Detail of "61-16-5"

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The effects of denervation, cocaine, 6-hydroxydopamine and reserpine on the characteristics of drug-induced contractions of the depolarized smooth muscle of the rat and guinea-pig vas deferens

The effects of denervation, cocaine, 6-hydroxydopamine and reserpine on the characteristics of drug-induced contractions of the depolarized smooth muscle of the rat and guinea-pig vas deferens. Westfall, David P. (Med. Cent., West Virginia Univ., Morgantown, W. Va., USA). J. Pharmacol. Exp. Ther., 201(2), 267-75 (English) 1977. CODEN: JPETAB. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacodynamics) Previous studies have suggested that postjunctional supersensitivity of the vas deferens in due in part to altered electrophysiol. properties, the sensitivity of the muscle being increased to any agonist which initiates contraction by means of depolarizing the cell membrane. Results of the present study indicate that altered elec. properties are not the only postjunctional changes which can account for the enhanced response. Dose-response curves for stimulant agonists were obtained in isolated vasa deferentia which were depolarized by a K-rich, Na-free soln. Chronic denervation resulted in a 2- to 3-fold displacement of the dose-response curve for norepinephrine bitartrate [51-40-1] to the left of control. In contrast, cocaine [50-36-2] (10-5 M) did not potentiate the response to norepinephrine of the innervated, depolarized smooth muscle. Supporting the contention that the supersensitivity of the depolarized tissue is postjunctional in nature was the finding that the denervated vas deferens was supersensitive to methoxamine-HCl [61-16-5] , an agent which is not taken up by the neuronal amine transnport system. Pretreatment of rats with reserpine [50-55-5] (1.0 mg/kg/day for 5-7 days) also produced supersensitivity of the depolarized vas deferens. The increased maximal response to drugs of the denervation rat vas deferens which is obsd. in normally polarized tissues is absent in depolarized tissues suggesting that the phenomenon of increased max. requires the existence of a membrane potential in order to be manifest. The denervated vas deferens, but not the vas deferens from reserpine-pretreated animals, exhibits an increase in the duration of drug-induced contractions. This effect occurs in both normal and depolarizing salt solns. suggesting that the change which leads to this phenomenon differs from those alterations which lead to postjunctional supersensitivity and to the enhanced max. response.

Prostaglandin-mediated inhibition of noradrenaline release

Prostaglandin-mediated inhibition of noradrenaline release. IV. Prostaglandin synthesis is stimulated by myocardial adrenoceptors differing from the a- and b-type. Wennmalm, A.; Brundin, T. (Dep. Clin. Physiol., Karolinska Inst., Swed.). Acta Physiol. Scand., 102(3), 374-81 (English) 1978. CODEN: APSCAX. ISSN: 0001-6772. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Section cross-reference(s): 1 In the isolated rabbit heart, assays were made of the outflow of prostaglandin E (PGE) during exposure to equimolar concns. of methoxamine-HCl [61-16-5] noradrenaline bitartrate [51-40-1] adrenaline bitartrate [51-42-3], and isoprenaline [7683-59-2] in the absence and in the presence of phentolamine or propranolol. Noradrenaline caused an almost 4-fold increase in the basal outflow of PGE from the heart, whereas methoxamine (an a-adrenoceptor agonist) and isoprenaline (a b-adrenoceptor agonist) were both ineffective in this respect. Thus, the PGE-releasing capacity of the drugs was not correlated to their ability to activate a- or b-adrenoceptors. Furthermore, no relation was obtained between the PGE release induced by the drugs and the increase in heart rate and contractile force elicited by them. Apparently, sympathomimetic drugs trigger PGE synthesis and release in the rabbit myocardium following activation of a hitherto unobsd. adrenoceptive mechanism, optimally stimulated by noradrenaline.