Background. This study assessed the calcium-activating mechanisms mediating glomerular arteriolar constriction by angiotensin II (Ang II). Methods. Immunohistochemical and physiological studies were carried out, using antibody against transient receptor potential (TRP)-1 and an isolated perfused kidney model. Results. Immunohistochemical experiments demonstrated that TRP-1 proteins were transcribed on both afferent and efferent arteriolar myocytes. In the first series of physiological experiments, Ang II (0.3 nmol/L) considerably constricted afferent (20.2 ± 0.9 to 14.9 ± 0.7 μm) and efferent arterioles (18.4 ± 0.7 to 14.0 ± 0.7 μm). The addition of nifedipine (1 μmol/L) restored decrements in afferent (to 20.0 ± 0.8 μm) but not efferent arteriolar diameters. Further administration of SKF-96365 (100 μmol/L), a TRP channel blocker, reversed efferent arteriolar constriction (to 16.2 ± 0.8 μmol/L). In the second group, although 2-aminoethoxydiphenyl borate (100 μmol/L), an inhibitor of inositol trisphosphate-induced calcium release (IP3CR), did not alter glomerular arteriolar diameters, it prevented Ang II-induced afferent arteriolar constriction and attenuated efferent arteriolar constriction (18.8 ± 0.8 to 16.9 ± μm). Subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 ± 0.8 μm). Conclusions. Our data provide evidence that Ang II elicits IP3CR, possibly inducing a cellular response that activates voltage-dependent calcium channels on afferent arterioles. The present results suggest that Ang II-induced efferent arteriolar constriction involves IP3CR and calcium influx sensitive to SKF-96365.
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