P-450 and the time available to titrate the dosage before surgery (titration time) may interact; dependence on P-450 may be most harmful when titration time is short. Second, beta-blockers vary in their selectivity for
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Wakamatsu, Hiroki, Toshiki Watanabe, Yoshiyuki Sato, Shinya Takase, Sadao Omata, and Hitoshi Yokoyama. "Selective Beta-1 Receptor Blockade Further Reduces the Mechanically Stabilized Target Coronary Artery Motion during Beating Heart Surgery." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 5, no. 5 (September 2010): 349–54. http://dx.doi.org/10.1097/imi.0b013e3181f6536b.

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Objective Adequate stabilization of anastomosis sites during off-pump coronary artery bypass is essential to obtain excellent graft patency. We examined the effect of beta-1 adrenergic receptor blockade on the target coronary artery motion by three-dimensional (3D) digital motion capture and reconstruction technology. Methods Eight pigs underwent a sternotomy. Reflection markers were attached to the surface coronary arteries, followed by a mechanical stabilizer application. Two high-speed digital cameras captured two-dimensional (2D) motion of the markers from different angles. These 2D data w
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Hintze, T. H., F. L. Belloni, J. E. Harrison, and G. C. Shapiro. "Apparent reduction in baroreflex sensitivity to adenosine in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 249, no. 3 (September 1, 1985): H554—H559. http://dx.doi.org/10.1152/ajpheart.1985.249.3.h554.

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Relative effects of equihypotensive doses (-35 mmHg) of adenosine (5.0 mumol/kg) and nitroglycerin (25 micrograms/kg) on heart rate and, therefore, baroreflex sensitivity were studied in conscious dogs. Nitroglycerin increased heart rate 133 +/- 24% from 78 +/- 5.5 beats/min, whereas adenosine increased heart rate only 79 +/- 16% from 78 +/- 5.2 beats/min (P less than 0.01). Injection of nitroglycerin during combined beta-adrenergic and muscarinic receptor blockades caused arterial pressure to fall 38 +/- 3.4% from 107 +/- 3.2 mmHg without any significant change in heart rate (3.8 +/- 3.8 from
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47

Fujii, A. M., and S. F. Vatner. "Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 4 (October 1, 1987): H728—H736. http://dx.doi.org/10.1152/ajpheart.1987.253.4.h728.

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To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the c
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48

Nganele, D. M., and T. H. Hintze. "Cardiac chemical reflex control of preload in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 4 (April 1, 1990): H1055—H1063. http://dx.doi.org/10.1152/ajpheart.1990.258.4.h1055.

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The purpose of our study was to determine the effects of cardiac chemical reflexes on left ventricular (LV) preload in conscious dogs. Adult mongrel dogs were instrumented to measure LV pressure and, with ultrasonic dimension crystals, to measure LV internal diameter. A catheter was inserted in the left circumflex coronary artery for the administration of increasing doses of veratridine, arachidonic acid (AA), and prostacyclin (PGI2). LV end-diastolic diameter (EDD) and end-diastolic pressure (EDP) were used as indexes of preload. Veratridine (0.4 micrograms/kg) reduced EDD 3.0 +/- 0.5% from 3
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Mandic, Danijela, Lana Nezic, and Ranko Skrbic. "Severe hyperkalemia induced by propranolol." Medical review 67, no. 5-6 (2014): 181–84. http://dx.doi.org/10.2298/mpns1406181m.

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Introduction. Hyperkalemia secondary to beta-adrenergic receptor blockade occurs in 1-5% of patients and is likely to develop with non-cardio-selective beta-blockers. Case Report. We have described hyperkalemia in a patient with angina pectoris receiving propranolol, clinically manifested as weakness, tightness behind the sternum and numbness in the limbs. Laboratory tests showed hyperkalemia (6.6 mmol/L), peaked T wave and a corrected QT interval of 510 ms. After discontinuation of propranolol, decline in potassium level, normalisation of electrocardiographic changes and clinical improvement
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Kruse, P., J. Ladefoged, U. Nielsen, P. E. Paulev, and J. P. Sorensen. "beta-Blockade used in precision sports: effect on pistol shooting performance." Journal of Applied Physiology 61, no. 2 (August 1, 1986): 417–20. http://dx.doi.org/10.1152/jappl.1986.61.2.417.

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In a double-blind cross-over study of 33 marksmen (standard pistol, 25 m) the adrenergic beta 1-receptor blocker, metoprolol, was compared to placebo. Metoprolol obviously improved the pistol shooting performance compared with placebo. Shooting improved by 13.4% of possible improvement (i.e., 600 points minus actual points obtained) as an average (SE = 4%, 2P less than 0.002). The most skilled athletes demonstrated the clearest metoprolol improvement. We found no correlation between the shooting improvement and changes in the cardiovascular variables (i.e., changes of heart rate and systolic b
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