Adrenergic stimulation and blockade in colonic circulation of the rhesus monkey

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.

Effects of beta-adrenergic receptor blockade on glycogenolysis during exercise

1982 ◽  
Vol 53 (3) ◽  
pp. 549-554 ◽  
Author(s):  
A. C. Juhlin-Dannfelt ◽  
S. E. Terblanche ◽  
R. D. Fell ◽  
J. C. Young ◽  
J. O. Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Adrenergic Receptor ◽  
Beta Blockade ◽  
Receptor Blockade ◽  
Adrenergic Stimulation ◽  
Glycogen Depletion ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Adrenergic Receptor Blockade ◽  
Exogenous Substrates

The purpose of this study was to determine whether beta-adrenergic receptor blockade inhibits glycogen utilization in rats during exercise. Propranolol (1 mg/kg body wt) completely blocked the glycogenolytic effect of a large dose of epinephrine given by injection but did not prevent glycogen breakdown in skeletal muscle or liver during a bout of treadmill exercise. On the contrary, exercise resulted in greater glycogen depletion in plantaris muscles of beta-blocked rats than in those of control rats, probably as a result of decreased availability of fatty acids. Increasing the availability of exogenous substrates slowed the rate of skeletal muscle glycogen depletion during exercise. However, even with increased availability of exogenous substrates, beta-blockade did not result in reduced utilization of skeletal muscle or liver glycogen. In contrast to its effect on skeletal muscle, beta-blockade markedly reduced glycogen depletion in the heart during exercise. We conclude that beta-adrenergic stimulation is of major importance in mediating glycogenolysis in the heart but is not necessary for glycogenolysis in skeletal muscle or liver during prolonged exercise.

Contribution of Hypercapnia and Hypoxia to the Vascular Response to Ischaemia

1970 ◽  
Vol 39 (2) ◽  
pp. 203-222 ◽  
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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