SUMMARY Increased dietary calcium intake in the adult spontaneously hypertensive rat (SHR) has been reported to correct low serum ionized calcium concentration ([Ca ++ ]) and to result in a significant amelioration of the prevailing hypertension. In the present study we examined several parameters of calcium metabolism in young (6-week-old) SHR and compared them with those observed in normotensive Wistar-Kyoto (WKY) rats fed equal amounts of a diet containing normal quantities of calcium (0.4%, wt/wt) for 4 weeks. A separate group of SHR was placed on an equal amount of a high calcium (2.8%, wt/wt) but otherwise identical diet. In SHR and WKY eating a normal calcium diet, serum total calcium concentration was not different, but [Ca + + ] was lower in SHR (1.58 ± 0.06 vs 1.91 ± 0.07 mmol/liter, p< 0.01). Serum immunoreactive parathyroid hormone (PTH) was increased in some, but not all, SHR. No difference was noted between the two groups in the following parameters: calcium intake, serum 1,25 dihydroxycholecalciferol (1,25(OH) 2 D 3 ), urinary calcium excretion, fractional stool calcium content ([stool calcium/calcium intake] x 100), and in vitro 4SCa uptake by everted gut sacs constructed from segments of duodenum, mid-jejunum, ileum, and proximal colon. A high calcium diet corrected the abnormal serum [Ca + + ] and PTH but did not alter the progression or severity of the hypertension in SHR. A lower net weight gain was observed in SHR on a high calcium diet when compared to SHR eating normal calcium diet (9.1 ± 1.8 vs 27.0 ± 2.0 g). This was attributed, at least in part, to a consistently higher urinary sodium loss in the former group of rats (p < 0.05-0.001 throughout the study period). The progression of hypertension, even in the face of normalized serum [Ca + + ] in young SHR, suggests that low [Ca + + ] and hypertension do not have a cause-and-effect relationship. Sustained natriuresis caused by the augmented dietary calcium intake and increased urinary calcium excretion may contribute to the blood-pressure-lowering effect reported in adult SHR. (Hypertension 6: 639-646, 1984) KEY WORDS • calcium • 1,25(OH) 2 D • sodium • spontaneously hypertensive rat A LTERATIONS in calcium homeostasis in humans with essential hypertension and in spontaneously hypertensive rats (SHR) have been described in recent years.1 " 3 Similar findings in human and rat hypertension include reduced serum ionized calcium concentration [Ca ++ ], increased immunoreactive parathyroid hormone (PTH) levels, and enhanced urinary calcium excretion. Whereas a unify-
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