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Abnormal calcium (Ca) homeostasis has been reported in essential hypertension and in the Okamoto-Aoki strain of spontaneously hypertensive rats. These abnormalities include increased urinary excretion of calcium and decreased ionized serum calcium (Ca2+). To pursue these abnormalities we studied the chronology of urinary excretion of electrolytes in a genetically homogeneous strain of hypertensive rat, the Dahl/Rapp salt sensitive (S) and resistant (R) rat (at ages 3, 5, 7, 9, 12, 20 and 32 weeks). We also characterized the renal adenylate cyclase-cAMP, system by measuring urinary cAMP excretion and adenylate cyclase response to membrane receptor agonists in renal membranes from S and R rats at day 2 and at 6 and 28 weeks of age. Urinary calcium excretion was higher in S than in R at 3, 5 and 7 weeks (0.48 ± 0.04 versus 0.24 ± 0.01 mg/mg creatinine at 7 weeks, P<0.01). Sodium and phosphorous excretion were lower in S than in R rats at 5, 7, 9, and 12 weeks, and at 5, 7, 9, 12, 20 and 32 weeks, respectively. Potassium excretion was similar in the two groups. Plasma ionized calcium was lower in S than in R rats (3.9 ± 0.1 versus 4.5 ± 0.1 mg/dl, P<0.01) only at 7 weeks of age. Plasma parathyroid hormone (PTH) was not different between S and R rats. Cyclic AMP excretion and the renal adenylate cyclase response to PTH when referenced to basal activity was lower in S than in R rats at all ages. These studies demonstrate that in the Dahl S rats, there is increased urinary calcium excretion and decreased urinary cAMP excretion associated with decreased adenylate cyclase response to PTH in the kidney. This decreased adenylate cyclase response to PTH may be a causal factor in the increased urinary calcium in Dahl S rats. The relationship between altered calcium homeostasis and the hypertension mechanism is unknown.