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Angiotensin II (AngII) is a potent physiological vasoconstrictor peptide and a growth factor of smooth muscle cells. AngII also induces NO release from the endothelium and relaxes smooth muscle. We have reported that AngII-induced endothelium-dependent relaxation in the thoracic aorta from SHRSP at developmental ages of hypertension was significantly enhanced in comparison with that of age-matched WKY (Mashiko et al., Jpn. Heart J. 1995, 36, 528). Binding of AngII to AT1 receptor in the smooth muscle cell surface activates PLC-ƒÁ which generates the second messengers, inositol1,4,5-trisphosphate (IP3) and diacylglycerols (DAG). IP3 mobilizes Ca2+ from endoplasmic reticulum (ER), intracellular Ca2+ store and induces a rapid increase in intracellular free calcium ion concentration ([Ca2+]i). This rise in [Ca2+]i mediates the phasic contraction in response to AngII. [Ca2+]i returns to the basal levels by Ca2+-sequestration via Ca2+-pump in ER, Ca2+efflux via Ca2+-pump and Ca2+-efflux via Na+/Ca2+ exchanger in plasma membrane, inducing muscle relaxation. In this study, effects of AngII on contractile responses of smooth muscle, and changes in intracellular free calcium concentration ([Ca2+]i) in cultured vascular smooth muscle cells (VSMC) were compared between SHRSP and WKY. Male SHRSP at established ages of hypertension (12-17 weeks old) and age-matched WKY were used in this study. The thoracic aorta was excised and aortic rings (3mm long) were prepared. For endothelium-denuded

Sustained Contraction to Angiotensin II and Impaired Calcium-Pump Activity in Smooth Muscle from SHRSP