Renal arteriolar Na+/Ca2+ exchange in salt-sensitive hypertension

he present studies were performed to assess Na+/Ca2+ exchange activity in a fferent and efferent arterioles from Dahl/Rapp salt-resistant (R) and salt- sensitive (R) rats. Renal arterioles were obtained by microdissection from S and R rats on either a low-salt (0.3% NaCl) or high-salt (8.0% NaCl) diet . On the high-salt diet, 8 rats become markedly hypertensive. Cytosolic cal cium concentration (([Ca2+](i))) was measured in fura 2-loaded arterioles b athed in a Ringer solution in which extracellular Na (Na,) was varied from 150 to 2 mM (Na was replaced with N-methyl-D-glucamine). Baseline [Ca2+](i) was similar in afferent arterioles of R and 8 rats fed low- and high-salt diet. The change in [Ca2+](i) (Delta[Ca2+]i)during reduction in Na, from 15 0 to 2 mM was 80 +/- 10 and 61 +/- 3 nM (not significant) in afferent arter ioles from R rats fed the low- and high-salt diet, respectively. Tn afferen t arterioles from 8 rats on a high-salt diet, Delta[Ca2+](i) during reducti ons in Na-e from 150 to 2 mM was attenuated (39 +/- 4 nM) relative to the D elta[Ca2+](i) of 79 +/- 13 nM (P < 0.05) obtained in afferent arterioles fr om 8 rats on a low-salt diet. Tn efferent arterioles, baseline [Ca2+]i was similar in R and S rats fed low- and high-salt diets, and Delta[Ca2+](i) in response to reduction in Na, was also not different in efferent arterioles from R and S rats fed low- or high-salt diets. Differences in regulation o f the exchanger in afferent arterioles of S and R rats were assessed by det ermining the effects of protein kinase C (PKC) activation by phorbol 12-myr istate 13-acetate (PMA, 100 nM) on a[Ca2+]i in response to reductions in Na , from 150 to 2 mM. PMA increased Delta[Ca2+](i) in afferent arterioles fro m R rats but not from S rats. These results suggest that Na+/Ca2+ exchange activity is suppressed in afferent arterioles of S rats that are on a high- salt diet. Tn addition, there appears to be a defect in the PKC-Na+/Ca2+ ex change pathway that might contribute to altered [Ca2+](i) regulation in thi s important renal vascular segment in salt-sensitive hypertension.