A single mechanism to explain the effect of calcium on renal-function
Lahera, V; Ruilope, LM; Romero, JC
HERO ID
4941708
Reference Type
Journal Article
Year
1991
Language
English
| HERO ID | 4941708 |
|---|---|
| In Press | No |
| Year | 1991 |
| Title | A single mechanism to explain the effect of calcium on renal-function |
| Authors | Lahera, V; Ruilope, LM; Romero, JC |
| Journal | American Journal of Hypertension |
| Volume | 4 |
| Issue | 7 |
| Page Numbers | S473-S481 |
| Abstract | It is known that calcium induces the formation of potent vasodilators in endothelial cells and vasocontriction in smooth muscle cells, whereas in the renal parenchyma, it modulates sodium excretion through vascular and tubular mechanisms. Consequently, an increased concentration of calcium in renal circulation may induce a sequence of contrasting hemodynamics and excretory effects depending on the threshold of a particular mechanism that is first being stimulated. In order to identify this sequence of responses and their respective thresholds, we infused into the renal artery of anesthetized dogs progressively increasing doses of calcium gluconate that ranged from 1 to 400-mu-g/kg/min. <br> <br>The administration of 1, 10, and 100-mu-g/kg/min of calcium gluconate was followed by a significant increase in urinary excretion of PGE2 and 6-keto-PGF1-alpha and by a marked diuresis and natriuresis without altering renal blood flow (RBF) or glomerular filtration rate (GFR). Renin release was increased by 80% only during the infusion of the 10-mu-g/kg/min dose. The intrarenal infusion of a 400-mu-g/kg/min dose of calcium produced marked decreases in RBF and GFR, while urine sodium excretion (U(Na)V), U(PGE2)V, and U6-keto-PGF1-alpha-V continued and were markedly elevated. During all these maneuvers, mean arterial pressure remained unchanged. After the administration of indomethacin, the intrarenal infusion of 10 and 100-mu-g/kg/min of calcium produced marked reductions in urine prostaglandins and caused a decrease in RBF and GFR comparable to those obtained with the 400-mu-g/kg/min dose, abolished completely the increments in urine volume and urine sodium, and prevented the increase in renin produced by the 10-mu-g/kg/min dose. These studies show that all the intrarenal effects of low doses of calcium are dependent on the production of prostaglandins. The use of systemic infusion of calcium gluconate as a specific probe to test the renal ability to produce prostaglandins is further emphasized by the finding that in humans the threshold of renal responses to calcium is much greater than that of the systemic circulation. |
| Doi | 10.1093/ajh/4.7.473S |
| Wosid | WOS:A1991FX09800014 |
| Url | https://academic.oup.com/ajh/article/176452/A |
| Is Certified Translation | No |
| Dupe Override | No |
| Comments | ISSN: 1941-7225 |
| Is Public | Yes |
| Language Text | English |
| Keyword | CALCIUM; PROSTAGLANDINS; INDOMETHACIN; RENAL HEMODYNAMICS; RENAL FUNCTION |