Calcium buffering of resting, voltage-dependent Ca2+ influx by sarcoplasmic reticulum in femoral arteries from spontaneously hypertensive rats at prehypertensive stage

We examined the Ca2+-buffering function of the sarcoplasmic reticulum (SR) in the resting state of arteries from spontaneously hypertensive rats (SHR) at a prehypertensive stage. Differences in the effects of cyclopiazonic ac id (CPA) and thapsigargin, agents that inhibit SR Ca2+-ATPase, and of ryano dine, which depletes SR Ca2+, on tension and cellular Ca2+ level were asses sed in endothelium-denuded strips of femoral arteries from 4-week-old SHR a nd normotensive Wistar-Kyoto rats (WKY), Addition of CPA, thapsigargin or r yanodine to the resting state of the strips caused an elevation of cytosoli c Ca2+ level and a contraction in both WKY and SHR. These responses were la rger in SHR than in WKY, The contractions were inhibited strongly by 100 nM nifedipine or 3 muM verapamil and were abolished by Ca2+-free solution. Ni fedipine, verapamil or Ca2+-free solution itself caused a relaxation from t he resting state of SHR strips, but not from that of WKY strips. The restin g Ca2+ influx in arteries measured by a 5-min incubation with Ca-45 was sig nificantly larger in SHR than in WKY. This influx was decreased by 10 muM C PA or 10 muM ryanodine in both WKY and SHR, These results suggest that in t he resting state of the femoral artery from 4-week-old SHR, the greater par t of the increased Ca2+ influx via L-type Ca2+ channels is buffered by Ca2 uptake into the SR, while some Ca2+ reaches the myofilaments, resulting in the maintenance of resting tone.