Effects of hypercalcemia on kidney function in anesthetized dogs.
The effects of acute hypercalcemia on renal function were evaluated in anesthetized mongrel dogs. Calcium concentration was increased by infusion of CaCl2 solution into the left renal artery at two different rates. At the lower rate of infusion (0.010 mM/kg/min) the plasma total calcium concentration in the left kidney increased from 2.5 mM/l to 3.76 mM/l and the arterial plasma total calcium concentration to 2.94 mM/l. Renal vascular resistance in the left kidney did not change in association with a small decrement in the renal blood flow (9.5%). The glomerular filtration rate decreased from 82.9 ml/min to 65.9 ml/min in association with a small decrease in the urine output. The calcium excretion increased slightly from 3.3 microM/min to 4.05 microM/min. When this amount of CaCl2 was infused into the left renal artery the parameters of the right intact kidney did not change. During the higher rate of infusion (0.020 mM/kg/min) in the left kidney the plasma total calcium concentration in the left kidney increased from 2.3 mM/l to 6.15 mM/l and in the arterial plasma to 3.4 mM/l. Renal vascular resistance increased considerably from 1.66 to 4.0 and the renal blood flow decreased from 482 ml/min to 311 ml/min. The glomerular filtration rate dropped from 78.7 ml/min to 43 ml/min with a significant decrease in the urine output. The calcium excretion increased from 4.35 microM/min to 7.5 microM/min. In the right kidney during the CaCl2 infusion the CPAH decreased from 304 ml/min to 239 ml/min showing that there was an increase in the vascular resistance in association with decrements in Cinulin from 85 ml/min to 67.2 ml/min. These data prove a direct, but not linear relationship between the total plasma calcium concentration and the renal vascular resistance. We suppose that the distal tubular calcium load participates in the distal tubular feedback regulation, when the calcium ion concentration in the tubular fluid at the macula densa increases. This increment elicits vasoconstriction in the afferent arteriole decreasing the filtered calcium load in the glomeruli.
Kövér
G
G
Department of Physiology, Semmelweis University Medical School, Budapest, Hungary.
Tost
H
H
D000208:Acute Disease; D000771:Anesthesia, Intravenous; D000818:Animals; D001794:Blood Pressure; D002118:Calcium / Q000032:analysis / Q000097:blood; D002122:Calcium Chloride / Q000008:administration & dosage; D003627:Data Interpretation, Statistical; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate; D006934:Hypercalcemia / Q000503:physiopathology*; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D009994:Osmolar Concentration; D011188:Potassium / Q000032:analysis; D012077:Renal Artery; D012079:Renal Circulation; D012964:Sodium / Q000032:analysis; D014655:Vascular Resistance
D012964:Sodium; D002122:Calcium Chloride; D011188:Potassium; D002118:Calcium