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Angiotensin II-stimulated secretion by adrenal glomerulosa cells and contraction by vascular smooth muscle (VSM) are dependent on calcium influx through membrane calcium channels. We have examined the hypothesis that the altered responsiveness of ad-renal glomerulosa cells and VSM to angiotensin II during NaCl restriction may be associated with a change in membrane calcium channel number. To test this hypothesis, female rats were placed on a high or low NaCl diet. On the 14th day, membranes were prepared from the zona glomerulosa, aorta, mesenteric artery, and uterus. I3HNitrendipine binding was used to monitor calcium channel number. The PHlnitrendipine binding capacity was ob-served to be higher in the zona glomerulosa during NaCl restric-tion than during high NaCl intake (83±18 vs. 49±9 fmol/mg protein, P < 0.025, n = 6 paired experiments). The binding ca-pacities of 13Hlnitrendipine on the low and high NaCl diet were similar in the mesenteric artery (10±1 vs. 9±1 fmol/mg protein, n = 8), aorta (33±5 vs. 35±8 fmol/mg protein, n = 5), or uterus (87±15 vs. 85±16 fmol/mg protein, n = 4), respectively. The dissociation constants of PHInitrendipine binding did not differ on a low or high NaCl intake in the zona glomerulosa (0.84±.12 vs. 0.79±.10 nM), mesenteric artery (0.82±.06 vs. 83±.05 nM), aorta (0.90±.11 vs. 0.92±.12 nM), or uterus (0.55±.12 vs. 0.56±.10 nM), respectively. We conclude that the blunted re-sponse of VSM to angiotensin II during NaCI restriction is best explained by the previously reported lower number of angiotensin II receptors since calcium channel number does not change. In the adrenal glomerulosa cell, NaCl restriction is associated with a higher number of membrane calcium channels and angiotensin II receptors. The increase in calcium channel number may reflect the influence of an unknown factor(s) believed to be necessary for the full expression of the adrenal glomerulosa cell response to NaCl restriction