Beta-adrenergic receptors predict heart rate reactivity to a psychosocial stressor.

1990 ◽  
Vol 52 (6) ◽  
pp. 621-623 ◽  
Author(s):  
P J Mills ◽  
J E Dimsdale ◽  
M G Ziegler ◽  
C C Berry ◽  
R D Bain
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Beta Adrenergic Receptors ◽  
Psychosocial Stressor ◽  
Heart Rate Reactivity ◽  
Beta Adrenergic

Effect of exercise duration on density and coupling of beta-adrenergic receptors on human mononuclear cells

1989 ◽  
Vol 66 (3) ◽  
pp. 1494-1500 ◽  
Author(s):  
M. J. Frey ◽  
D. Mancini ◽  
D. Fischberg ◽  
J. R. Wilson ◽  
P. B. Molinoff
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Regulatory Protein ◽  
Nucleotide Binding ◽  
Plasma Norepinephrine ◽  
Base Line ◽  
Guanine Nucleotide ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Guanine Nucleotide Binding

The effect of maximal exercise on lymphocyte beta-adrenergic receptors was examined in 26 normal subjects. Exercise increased O2 consumption (Vo2) from 5 +/- 1 to 50 +/- 4 ml.min-1.kg-1, plasma norepinephrine level from 188 +/- 28 to 2,682 +/- 160 pg/ml, and plasma epinephrine level from 94 +/- 72 to 857 +/- 180 pg/ml. The density of beta-adrenergic receptors on lymphocytes obtained at rest was 31 +/- 3.7 fmol/mg protein; exercise increased the density of receptors by 86 +/- 33% (range 0–257%) to 58.3 +/- 1.5 fmol/mg protein but did not alter the affinity of the receptor for [125I]iodopindolol or the coupling of the receptor to the guanine nucleotide-binding regulatory protein. The density of beta-adrenergic receptors increased progressively throughout exercise and paralleled the increase in heart rate. The magnitude of the change in the density of beta-adrenergic receptors did not correlate with the magnitude of the increase in heart rate, Vo2, or plasma levels of catecholamines. The density of receptors was still elevated 15 min after completion of exercise but fell below base line 1 h after peak exercise to 18.2 +/- 6.7 fmol/mg protein (P less than 0.05 vs. base-line levels). These results demonstrate that exhaustive exercise results in a progressive increase in the number of beta-adrenergic receptors on lymphocyte membranes, followed by a reduction in the density of receptors during the recovery phase of exercise. Despite a significant increase in the level of plasma catecholamines, the receptor remains coupled to the guanine nucleotide-binding regulatory protein.

Regulation of atrial autonomic receptors in experimental cyanotic heart disease

1991 ◽  
Vol 261 (4) ◽  
pp. H1135-H1140 ◽  
Author(s):  
R. Doshi ◽  
E. Strandness ◽  
D. Bernstein
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Receptor Subtypes ◽  
Receptor Density ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Beta 2 ◽  
The Right ◽  
Chronic Hypoxemia ◽  
Inotropic Responses

During chronic hypoxemia, left ventricular beta-adrenergic receptor density is decreased and a dissociation occurs between increased chronotropic and decreased inotropic responses to chronically elevated sympathetic tone. To determine whether this dissociation was related to alterations in autonomic receptor populations in the right atrium, we studied right atrial cholinergic and beta-adrenergic receptors in chronically hypoxemic newborn lambs and in normoxemic controls. Heart rate response was determined by infusing isoproterenol at 0.1 or 0.5 microgram.kg-1.min-1. Muscarinic receptors were quantified with [3H]quinuclidinyl benzilate and beta-adrenergic receptors with [125I]iodocyanopindolol. Competition with ICI 118,551 was used to determine beta 1- vs. beta 2-receptor subtypes. In the hypoxemic lambs, isoproterenol resulted in a lesser percentage increase in heart rate (hypoxemic, 46 +/- 6% vs. control, 89 +/- 17%, P less than 0.05); however, because baseline heart rate was higher in the hypoxemic lambs (213 +/- 7 vs. 177 +/- 12 beats/min, P less than 0.05), maximal heart rate responses were similar (310 +/- 7 vs. 326 +/- 6 beats/min, NS). There was no change in receptor density or affinity of either muscarinic or beta-adrenergic receptors and no change in the proportion of beta 1- vs. beta 2-receptor subtypes. Thus the dissociation between the chronotropic and inotropic responses to chronic hypoxemia may be in part secondary to a differential regulation of beta-adrenergic receptors between the left ventricle and the right atrium.

Exercise-induced functional desensitization of canine cardiac beta-adrenergic receptors

1987 ◽  
Vol 62 (4) ◽  
pp. 1721-1723 ◽  
Author(s):  
D. B. Friedman ◽  
G. A. Ordway ◽  
R. S. Williams
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Treadmill Running ◽  
Strenuous Exercise ◽  
Beta Adrenergic Receptors ◽  
Similar Reduction ◽  
Beta Adrenergic ◽  
Single Bout ◽  
Chronotropic Effects ◽  
Exercise Induced

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 to 3.50 +/- 0.98 micrograms (P less than 0.02). A similar reduction in isoproterenol sensitivity was evident regardless of whether testing was performed in the presence or absence of vagal blockade with atropine. By 3 h after exercise, CD25 had returned to the preexercise level, with no further change noted 24 h after exercise. There was no change in the CD25 when measured serially in three unexercised dogs. We conclude that a single bout of dynamic exercise is sufficient to produce a significantly decreased chronotropic responsiveness to isoproterenol. This phenomenon may represent an acute but transient desensitization of cardiac beta-adrenergic receptors.

scholarly journals Autonomous regulation of heart rate in conditions of blocking the beta 1-adrenergic receptors in associative cortex of young rats with hypoxic exposure

2015 ◽  
Vol 17 (3) ◽  
Author(s):  
N. M. Volkova
Keyword(s):  
Heart Rate ◽  
Cerebral Cortex ◽  
Atmospheric Pressure ◽  
Adrenergic Receptors ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Young Rats ◽  
Associative Cortex ◽  
Hypoxic Environment ◽  
Low Atmospheric Pressure

<p>The literature discusses modulation of beta-adrenergic receptors sensitivity of the cerebral cortex under changed<br />conditions for the functioning of the body. However, very little data on the effect of the hypoxic environment to the<br />sensitivity of beta-adrenergic receptors of the cerebral cortex in a young body, which possible to investigate in<br />experiments on rats. The aim of the experiment was to determine the functional consequences of the exclusion of<br />beta1-adrenergic receptors in the associative cortex in young rats after incubation in hypoxic environment under<br />conditions of low atmospheric pressure. Blocking the beta1-adrenergic receptors in young rat’s associative cortex<br />can significantly offset the regulatory effects on heart rate that occurred during incubation in the hypoxic environment<br />under conditions of low atmospheric pressure. Hypoxic effect in young rats resulted in a significant decrease in<br />sensitivity beta1-adrenergic receptors in the associative cortex.</p>

Autonomic mechanisms of training bradycardia: beta-adrenergic receptors in humans

1981 ◽  
Vol 51 (5) ◽  
pp. 1232-1237 ◽  
Author(s):  
R. S. Williams ◽  
R. S. Eden ◽  
M. E. Moll ◽  
R. M. Lester ◽  
A. G. Wallace
Keyword(s):  
Heart Rate ◽  
Physical Training ◽  
Adrenergic Receptors ◽  
Human Subjects ◽  
Sinus Node ◽  
Cross Sectional Study ◽  
Beta Adrenergic Receptors ◽  
Cross Sectional ◽  
Beta Adrenergic ◽  
Marathon Runners

To address the autonomic mechanisms underlying the bradycardia of physical training in human subjects, we performed a cross-sectional study comparing the heart-rate responses to graded doses of isoproterenol in 7 elite marathon runners and 7 age-matched controls, and a longitudinal study in 12 normal volunteers of the effects of 6 wk of intense physical training on lymphocyte beta-adrenergic receptors identified by l-[3H]dihydroalprenolol. We observed no significant differences between marathoners and controls in the dose of isoproterenol that produced a 25-beat/min increment in heart rate, either in the absence (1.9 +/- 0.6 vs. 2.5 +/- 0.6 microgram; P, 0.509) or in the presence of cholinergic blockade (4.4 +/- 1.3 vs. 3.1 +/- 0.4 microgram: P, 0.320). Likewise, we observed no effects of physical training on lymphocyte beta-adrenergic receptors in terms of receptors number (53 +/- 11 vs. 56 +/- 10 fmol/mg protein) or receptor affinity (Kd 4.0 +/- 0.7 vs. 3.6 +/- 0.7 nM) (P, 0.9178). Although our data cannot exclude reduced chronotropic sensitivity to catecholamines as contributing to lowered heart rate in some highly conditioned individuals, these results are consistent with the hypothesis that altered neuronal input to the sinus node is usually a more important mechanism of training bradycardia.

Decreased cardiac response to isoproterenol infusion in acute and chronic hypoxia

1988 ◽  
Vol 65 (5) ◽  
pp. 1957-1961 ◽  
Author(s):  
J. P. Richalet ◽  
P. Larmignat ◽  
C. Rathat ◽  
A. Keromes ◽  
P. Baud ◽  
...  
Keyword(s):  
Heart Rate ◽  
Adrenergic Receptors ◽  
Chronic Hypoxia ◽  
Diastolic Pressure ◽  
Acute Hypoxia ◽  
Cardiac Response ◽  
Beta Adrenergic Receptors ◽  
Beta Adrenergic ◽  
Chronotropic Response ◽  
Isoproterenol Infusion

The hypothesis of a blunted chronotropic response of cardiac beta-adrenergic receptors in altitude hypoxia was tested in nine subjects at sea level (SL) by infusion of isoproterenol. Observations were made at SL, in acute hypoxia (2 days at 4,350 m, condition H1), in more prolonged hypoxia [13 days between 850 and 4,800 m, condition H2] and in chronic hypoxia [21 days at 4,800 m, condition H3]. Resting heart rate was higher in all hypoxic conditions. Resting norepinephrine concentrations were found to be significantly higher in conditions H2 (1.64 +/- 0.59) and H3 (1.74 +/- 0.76) than at SL (0.77 +/- 0.18 ng/ml). Isoproterenol, diluted in saline, was infused at increasing doses of 0.0, 0.02, 0.04, and 0.06 micrograms.kg-1.min-1. For the highest dose, there was a significantly smaller increase in heart rate in conditions H1 (35 +/- 9), H2 (33 +/- 11), and H3 (31 +/- 11) than at SL (45 +/- 8 min-1). The increase in pulse (systolic/diastolic) pressure, considered as the vascular response to isoproterenol infusion, was smaller in condition H3 (29 +/- 16) than at SL (51 +/- 24 mmHg). There was a significant increase in the dose of isoproterenol required to increase heart rate by 25 min-1 and decrease in slope of heart rate increase vs. log(dose) relationship in conditions H2 and H3. Thus an hypoxia-related attenuated response of beta-adrenergic receptors to exogenous stimulation was found in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

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