Effect of propranolol on sympathetic nervous activity in hydrallazine‐ treated hypertensive patients.

Velasco, Manuel; Romero, Eduardo; Bertoncini, H.; Urbina-Quintana, A.; Guevara, José Cordero; Pieretti, Otto Hernandez

doi:10.1111/j.1365-2125.1978.tb04587.x

Cited by 7 publications

(1 citation statement)

References 6 publications

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“…The haemodynamic effects of cold exposure during blockade with propranolol have been extensively studied (Nicotero et al, 1968;Guazzi et al, 1976;Maconochie et at., 1977;Velasco et al, 1978). As far 0306-5251/82/12086704 $01.00 as we know only one study has been published on the influence of one of the now available selective 8-adrenoceptor blockers, i.e.…”

Section: Introductionmentioning

confidence: 99%

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non‐selective beta‐ adrenoceptor blockade.

Houben¹,

Thien²,

Wijnands³

et al. 1982

Brit J Clinical Pharma

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Haemodynamic effects of a cold pressor test (foot immersion for 6 min in water at 5°C) without medication and after the non-selective 3-adrenoceptor blocker propranolol and the selective 3-adrenoceptor blocker metoprolol were studied in 17 volunteers. In the control study as well as in the study with the 8-adrenoceptor blockers cold exposure caused comparable changes, namely a blood pressure rise and a reduction of forearm blood flow. The increase in heart rate during cold exposure was clearly and equally reduced by both ,8-adrenoceptor blockers. Plasma noradrenaline rose significantly by 47%, plasma adrenaline did not change. It is concluded, that as to this kind of stress, ,81-selective-adrenoceptor blockade confers no important advantage over non-selective X3-adrenoceptor blockade.

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Section: Introductionmentioning

confidence: 99%

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non‐selective beta‐ adrenoceptor blockade.

Houben¹,

Thien²,

Wijnands³

et al. 1982

Brit J Clinical Pharma

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Comparative Effects of Dopaminergic Agonists on Cardiovascular, Renal, and Renin‐Angiotensin Systems in Hypertensive Patients

Luchsinger¹,

Velasco

Urbina

et al. 1992

The Journal of Clinical Pharma

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The role of dopaminergic receptors on renal function has been extensively studied. Recently dopaminergic receptor has been classified in two subtypes D1 and D2, which seem to have different modulatory function. However, the role of dopaminergic receptors on cardiovascular function and more specifically the potential role of dopaminergic agonists as antihypertensive agents has not yet been clarified. Nine outpatients with mild and moderate hypertension were studied in the Cardiology Service of Vargas Hospital with a D1 agonist, piribedil, at 50-100 mg/day, orally, for 8 weeks, and with a D2 agonist, bromocriptine, at 2.5 - 5 mg/day, orally, for an another 8 weeks by using a placebo comparative crossover design. Piribedil reduced blood pressure with a modest increase in heart rate, plasma renin activity, and of plasma aldosterone, and an important increment of renal function. Bromocriptine reduced blood pressure with a decrease in heart rate and plasma aldosterone without altering renal function. There was no orthostatic hypotension with either agent. The authors conclude that activation of dopaminergic D1 receptor induces a vasodilatory and antihypertensive effect with a reflex increase in sympathetic tone, whereas activation of dopaminergic D2 receptor induces a decrease in sympathetic tone, probably due to a decrease in norepinephrine release at adrenergic endings. The potential effect of these compounds as antihypertensive agents is of great interest because blood pressure reduction can be induced by a new mechanism, i.e. activation of dopaminergic receptors which results in a decrease of the renin angiotensin system or a vasodilatory action.(ABSTRACT TRUNCATED AT 250 WORDS)

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The changing concept of cardiovascular reactivity

Rosenman¹,

Ward²

1988

Stress Med.

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Cardiovascular reactivity has long been measured in laboratory responses to a wide variety of cognitive and physical stressors, with the hypothesis that exaggerated reactivity plays a pathogenetic role in the development of essential hypertension. However there are few data to support the belief that behavioural differences of cognitive perception of stressors account for observed differences of reactivity. Cardiovascular reactivity in the laboratory does not predict hypertension or account for differences of blood pressure variability in the natural environment. Hypertensives do not exhibit increased blood pressure variability. Antihypertensive therapy consistently fails to lower cardiovascular reactivity in either the laboratory or natural milieu, supporting the dual and largely independent regulation of the basal and reactive blood pressures. It is concluded that there is little support for the use of laboratory stress testing to delineate either the pathogenesis of hypertension, the evaluation of hypertensive subjects, or the efficacy of antihypertensive therapy.

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Effect of propranolol on sympathetic nervous activity in hydrallazine‐ treated hypertensive patients.

Cited by 7 publications

References 6 publications

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non‐selective beta‐ adrenoceptor blockade.

Effects of cold exposure on blood pressure, heart rate and forearm blood flow in normotensives during selective and non‐selective beta‐ adrenoceptor blockade.

Comparative Effects of Dopaminergic Agonists on Cardiovascular, Renal, and Renin‐Angiotensin Systems in Hypertensive Patients

The changing concept of cardiovascular reactivity

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