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Research Article Free access | 10.1172/JCI107873
Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Surgery, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20012
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Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Surgery, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20012
Find articles by Mauli, K. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Surgery, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20012
Find articles by Luke, R. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Surgery, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20012
Find articles by Rees, D. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Surgery, University of Kentucky School of Medicine, Lexington, Kentucky 40506
Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20012
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Published December 1, 1974 - More info
To evaluate the effect of Ca++ on renin release, plasma renin activity (PRA) was measured after acute and chronic Ca++ administration. 1% CaCl2 was infused into one renal artery of 10 anesthetized dogs (0.3 mg/kg/min). The excreted fraction of filtered calcium (EFca++) and EFNa+ from the infused kidney were elevated (P < 0.04) during three successive 15-min infusion periods. Serum calcium concentration was significantly elevated (P < 0.001). Creatinine clearance, systemic arterial pressure, and renal blood flow did not change (P > 0.10). Compared to control (45 ng/ml/h±5.2 SE), renal venous PRA was suppressed (P < 0.0001) after infusion of Ca++ for 15, 30, and 45 min (20 ng/ml/h±4.6, 16 ng/ml/h±4.0, and 13 ng/ml/h±2.7, respectively). 15 and 30-min after infusion, PRA did not differ from control (P > 0.20). Chronic Ca++ loading was achieved in Sprague-Dawley rats by replacing drinking water with 1% CaCl2 for 17 days. At sacrifice, serum Ca++, Na+, and K+ of controls (n = 12) did not differ (P > 0.60) from Ca++-loaded rats (n = 12). Ca++ excretion (467 μeq/24 h±51) was elevated (P < 0.001) compared to controls (85 μeq/24 h±12). PRA (8.6 ng/ml/h±1.4) and renal renin content of Ca++-loaded rats did not differ from controls (P > 0.80). However, after 8 days of sodium deprivation, both PRA and renal renin content of calcium-loaded animals were significantly lower than the respective values in pair-fed controls (P < 0.005). During the period of sodium deprivation, calcium-drinking animals were in greater negative sodium balance than controls (P < 0.005). The data are consistent with the hypothesis that acute and chronic calcium administration inhibit renin secretion.