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

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 endotheliumdenuded 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 10μM 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 μM)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 μM CPA, 100 nM thapsigargin or 10 μM 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.