Effect of renal perfusion pressure on excretion of calcium, magnesium, and phosphate in the rat.
Abnormalities in renal handling of calcium, magnesium, or phosphate have been implicated in the development and/or maintenance of human hypertension. We have shown recently that renal excretion of these ions is correlated to blood pressure in Dahl salt-sensitive as well as salt-resistant rats. The present study was designed to determine whether renal perfusion pressure per se could affect excretion of these ions. Urinary excretion of calcium, magnesium, and phosphate was studied in anaesthetized Sprague-Dawley rats under basal conditions and during an intravenous infusion of angiotensin II (ANG II), vasopressin (AVP) or phenylephrine (PE). A cuff, placed around the aorta between the two renal arteries, allowed maintenance of normal perfusion pressure in the left kidney, while that in the right kidney was allowed to rise. Infusion of pressor agents raised mean arterial blood pressure to comparable levels (means +/- SE): ANG II (n = 7), before = 102 +/- 4, during = 133 +/- 3 mmHg, AVP (n = 8), before = 110 +/- 7, during = 136 +/- 5 mmHg, PE (n = 6), before = 111 +/- 6, during = 141 +/- 6 mmHg. Although there was no difference in excretion of calcium, magnesium and phosphate between the two kidneys under basal conditions, infusion of ANG II or PE induced hypercalciuria, hypermagnesiuria and hyperphosphaturia in the right kidney which was exposed to the increased arterial pressure. Such effects did not appear in the pressure-controlled left kidney. Infusion of AVP was associated with reduced excretion of calcium and magnesium, and increased excretion of phosphate, in the normotensive kidney. The response to the similarly increased renal perfusion pressure in this group was also reduced for calcium and magnesium, and enhanced for phosphate. The results indicate (1) renal excretion of calcium, magnesium and phosphate is renal perfusion pressure-dependent; the higher the renal perfusion pressure, the greater the excretion of these ions. (2) Independently of perfusion pressure, AVP can inhibit phosphate reabsorption and stimulate divalent cation reabsorption.
Wu
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Department of Physiology, University of Toronto, Ontario, Canada.
Sonnenberg
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H
D000804:Angiotensin II / Q000008:administration & dosage; D000818:Animals; D002118:Calcium / Q000652:urine*; D007668:Kidney / Q000378:metabolism* / Q000503:physiopathology; D008274:Magnesium / Q000652:urine*; D008297:Male; D010477:Perfusion; D010656:Phenylephrine / Q000008:administration & dosage; D010710:Phosphates / Q000652:urine*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014662:Vasoconstrictor Agents / Q000008:administration & dosage; D014667:Vasopressins / Q000008:administration & dosage
D010710:Phosphates; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D000804:Angiotensin II; D010656:Phenylephrine; D008274:Magnesium; D002118:Calcium