Open AccessCa2+ Buffering Function of Sarcoplasmic Reticulum in Rat Tail Arteries:Comparison in Normotensive and Spontaneously Hypertensive Rats
Author(s) -
Yukiko Nomura,
Masahisa Asano
Publication year - 2000
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.83.335
Subject(s) - cyclopiazonic acid , thapsigargin , ryanodine receptor , contraction (grammar) , medicine , endocrinology , nifedipine , endoplasmic reticulum , chemistry , stimulation , vascular smooth muscle , muscle contraction , calcium , biophysics , biology , smooth muscle , biochemistry
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 microM 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 microM) 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 microM CPA, 100 nM thapsigargin or 10 microM 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.