The effect of diltiazem on noradrenaline release

Wolchinsky, C.; Zsoter, T

doi:10.1111/j.1476-5381.1985.tb08873.x

Cited by 15 publications

(6 citation statements)

References 17 publications

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“…Since the NA-depleting activity of verapamil that is described here was accompanied by a similar reduction in tissue DA and DHPG, it is unlikely that the depletion is due to an altered rate of synthesis or degradation. Other investigators have already established that the NA-depleting activity of verapamil is unaIfected by K+ channel blockade, inhibition of uptake1 and uptakez, or a2-adrenoceptor antagonism induced with yohimbine (Chaudhry & Vohra 1984Wolchinsky & Zsoter 1985).…”

Section: Discussionmentioning

confidence: 99%

Calcium Antagonists and Hypertension

Nayler

Dillon

Sturrock

1988

Clin Exp Pharma Physio

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1. Calcium antagonists, including verapamil, are now used widely in the management of patients with hypertension. 2. Six weeks of chronic therapy with verapamil (50 mg/kg per day, orally) to produce a plasma level of 80-100 ng/ml in Sprague-Dawley rats depletes cardiac noradrenaline (NA) without apparently causing beta 1 adrenoceptor 'up' regulation. 3. The effect of verapamil on cardiac NA is rapidly reversed upon verapamil withdrawal. 4. Chronic therapy with nisoldipine (100 mg/kg per day, orally) had no effect on cardiac NA. 5. Verapamil (50 mg/kg per day, orally) and nisoldipine (100 mg/kg per day, orally) therapy for 6 weeks prevented the time-dependent increase in systolic blood pressure in SHR rats. 6. Binding studies with (-)[3H]-D888 (desmethoxyverapamil) indicated that the affinity of the phenylalkylamine binding sites is higher in hearts of SHR relative to hearts from age-matched (25 weeks) WKY and SD, without any change in density.

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Section: Discussionmentioning

confidence: 99%

Calcium Antagonists and Hypertension

Nayler

Dillon

Sturrock

1988

Clin Exp Pharma Physio

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“…One possibility is that pinacidil directly affects, in a non-specific manner, the storage sites for catecholamines, as does tyramine (Lindmar et al, 1967). Calcium channel blockers, like nifedipine or diltiazem, do have such properties (Wolchinsky & Zsoster, 1985;Zsoster & Wolchinsky, 1986). Moreover, this hypothesis of a 'non-specific' effect agrees with a recent communication from Cook et al (1989) who found, in in vitro experiments, that the vasodilator activity of pinacidil cannot be solely explained by potassium channel opening.…”

Section: Controlsmentioning

confidence: 99%

Effects of pinacidil on the sympatho‐adrenal system in dogs

Damase‐Michel

Tran

Montastruc

et al. 1989

British J Pharmacology

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The aim of the present work was to study the antihypertensive effect of pinacidil, a potassium channel opener, in sinoaortic denervated (SAD) conscious dogs and to investigate whether the involvement of the sympathetic nervous system induced by this vasodilator compound is only of baroceptor reflex origin. Pinacidil (0.1, 0.2, 0.4 mg kg−1 i.v.) induced a dose‐dependent decrease in blood pressure in normal as well as in SAD dogs. In contrast, the induced‐tachycardia observed in normal dogs was not found in SAD animals. Since pinacidil induced an increase in plasma catecholamines, free fatty acids, glucose, plasma renin activity and aldosterone in SAD dogs, it is suggested that this sympathetic activation is independent of the baroreceptor reflex pathways. The sympathetic activation is mainly of peripheral origin, since pinacidil (0.7 mg kg−1 i.v.) induced an increase in adrenaline release from the adrenal gland after section of the great splanchnic nerve in anaesthetized dogs. This increase is probably due to an effect that does not involve K+ channel opening. However, this effect of pinacidil was not observed during splanchnic nerve stimulation (in this case, the involvement of K+ channel opening is suggested).

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“…The precise mechanisms responsible for these hemodynamic effects and the inhibited norepinephrine release during diltiazem administration shown in the present study have not been established. In rats, diltiazem has been shown to inhibit norepinephrine release from sympathetic nerve terminals and the adrenal gland through an alteration in adrenergic cardiovascular stimulation [21]. Imai et al [22], however, reported that continuous infusion of diltiazem induced a gradual decrease in both arterial pressure and heart rate in rats, whereas it also induced activation of the sympathetic nervous system, as assessed by the correlation between systolic pressure and norepinephrine.…”

Section: Discussionmentioning

confidence: 98%