The mechanism of beta-adrenergic receptor blockade-induced elevation of arterial blood pressure in rats

Abstract Background: Beta-blockers are increasingly prescribed while the effects of beta-adrenergic receptor blockade on cardio-pulmonary exercise test (CPET) derived parameters remain under-studied. Methods: 21 young healthy adults repeated 3 CPET at an interval of 7 days at the same time of the day. The tests were performed 3 hours after a random, double blind, cross-over single dose intake of placebo, 2.5 mg bisoprolol or 5 mg bisoprolol. Gaz exchange, heart rate and blood pressure were measured at rest and during cyclo-ergometric CPET.Results: Maximal workload and VO2max were unaffected by the treatment, with maximal respiratory exchange ratio > 1.15 in all tests. A beta-blocker dose-dependent effect reduced resting and maximal blood pressure and heart rate and the chronotropic response to exercise, evaluated by the heart rate/VO2 slope (placebo: 2,9 ± 0,4 beat/ml/kg; 2,5 mg bisoprolol: 2,4 ± 0,5 beat/ml/kg; 5 mg bisoprolol: 2,3 ± 0,4 beat/ml/kg, p<0.001). Ventilation efficiency measured by the VE/VCO2 slope and the ventilatory equivalent for CO2 at the ventilatory threshold were not affected by beta1-receptor blockade. Post-exercise chronotropic recovery measured after 1 min was enhanced under beta1-blocker (placebo: 26 ± 7 bpm; 2,5 mg bisoprolol: 32 ± 6 bpm; 5 mg bisoprolol: 33 ± 6 bpm, p<0.01).Conclusion: The present results suggest that a single dose of bisoprolol does not affect metabolism, respiratory response and exercise capacity. However, beta-adrenergic blockade dose-dependently reduced exercise hemodynamic response by lowering the pressure and chronotropic responses.

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Adrenergic stimulation and blockade in colonic circulation of the rhesus monkey

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.240.1.g25 ◽

1981 ◽

Vol 240 (1) ◽

pp. G25-G31

Author(s):

J. C. Kerr ◽

K. G. Swan

Keyword(s):

Adrenergic Receptor ◽

Arterial Blood Flow ◽

Receptor Blockade ◽

Adrenergic Stimulation ◽

Beta Adrenergic Receptor ◽

Receptor Stimulation ◽

Beta Adrenergic ◽

Alpha Adrenergic Receptor ◽

Arterial Blood ◽

Adrenergic Receptor Blockade

Adrenergic stimulation and blockade on inferior mesenteric arterial blood flow (Q) were measured in anesthetized rhesus monkeys. Control Q was 25 +/- 2 (mean +/- SE) ml/min; aortic and portal venous pressures were 121 +/- 5 and 6.5 +/- 1.0 mmHg. Calculated inferior mesenteric arterial resistance was 5.10 +/- 0.42 peripheral resistance units. Norepinephrine (N), 10(-3) to 1.0 microgram/kg intra-arterially, caused dose-dependent decreases in Q. Epinephrine (E) increased Q at 10(-3) microgram/kg in 60% of the animals studied and decreased Q at the higher doses (10(-2) to 1.0 microgram/kg). Isoproterenol (I) increased Q at all four doses studied. Ten-minute infusions of N and E (0.5 microgram x kg-1 x min-1) caused sustained decreases, and I caused sustained increases in Q. Autoregulatory escape was not observed. alpha-Adrenergic receptor blockade (phenoxybenzamine) attenuated the vasoconstrictor responses to N, but did not "reverse" the vasoconstrictor response to E (vasodilation). beta-adrenergic receptor blockade (propranolol) attenuated the vasodilator responses to I, but did not alter significantly the responses to E or N. These data indicate that in the monkey colonic circulation, alpha-adrenergic receptor stimulation causes vasoconstriction and beta-adrenergic receptor stimulation causes vasodilation.

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Contribution of Hypercapnia and Hypoxia to the Vascular Response to Ischaemia

Clinical Science ◽

10.1042/cs0390203 ◽

1970 ◽

Vol 39 (2) ◽

pp. 203-222 ◽

Cited By ~ 7

Author(s):

H. A. Kontos ◽

D. W. Richardson ◽

A. J. Raper ◽

J. L. Patterson

Keyword(s):

Adrenergic Receptor ◽

Circulatory Arrest ◽

Venous Blood ◽

Receptor Blockade ◽

Beta Adrenergic Receptor ◽

Beta Adrenergic ◽

Air Breathing ◽

Vasodilator Response ◽

Arterial Blood ◽

Adrenergic Receptor Blockade

1. Hypoxia, induced by 7–12% oxygen breathing, produced vasodilatation in the intact or in the phenoxybenzamine and propranolol treated forearm of human volunteers when arterial blood PO2 decreased below 45 mmHg, or when deep forearm venous blood PO2 decreased below 35–40 mmHg. 2. Circulatory arrest of the forearm following alpha and beta adrenergic receptor blockade was followed by greater increases in blood flow and greater decreases in forearm vascular resistance during CO2 breathing than during room air breathing. The increased flow following ischaemia was maintained at a high level until CO2 administration was stopped. 3. The vasodilator response following ischaemia of the human forearm, produced by digital occlusion of the brachial artery, was compared to that produced by hypercapnia or hypoxia or a combination of the two, produced by breathing the appropriate gas mixtures. The forearm was pre-treated with phenoxybenzamine and propranolol to produce alpha and beta adrenergic receptor blockade. For equal increases in deep forearm venous blood PCO2 the vasodilator response to hypercapnia averaged 60% of that following ischaemia. For equal decreases in deep forearm venous blood PO2 the vasodilator response to hypoxia averaged 26% of that produced by ischaemia. The vasodilator response to ischaemia was not modified by breathing 100% oxygen to maintain the deep forearm venous blood PO2 at a level above that seen with the circulation free during room air breathing. Combined hypoxia and hypercapnia of equal severity as those produced by ischaemia resulted in a vasodilator response which averaged 64% of that produced by ischaemia.

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