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Amiloride‐sensitive pressure‐induced myogenic contraction in rat cerebral artery
Author(s) -
Oyabe Akihiro,
Masumoto Naohiro,
Ueta Kiichiro,
Nakayama Koichi
Publication year - 2000
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2000.tb00418.x
Subject(s) - amiloride , cyclopiazonic acid , calphostin c , contraction (grammar) , thapsigargin , myogenic contraction , endocrinology , medicine , chemistry , extracellular , vasoconstriction , muscle contraction , nicardipine , pharmacology , protein kinase c , calcium , biochemistry , enzyme , organic chemistry , smooth muscle , sodium
— The inhibitory action of amiloride on the pressure‐induced contraction was assessed in isolated rat cerebral artery. The artery was mounted in an arteriograph, and the change in intracellular Ca 2+ concentration ([Ca 2+ ] i ) and vessel diameter were simultaneously measured. The contractile response elicited by intraluminal pressurization was independent of endothelium, i.e. myogenic in nature, and abolished by nicardipine, a Ca 2+ antagonist or by removal of extracellular Ca 2+ , and was potentiated by 25 mM KCl. Cyclopiazonic acid and thapsigargin, inhibitors of the Ca 2+ ‐ATPase pump of the sarcoplasmic reticulum, and a protein kinase C inhibitor calphostin C did not suppress the pressure‐induced contraction. Amiloride, a putative stretch‐activated cation channel blocker, attenuated with an IC 50 (50% inhibitory concentration) of about 3 μM the increase in [Ca 2+ ] i and contractile activity in response to pressure, whereas the drug showed no apparent effect on the contraction produced by high KCl or 9,11‐dideoxy‐11α,9α‐epoxymethano prostaglandin F 2α , (U46619). Furthermore, amiloride (100 μM) did not significantly affect intracellular pH in the artery. In spite of its multiple pharmacological actions, it seems possible that amiloride is a useful alternative tool at the cellular or tissue level to study the mechanotransduction mechanisms involved in the pressure‐induced contraction in rat cerebral artery.