Effect of Diltiazem on the Membrane Potential of Uterine Smooth Muscle

Abstract

On the other hand, methoxamine usually induced negative chronotropic and inotropic effects in both preparations, and these negative effects were not blocked by atropine, tetrodotoxin and phentolamine. These results suggest that phenylephrine produces a cholinergic excitation which may occur through an adrenergic alpha-mechanism in parasympathetic nerve terminals, in addition to its adrenergic beta-stimulating effect.In 1968, James et al.(1) reported that sinus deceleration with the adrenergic alpha stimulant, methoxamine was prevented by phenoxybenzamine but not by atropine. These workers had directly perfused the sinus node artery of the dog heart in situ (2). They con cluded that this phenomenon was "evidence for alpha receptor depressant activity". The negative chronotropic effect was not however, observed when phenylephrine was adminis perfused atria] preparation of the dog, which allows for a well controlled study of such local mechanisms and perfusion is carried out only through the sinus node artery.In the present study, the isolated canine atria] preparation was employed to determine

Cardiovascular effects of topical ophthalmic 10% phenylephrine in dogs

“…In a similar study, negative, positive and combined chronotropic responses were observed but the specific effects did not appear to be dose related 14 . A study using isolated canine atrial and ventricular preparations also produced mixed chronotropic responses 15 . Others have shown that, through α 1 ‐adrenergic mediated reduction in acetylcholine release from parasympathetic neurons, phenylephrine reduces the magnitude of bradycardia produced by direct vagal stimulation 16,17 .…”

Mechanism of epinephrine-induced dysrhythmias in rat involves local cholinergic activation

“…The hypothesis that epinephrine induced ACh release by cardiac parasympathetic efferent postganglionic neurons is supported by findings that ACh liberation from parasympathetic cardiac nerve fibers is facilitated by α 1 -adrenoceptors (Chiba 1977;Flavahan and McGrath 1982;Bognar et al 1990). However, vagal efferent postganglionic axon terminals are not equipped with α 1 -or α 2 -adrenoceptors (Manabe et al 1991).…”

Pharmacological analysis of positive chronotropic and inotropic responses to etilefrine in isolated dog heart preparations

“…However, Mukherjee et al (8) found more 13-adrenoceptors and fewer «-1 adrenoceptor binding sites in the dog myocardium than rabbit or rat heart. Furthermore, Chiba [9] and Endoh et al [10] reported that adrenoceptors mediating positive chronotropic and inotropic responses in the dog heart were ]3-adrenoceptors not post-synaptic ct-adrenoceptors.…”

“…They found more 13-adrenoceptor and fewer post-synaptic c~-1 adrenoceptor binding sites in the dog myocardium. Moreover, functional observations in the isolated dog heart preparations showed that positive cardiac effects of sympathomimetic amines were mostly mediated by 13-adrenoceptors [9,10]. Etilefrine has been postulated as a cardioselective 13-adrenoceptor or 13-1 adrenoceptor agonist [4,11].…”