Differential modulation of norepinephrine-induced contractile response by ryanodine and verapamil in the isolated aortic ring of spontaneously hypertensive and Wistar-Kyoto rats.

Using ryanodine and verapamil, we compared the relative contributions of SR Ca2+ release and gated Ca2+ entry in arterial contractions induced by norepinephrine (NE) between spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Aortic rings of 10 SHR and 10 WKY aged 10-12 weeks were superfused in small water-jacketed tissue chambers with physiological salt solution and isometric tension was measured. The inhibition of the NE(3 x 10(-8) M)-induced contraction of aortic rings by ryanodine (10-mu-M) was significantly greater in WKY (40.1 +/- 6.9%) than in SHR (2.2 +/- 9.0%) (p < 0.01). The inhibition of the NE-induced contraction by verapamil (10-mu-M) in the presence or absence of ryanodine (10-mu-M) was significantly greater in SHR than in WKY. The residual, ryanodine and verapamil-insensitive component of NE-induced contraction was significantly greater in WKY than in SHR. Caffeine(5 mM)-induced contraction in the presence of verapamil and phentolamine was significantly smaller in SHR than in WKY. These results suggest that gated Ca2+ entry plays a more important role in Ca2+ control and that ryanodine-sensitive Ca2+ store is smaller, or the ryanodine receptor is altered in these tissues of SHR compared with those of WKY.