Calcium mobilization and phosphatidylinositol turnover in vas deferens smooth muscle of diabetic rats
Y Sakai, K Aihara, H Honda, M Inazu - European journal of pharmacology, 1989 - Elsevier
Y Sakai, K Aihara, H Honda, M Inazu
European journal of pharmacology, 1989•ElsevierThe study concerned Ca 2+ channels that are receptor-operated by norepinephrine (NE)
and mediate hyper-reactivity of vas deferens smooth muscle from rats with streptozotocin
(STZ)-induced diabetes, and the mediatory responses of these channels, such as tension
development, Ca 2+ uptake and phosphatidylinositol (PI) turnover. The contractile
responses induced by adrenoceptor agonists were significantly greater in diabetic rat vas
deferens than in the controls. A greater Ca 2+ uptake was induced by 10− 5 M NE in strips …
and mediate hyper-reactivity of vas deferens smooth muscle from rats with streptozotocin
(STZ)-induced diabetes, and the mediatory responses of these channels, such as tension
development, Ca 2+ uptake and phosphatidylinositol (PI) turnover. The contractile
responses induced by adrenoceptor agonists were significantly greater in diabetic rat vas
deferens than in the controls. A greater Ca 2+ uptake was induced by 10− 5 M NE in strips …
Abstract
The study concerned Ca2+ channels that are receptor-operated by norepinephrine (NE) and mediate hyper-reactivity of vas deferens smooth muscle from rats with streptozotocin (STZ)-induced diabetes, and the mediatory responses of these channels, such as tension development, Ca2+ uptake and phosphatidylinositol (PI) turnover. The contractile responses induced by adrenoceptor agonists were significantly greater in diabetic rat vas deferens than in the controls. A greater Ca2+ uptake was induced by 10−5 M NE in strips from diabetic rats than in the controls. The uptake of Ca2+ was completely inhibited by 10−6 M prazosin but not by 10−5 M verapamil. Enhancement of Ca2+ release by 10−5 M NE was faster and greater in diabetic muscles than in the controls. The accumulation of [3H]inositol phosphates was increased 4-fold in the controls and 7-fold in diabetic muscles by 10−5 M NE. This increase was completely inhibited by 10−6 M prazosin but not by 10−6 M yohimbine. The data suggest that vas deferens smooth muscle hyper-reactivity in diabetic rats is due to increased PI turnover mediated by α1-adrenoceptors, to the release of intracellular bound Ca2+ and to an increase of Ca2+ uptake through receptor-operated Ca2+ channels.
Elsevier
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