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 microm) and efferent arterioles (18.4 +/- 0.7 to 14.0 +/- 0.7 microm). the addition of nifedipine (1 micromol/l) restored decrements in afferent (to 20.0 +/- 0.8 microm) but not efferent arteriolar diameters. further administration of skf-96365 (100 micromol/l), a trp channel blocker, reversed efferent arteriolar constriction (to 16.2 +/- 0.8 micromol/l). in the second group, although 2-aminoethoxydiphenyl borate (100 micromol/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 +/- microm). subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 +/- 0.8 microm).
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.