Effects of propranolol on peripheral vessels in man

Brick, I.; Glover, W. E.; Hutchison, K.J.; Roddie, I. C.

doi:10.1016/0002-9149(66)90050-6

Cited by 69 publications

(20 citation statements)

References 2 publications

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“…Judging by the test results found in literature (11,21,13,7) and by our own results it may be concluded that propranolol has a marked blocking effect on the adrenergic beta-receptors in the blood vessels supplying the muscles. The typical vasodilation after small intra arterial or intravenous injections o f adrenaline is completely prevented and replaced by a sole vasoconstriction, the alpha-receptor stimulating effect of the adrenaline.…”

Section: Discussionsupporting

confidence: 60%

The Effect of Beta-Adrenergic Blocking Substances on Muscle Bloodflow in Man

Schoop¹,

Schmidtke²

1966

J Vasc Res

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Section: Discussionsupporting

confidence: 60%

The Effect of Beta-Adrenergic Blocking Substances on Muscle Bloodflow in Man

Schoop¹,

Schmidtke²

1966

J Vasc Res

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“…First, propranolol is an exceptionally specific /3-receptor blocker and is apparently devoid of direct sympathomimetic or vascular actions (8,9). Among its effects in this study were an increase in splanchnic vascular resistance and a reduction in blood flow and oxygen consumption.…”

Section: Discussionmentioning

confidence: 69%

Control of the Splanchnic Circulation in Man

Price

Cooperman

Warden

1967

Circulation Research

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Some effects of the /3-adrenergic receptor blocker, propranolol, were studied in 20 normal, fasting, conscious men. The measurements made included cardiac output, splanchnic blood flow and oxygen consumption, arterial and hepatic venous blood pressure, and heart rate. The intravenous administration of propranolol (0.13 mg/kg) was followed by significant reductions in splanchnic blood flow and oxygen consumption, in cardiac output and in heart rate. Splanchnic perfusion pressure was unchanged; the splanchnic vascular resistance was significantly elevated. Previous treatment with glucose did not alter these findings. Phenoxybenzamine prerreatment lessened the increase in splanchnic vascular resistance which propranolol ordinarily caused. Ganglionic blockade with hexamethonium prevented all of the changes which propranolol produced in untreated individuals. These results may best be explained by assuming that the splanchnic circulation in man is influenced both by a receptors, which cause vasoconstriction when activated, and by /9 receptors, which when activated cause vasodilatation and increase oxygen consumption.ADDITIONAL KEY WORDS alpha-adrenergic receptor blockade splanchnic vascular resistance beta-adrenergic receptor blockade propranolol hexamethonium splanchnic oxygen consumption phenoxybenzamine• One of us has reported (1) that the administration of propranolol (a /3-adrenergic receptor blocking drug of high specificity) to human subjects anesthetized with cyclopropane caused a marked reduction in splanchnic blood flow. This reduction resulted from increased vascular resistance and was usually accompanied by a diminution in local oxygen consumption. Since cyclopropane is believed to increase the impulse frequency in sympathetic nerves supplying the abdominal viscera (2), these observations raised the question whether some of the activity

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“…After 1 mg of propranolol, the effect of adrenaline on the heart was blocked and a bradycardia occurred. This can be attributed to a reflex increase in vagal activity (Glick & Braunwald, 1965) in response to the increase in arterial pressure which adrenaline produced as a result of propranolol blocking its peripheral vasodilator but not its vasoconstrictor action (Brick et al, 1966). I.C.I.…”

Section: Discussionmentioning

confidence: 99%

Comparison of the effects of I.C.I. 50172 and propranolol on the cardiovascular responses to adrenaline, isoprenaline and exercise

Brick

Hutchison

McDevitt

et al. 1968

British J Pharmacology

121

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The intravenous infusion of I.C.I. 50172 in doses up to 20 mg reduced, although not significantly, the increase in heart rate produced by the infusion of isoprenaline in healthy volunteers; the response to adrenaline was significantly reduced. The infusion of 1 mg propranolol abolished these responses After the pre‐treatment of subjects with atropine or hexamethonium, I.C.T. 50172 produced a significant reduction in an isoprenaline tachycardia. This reduction was not competitive and did not exceed 50%. The intravenous injection of 4 mg I.C.I. 50172 reduced an exercise tachycardia; its effect was less than that of 4 mg propranolol. This difference became greater as the doses of the two drugs were increased. The dextro isomer of propranolol had no effect on the exercise tachycardia; I.C.I. 45763 reduced it to the same extent as propranolol. The intravenous injection of I.C.I. 50172 reduced the increase in heart rate produced by tilting a normal subject from the supine to 80° head‐up position. After the administration of atropine, I.C.I. 50172 almost abolished the response. In the presence of atropine, I.C.I. 50172 was as active as propranolol in reducing the increase in heart rate on tilting. The reason for the differences in the effects of I.C.I. 50172 on the increases in heart rate brought about by the three procedures is not clear. The increase in forearm blood flow produced by the infusion of isoprenaline into the brachial artery was not reduced by the intra‐arterial administration of I.C.I. 50172.

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Effects of propranolol on peripheral vessels in man

Cited by 69 publications

References 2 publications

The Effect of Beta-Adrenergic Blocking Substances on Muscle Bloodflow in Man

The Effect of Beta-Adrenergic Blocking Substances on Muscle Bloodflow in Man

Control of the Splanchnic Circulation in Man

Comparison of the effects of I.C.I. 50172 and propranolol on the cardiovascular responses to adrenaline, isoprenaline and exercise

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