Effect of propranolol, a beta-adrenergic antagonist, on blood flow in the coronary and other vascular fields

Nayler, Winifred G.; McInnes, Iain B.; Swann, J. B.; Carson, Valerie; Lowe, T. E.

doi:10.1016/0002-8703(67)90150-0

Cited by 83 publications

(32 citation statements)

References 16 publications

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“…A NUMBER of investigators have demonstrated a propranolol-induced reduction in renal blood flow and, where measured, in glomerular filtration rate (Schirmeister et al, 1966;Nayler et al, 1967;Carriere, 1969;Fenyvesi & Kallay, 1970;Nies et al, 1971; Krauss et al, 1972;Ibsen & Sederberg-Olsen, 1973;Sullivan et al, 1976). Because a reduction in renal blood flow and glomerular filtration rate are common with agents that reduce cardiac output (Sannerstedt & Conway, 1970), as does propranolol, the renal response was widely attributed to the systemic effects of the agent.…”

Section: Introductionmentioning

confidence: 99%

beta‐Adrenoceptor‐blocking agents and the kidney: effect of nadolol and propranolol on the renal circulation.

Hollenberg¹,

Adams²,

McKinstry³

et al. 1979

Brit J Clinical Pharma

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1 Nadolol was administered intravenously to five hypertensive patients and three healthy volunteers in balance on a 10 mEq sodium intake. 2 Nadolol (0.3-10.0,ug/kg) induced a significant, dose-related increase in renal blood flow, measured with radioxenon, with a maximum increase of 72 ± 4 ml/100g/min (26%) at 3.0 .g/kg. 3 Heart rate and plasma renin activity decreased significantly over the same dose range. 4 The renal vascular response to nadolol contrasts sharply with those found with other P-adrenoceptor-blocking agents.5 The magnitude ofthe increase in renal blood flow, its time-course and the parallel fall in plasma renin activity raise the possibility that the renal vasodilatation reflects the reversal of angiotensin's influence on the renal arterial bed.

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Section: Introductionmentioning

confidence: 99%

beta‐Adrenoceptor‐blocking agents and the kidney: effect of nadolol and propranolol on the renal circulation.

Hollenberg¹,

Adams²,

McKinstry³

et al. 1979

Brit J Clinical Pharma

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“…These dogs survived for 24 hours after the onset of infarction, and myocardial CPK depletion was measured at this time.…”

Section: Methodsmentioning

confidence: 99%

“…Cardiac output, arterial, and left atrial pressures were recorded immediately before giving propranolol in the treated animals, immediately before two-stage ligation of the LAD in all animals (10 min after propranolol in the treated animals), and again in all animals at 15, 30, 60, 90 VOL 57, No 3, MARCH 1978 24 hr were excluded from the study, so that only results from the 25 surviving dogs were considered. Although there was a tendency for mortality rate to be higher in pretreated than in control animals, this was not statistically significant.…”

Section: Group 11mentioning

confidence: 99%

“…5 The findings have been consistent with the results of histological studies of the posterior papillary muscle after circumflex coronary artery ligation in the dog6 and with the reports that propranolol used experimentally preserved high energy stores in infarcting myocardium'5 and reduced gross anatomic infarct size.t1 Moreover, a recent clinical study has shown that propranolol may improve myocardial oxygenation in patients with uncomplicated infarction. 12 The present study was designed to re-examine the effect of high doses of propranolol, using our previously described model for the measurement of myocardial blood flow, both at 15 min and 24 hours after coronary occlusion, and measurement of the intensity of creatine phosphokinase (CPK) depletion at 24 hours after onset of infarction.,3 The effects of propranolol on these parameters were correlated with the hemodynamic alterations produced by the drug in relation to its plasma concentrations.…”

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confidence: 99%

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Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.

Peter¹,

Heng²,

Singh³

et al. 1978

Circulation

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SUMMARY Myocardial creatine phosphokinase (CPK) activity and myocardial blood flow (MBF, 15 ± 5 ,u microspheres) were measured at 24 hours after ligation of the left anterior descending coronary artery in nine untreated anesthetized dogs, in eight dogs pretreated with intravenous propranolol 5 mg/kg and in eight which had both pretreatment as well as infusion of propranolol (1.25 mg/kg/hour) after occlusion. Loss of CPK activity from the border and center zones of the myocardial infarct was similar in extent in dogs which had pretreatment but no infusion of propranolol as it was in the control group. Loss of CPK from the center zone was greater REDUCTION OF MYOCARDIAL OXYGEN CON-SUMPTION with beta-adrenergic blocking drugs1 is of proven clinical value for the treatment of angina pectoris and might also be beneficial in the treatment of the acute imbalance between oxygen supply and demand which occurs during the early stages of myocardial infarction. In spite of an initially encouraging report,2 however, oral administration of propranolol in early randomized trials3 was not found to reduce mortality from myocardial infarction in patients.More recently, Maroko et al. suggested that propranolol could reduce the intensity of experimental myocardial ischemia, as judged by electrocardiographic as well as other criteria.5 The findings have been consistent with the results of histological studies of the posterior papillary muscle after circumflex coronary artery ligation in the dog6 and with the reports that propranolol used experimentally preserved high energy stores in infarcting myocardium'5 and reduced gross anatomic infarct size.t1 Moreover, a recent clinical study has shown that propranolol may improve myocardial oxygenation in patients with uncomplicated infarction.12The present study was designed to re-examine the effect of high doses of propranolol, using our previously described model for the measurement of myocardial blood flow, both at 15 min and 24 hours after coronary occlusion, and measurement of the intensity of creatine phosphokinase (CPK) depletion at 24 hours after onset of infarction.,3 The effects of propranolol on these parameters were correlated with the hemodynamic alterations produced by the drug in relation to its plasma concentrations. (P < 0.005) in dogs receiving pretreatment followed by constant infusion of the drug. Propranolol had no significant effect on collateral blood flow to the border or center zone of the infarct. In separate experiments, there was no important difference in hemodynamic measurements, except a slower heart rate (P < 0.01), when pretreated dogs were compared with control dogs up to 2 hours after coronary ligation. We conclude that propranolol given in this dose does not influence myocardial damage, on the basis of regional myocardial blood flow or tissue CPK depletion values at 24 hr after coronary occlusion. MethodsForty-eight mongrel dogs, weighing 18-32 kg (mean 24 kg) were divided into two groups.Group 1 (25 dogs), designated the survival group, was divided into ...

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“…It has been shown that the noncardioselective 1,-and f2-adrenergic receptor blocking drug, propranolol, causes a reduction in renal blood flow and glomerular filtration rate when administered intravenously (Nayler, McInnes, Swann, Carson & Lowe, 1967;Shirmeister, Decot, Hallauer & Willmann, 1966). A similar reduction in glomerular filtration rate follows the intravenous injection of pindolol (Heierli, Thoelen & Radielovic, 1977).…”

Section: Introductionmentioning

confidence: 99%

A study of the effects of atenolol and propranolol on renal function in patients with essential hypertension.

Wilkinson¹,

Stevens²,

Pickering³

et al. 1980

Brit J Clinical Pharma

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1 The effects of propranolol and atenolol given in random order in a cross-over study to fifteen patients with essential hypertension have been studied. 2 Both drugs were effective in lowering blood pressure and side effects were not markedly different.3 There was no change in exchangeable sodium or potassium or in total body potassium during treatment with either drug. 4 Ambulant plasma renin activity was reduced by both drugs but the fall in blood pressure was not related to initial plasma renin. 5 Despite equal mean reduction in blood pressure with the two drugs, creatinine clearance fell significantly only during treatment with propranolol. 6 These observations suggest that intra-renal f2-adrenoceptors may be of importance in the regulation of renal function.

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Effect of propranolol, a beta-adrenergic antagonist, on blood flow in the coronary and other vascular fields

Cited by 83 publications

References 16 publications

beta‐Adrenoceptor‐blocking agents and the kidney: effect of nadolol and propranolol on the renal circulation.

beta‐Adrenoceptor‐blocking agents and the kidney: effect of nadolol and propranolol on the renal circulation.

Failure of high doses of propranolol to reduce experimental myocardial ischemic damage.

A study of the effects of atenolol and propranolol on renal function in patients with essential hypertension.

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