Interaction between L-type Ca2+ channels and sarcoplasmic reticulum in the regulation of vascular tone in isolated rat small arteries

Masaharu Takeuchi, Jun Watanabe, Satoru Horiguchi, Akihiko Karibe, Hiroshi Katoh, Shigeo Baba, Tsuyoshi Shinozaki, Masahito Miura, Mitsumasa Fukuchi, Yutaka Kagaya, Kunio Shirato

研究成果: Article査読

15 被引用数 (Scopus)


Summary: 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 μM) alone, but substantially constricted in the presence of ryanodine (1 μM). 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.

ジャーナルJournal of cardiovascular pharmacology
出版ステータスPublished - 2000

ASJC Scopus subject areas

  • 薬理学
  • 循環器および心血管医学


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