Influence of Adrenergic Beta‐receptor Blockade on the Acute Cardiovascular Effects of Hydralazine*

Brunner, H.; Hedwall, P. R.; Meier, M.

doi:10.1111/j.1476-5381.1967.tb02118.x

Cited by 45 publications

(14 citation statements)

References 11 publications

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“…The tachycardia observed after vasodilator therapy is mainly due to increased sympathetic activity (Glick & Braunwald, 1965;O'Malley et al, 1976;Davies et al, 1979), although a reduction in vagal tone may contribute to the response (Mroczec et al, 1976;Man in 'T Veld et al, 1980). The tachycardia observed after hydralazine therapy is reduced by 3-adrenoceptor blockade with propranolol (Brunner et al, 1967;Zacest et al, 1972;Velasco et al, 1978), oxprenolol (Davies et al, 1979) and alprenolol (Sannerstedt et al, 1971). Hydralazine may also stimulate the heart directly (Gershwin & Smith, 1967;Khatri et al, 1979;Wendling et al, 1979) but studies on animal isolated preparations (Koch-Weser, 1974) and in normal man (Barbat et al, 1981) indicate that such a direct effect occurs only at high doses.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Nicholls¹,

Harron²,

Shanks³

1983

Brit J Clinical Pharma

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1 The effect of single oral doses of alinidine 80 mg, propranolol 40 mg, hydralazine 50 mg, alinidine 80 mg combined with hydralazine 50 mg, propranolol 40 mg combined with hydralazine 50 mg, and placebo on arterial pressure and heart rate was studied in five normal volunteers in the supine and standing positions and during exercise. Observations were made before and at 1, 2, 3, 4 and 6 h after drug administration. 2 Alinidine 80 mg and propranolol 40 mg significantly reduced heart rate in the supine position, and on exercise. The reductions in supine heart rate produced by alinidine and propranolol were not significantly different, but the maximum effect of alinidine on exercise heart rate was observed later than that of propranolol. Propranolol reduced heart rate in the standing position at all time intervals after drug administration, but alinidine reduced standing heart rate only at 6 h (P < 0.01 when compared to placebo). 3 Hydralazine 50 mg increased supine heart rate by 8-10 beats min-' when compared to the pre-treatment value. These increases were significant (P < 0.05) when compared to the pre-treatment value, but not when compared to placebo. Hydralazine increased standing heart rate from 71.4 + 6.5 to 90.0 + 7.0 beats min-' (P < 0.05 when compared to placebo), but had no effect on exercise heart rate. The small increase in supine heart rate following hydralazine therapy was reduced by alinidine and propranolol, but only propranolol reduced the significant increase in standing heart rate produced by hydralazine. 4 Hydralazine reduced diastolic arterial pressure in the supine position at 2 and 4 h after drug administration (P < 0.05 when compared to placebo), but had no effect on systolic or diastolic arterial pressure in the standing position or on exercise. 5 Propranolol produced small reductions in systolic arterial pressure in the standing position, which were not significant when compared to placebo; diastolic pressure was unchanged. Propranolol reduced systolic pressure during exercise at 2, 4 and 6 h after drug administration (P < 0.05 when compared to placebo); diastolic pressure was unchanged. The effects of hydralazine and propranolol combined on arterial pressure in the standing position were similar to those observed after propranolol alone, but combined therapy produced a greater reduction in exercise systolic pressure, although these differences were not significant. 6 Alinidine reduced systolic arterial pressure in the supine position at 3, 4 and 6 h after drug administration (P < 0.01) and diastolic pressure at 2 and 4 h (P < 0.05 when compared to placebo). Alinidine reduced systolic arterial pressure in the standing position at 3, 4 and 6 h after drug administration (P < 0.05) and diastolic pressure at 2 h (P < 0.01) and 6 h (P < 0.05 when compared to placebo). During exercise, alinidine produced a small reduction in systolic arterial pressure which was not significant, and a reduction in diastolic pressure at 1 h (P < 0.05 when compared to placebo). The effects of hydralazine and alini...

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Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Nicholls¹,

Harron²,

Shanks³

1983

Brit J Clinical Pharma

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“…Indeed, activation of reactive vasoconstriction may greatly limit the therapeutic hypotensive response to vasodilator administration in hypertensive patients. 6 " 8 Our main purpose in the present study was to assess whether CCA circulation could influence the baroreceptor reflex response to arteriolar vasodilation. Hemodynamics of the CCA and the BA were measured in immediate succession in 10 subjects with essential hypertension before and after oral administration of ca-…”

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confidence: 99%

Hemodynamics of the carotid artery after vasodilation in essential hypertension.

et al. 1988

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SUMMARYWe performed simultaneous noninvasive measurements of common carotid artery and brachial artery hemodynamics in nine normal subjects and 10 subjects with sustained essential hypertension. In hypertensive subjects, brachial artery blood flow and forearm vascular resistance were in the normal range while carotid artery blood flow and carotid artery resistance were decreased and increased, respectively. The most important findings were the changes in the internal caliber of large arteries. Although the brachial and carotid artery diameters of hypertensive subjects were measured for the same level of mean arterial pressure, brachial artery diameter was significantly increased and carotid artery diameter was strictly normal as compared with values found in normal subjects. To assess whether carotid artery circulation could influence the baroreceptor reflex response to arteriolar vasodilation, carotid artery and brachial artery hemodynamics were measured in immediate succession in normotensive and hypertensive subjects before and after oral administration of cadralazine, a dihydralazine derivative. After cadralazine treatment, carotid artery tangential tension decreased in hypertensive subjects, and the changes were significantly correlated to the Increase in heart rate. A similar correlation was found in normal subjects, but it was reset toward higher heart rates. These results indicate that the carotid artery does not behave like the brachial artery in response to a chronic increase in blood pressure. This behavior indicates intrinsic alterations of the arterial wall and might be involved in the resetting of the carotid baroreceptor reflex. Carotid artery circulation could play a role in hypertension by modulating the carotid baroreceptor mechanisms involved in the response to drug-induced arteriolar vasodilation. Whether these findings represent a primary or a secondary event remains to be determined. (CCA) and the brachial artery (BA) to a chronic elevation of blood pressure may differ according to the regional circulation. Using a noninvasive pulsed Doppler system, we evaluated arterial diameter and blood flow of the straight superficial arteries. We measured simultaneously CCA and BA hemodynamics in normal and hypertensive subjects to assess the effect of essential hypertension on circulation in these arteries.The decrease in blood pressure and vascular resistance observed after treatment with dihydralazine or its derivative, cadralazine, was related to the dilation of small arteries, as has been shown extensively for dihyFrom the Diagnosis Center and the Hypertension Research Center, Broussais Hospital, Paris, France.Address for reprints: Prof. M. Safar, Centre de Diagnostic, H6pi-tal Broussais,

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“…It has recently been suggested that hydralazine may also have a direct positive inotropic effect (Opie, 1980;Khatri etal., 1977). Studies in animals (Brunner, Hedwall & Meier, 1967) and normotensive and hypertensive man (Sannerstedt et al, 1971) have demonstrated the attenuating effects of 18-adrenoceptor blocking agents on hydralazine-induced tachycardia. Oral administration of prizidilol hydrochloride at a dose of 5 mg/kg has significantly lowered systemic blood pressure without increasing standing heart rate (Bell et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects in man of intravenous prizidilol hydrochloride (SK&F 92657); a new antihypertensive agent.

Edmonstone¹,

Manghani²,

Bell³

et al. 1981

Brit J Clinical Pharma

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1 Cardiovascular responses to intravenous prizidilol hydrochloride (SK&F 92657) 0.86 mg/kg were studied in eight supine resting healthy volunteers. Five subjects were slow and the remaining three were fast acetylators of sulphamethazine. Compared with pre-infusion values, mean resting systolic and diastolic blood pressures were significantly reduced, while mean resting pulse rate was significantly increased at 30 min after the start of the twenty minute infusion. 2 During the 6 h study period the lowest mean ± s.e. mean systolic blood pressure (108.8 + 1.7) was recorded 30 min after the start of the infusion. This represented a mean reduction of 5.2 mmHg. Reductions in mean diastolic blood pressure were greater and of longer duration, the lowest mean value (44.8 + 2.0 mmHg) being recorded 3.5 h after the start of the infusion and representing a reduction of 18.5 mmHg from the pre-dosing value. At 6 h after the start of the infusion mean diastolic blood pressure was still significantly reduced (by 15.3 mmHg). 3 The maximum mean + s.e. mean resting pulse rate (79.3 ± 4.4 beats/min) occurred 3 h after the start of the infusion, an increase of 23.0 beats/min over the pre-infusion value. At the end of the study the pulse rate was still significantly raised (by 17.7 beats/min). 4 The left ventricular ejection fraction, evaluated in five subjects, 45 min after the start of the infusion, was not altered by prizidilol hydrochloride, but the left ventricular area decreased significantly. 5 Intravenous prizidilol hydrochloride decreases resting blood pressure and left ventricular area, increases pulse rate and has virtually no effect on left ventricular ejection fraction.

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Influence of Adrenergic Beta‐receptor Blockade on the Acute Cardiovascular Effects of Hydralazine*

Cited by 45 publications

References 11 publications

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Cardiovascular effects of alinidine and propranolol alone and in combination with hydralazine in normal man.

Hemodynamics of the carotid artery after vasodilation in essential hypertension.

Cardiovascular effects in man of intravenous prizidilol hydrochloride (SK&F 92657); a new antihypertensive agent.

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