Jpn. J. Pharmacol. 83 (4), 335-343 (2000)

Ca2+ Buffering Function of Sarcoplasmic Reticulum in Rat Tail Arteries: Comparison in Normotensive and Spontaneously Hypertensive Rats

Yukiko Nomura and Masahisa Asano*

Department of Pharmacology, Nagoya City University Medical School, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan
* To whom correspondence and reprints requests should be addressed.

Abstract: The superficial buffer barrier function of the sarcoplasmic reticulum (SR) during rest and that during stimulation with Bay╩k╩8644, an agonist of L-type Ca2+ channels, were compared in endothelium-denuded strips of tail arteries from 13-week-old normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), by measuring the effects of cyclopiazonic acid (CPA) and thapsigargin that inhibit SR Ca2+-ATPase and the effect of ryanodine that depletes SR Ca2+. The addition of 10╩mM CPA induced a transient contraction that was not significantly different between WKY and SHR. The CPA-induced contraction was strongly inhibited by 100╩nM nifedipine and was abolished by Ca2+-free solution in both strains. Thapsigargin (100╩nM) or ryanodine (10╩mM) induced similar, small transient contractions in the two strains. The addition of Bay╩k╩8644 (1-100╩nM) almost failed to induce a contraction in both WKY and SHR. When the strips were preincubated with 10╩mM CPA, 100╩nM thapsigargin or 10╩mM ryanodine, Bay╩k╩8644 induced similar concentration-dependent contractions in the two strains. The amount of Ca2+ stored in the SR, as estimated from the 20╩mM caffeine-induced contraction, was not significantly different between WKY and SHR. Our results suggest that the SR of rat tail arteries can buffer a large amount of Ca2+ that enters the cell during the rest and the Bay╩k╩8644 stimulation, and these functions are not altered in SHR.

Keywords: Superficial buffer barrier function, Sarcoplasmic reticulum Ca2+-ATPase,
Ca2+ influx via L-type Ca2+ channels, Tail artery, Spontaneously hypertensive rats (SHR)

Copyrightę The Japanese Pharmacological Society 2000

[Back to TOC]