Ryanodine-induced contraction in femoral artery from spontaneously hypertensive rats

Abstract

The mechanisms of ryanodine-induced contractions were studied in strips of femoral arteries from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Ryanodine (30 nM to 30 microM) alone contracted arterial strips in a dose-dependent manner. The maximum contraction in SHR was about 5 times greater than that in WKY. SHR strips had about a 30 times lower threshold than WKY strips. Pretreatment with ryanodine caused a more potent dose-dependent inhibition of 10 mM caffeine-induced contractions in SHR than in WKY. Ryanodine (10 microM) failed to contract SHR strips in a CaCl2-free solution, whereas caffeine induced a transient contraction in the solution. Under the conditions that the sarcoplasmic reticulum was depleted of Ca2+ by exposure of the strips to the CaCl2-free solution, ryanodine caused a contraction in the presence of extracellular Ca2+. Verapamil (1 nM) to 1 microM) relaxed the strips precontracted with ryanodine in a dose-dependent manner. In WKY strips exposed to a 15 mM K+ solution, ryanodine-induced contractions were potentiated and were not different from those of SHR strips in a normal K+ (5.9 mM) solution. These results suggest that ryanodine contracts rat femoral arteries by promoting Ca2+ influx through voltage-dependent Ca2+ channels, and that the ability of ryanodine to contract the arteries may depend on the state of the Ca2+ channels.