title: Interaction between L-type Ca2+ channels and sarcoplasmic reticulum in the regulation of vascular tone in isolated rat small arteries.
abstract: A dysfunction of the sarcoplasmic reticulum (SR) causes an increase in the myogenic tone of rat skeletal muscle small arteries (A(SK)), but not that of mesenteric small arteries (A(MS)). We hypothesized that the difference depends on the activity of voltage-dependent Ca2+ channels in these vessels. To test this, we measured the membrane potential of these vessels and examined ryanodine-induced constrictions by manipulating the activity of voltage-dependent Ca2+ channels. The isolated vessels were cannulated to control the transmural pressure. To assess the vascular tone, the inner diameter was measured with a video-digitizing system. The membrane potential of A(SK) was more depolarized between 20 to 100 mm Hg of transmural pressure. A(MS) was not constricted by the Ca2+ channel agonist Bay K 8644 (1 nM(-1) microM) alone, but substantially constricted in the presence of ryanodine (1 microM). Ryanodine also augmented the KCl (20 mM)-induced constriction. In A(SK), the Ca2+ channel blocker nisoldipine fully dilated the ryanodine-induced constriction: however, the ryanodine-induced constriction was less susceptible to nisoldipine than was the myogenic and phenylephrine-induced constriction caused mainly by increased Ca2+ influx. In conclusion, the contribution of the SR function to Ca2+ metabolism depends on the activity of dihydropyridine-sensitive Ca2+ channels. The dysfunction of SR by ryanodine may impair the Ca2+ extrusion rather than increase Ca2+ influx in rat small arteries.
authors.affiliation: Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Takeuchi
authors.forename: J
authors.initials: J
authors.lastname: Watanabe
authors.forename: S
authors.initials: S
authors.lastname: Horiguchi
authors.forename: A
authors.initials: A
authors.lastname: Karibe
authors.forename: H
authors.initials: H
authors.lastname: Katoh
authors.forename: S
authors.initials: S
authors.lastname: Baba
authors.forename: T
authors.initials: T
authors.lastname: Shinozaki
authors.forename: M
authors.initials: M
authors.lastname: Miura
authors.forename: M
authors.initials: M
authors.lastname: Fukuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Kagaya
authors.forename: K
authors.initials: K
authors.lastname: Shirato
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology*; D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects*; D004347:Drug Interactions; D008564:Membrane Potentials / Q000187:drug effects*; D008638:Mesenteric Arteries; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D015737:Nisoldipine / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D051381:Rats; D017208:Rats, Wistar; D012433:Ryanodine / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*
chemical_list: D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D012433:Ryanodine; D015737:Nisoldipine; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester