RESUMO
Cromakalim has been shown to inhibit naphazoline-induced contractions and spontaneous activity induced by exposure to naphazoline in the rat isolated vas deferens. Glibenclamide 10(-6) M blocked both these effects of cromakalim. Our data add to the list of data derived mainly from experiments on vascular smooth muscle; they suggest that the same glibenclamide-sensitive K+ channel is present in vascular and non-vascular smooth muscle and that it may be involved in the relaxant actions of cromakalim.
Assuntos
Benzopiranos/antagonistas & inibidores , Glibureto/farmacologia , Músculo Liso/efeitos dos fármacos , Nafazolina/farmacologia , Pirróis/antagonistas & inibidores , Animais , Benzopiranos/farmacologia , Cromakalim , Técnicas In Vitro , Masculino , Contração Muscular/efeitos dos fármacos , Nafazolina/antagonistas & inibidores , Parassimpatolíticos/farmacologia , Canais de Potássio/efeitos dos fármacos , Pirróis/farmacologia , Ratos , Ratos Endogâmicos , Ducto Deferente/efeitos dos fármacosRESUMO
In five conscious adult ewes at rest, chronically implanted with electrodes in the musculature of the omasal wall, intravenous (i.v.) infusion for 30 min of alpha 1- or alpha 2-adrenergic receptor blockers, prazosin (20 micrograms/kg/min) and yohimbine (30 micrograms/kg/min), respectively, had no significant effects on omasal myoelectrical activity. The i.v. administration for 15 min of alpha 1- or alpha 2-agonists phenylephrine (4 micrograms/kg/min) or naphazoline (2.5 micrograms/kg/min), respectively, increased the frequency and the amplitude of groups of myoelectrical discharges of omasum, as well as the duration of its activity. Pretreatment of animals with prazosin blocked the responses to phenylephrine. Yohimbine prevented the effects of naphazoline dose-dependently. It is suggested that both alpha 1- and alpha 2-adrenoreceptors are involved in regulation of the sheep's omasal notility. This regulation did not seem to be a simple consequence of the changes in the reticular motility.
