Effect of angiotensin II on calcium reabsorption by the luminal membranes of the nephron

Citation
A. Charbonneau et al., Effect of angiotensin II on calcium reabsorption by the luminal membranes of the nephron, AM J P-ENDO, 280(6), 2001, pp. E928-E936
Citations number
61
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN journal
01931849 → ACNP
Volume
280
Issue
6
Year of publication
2001
Pages
E928 - E936
Database
ISI
SICI code
0193-1849(200106)280:6<E928:EOAIOC>2.0.ZU;2-B
Abstract
In the rat and the rabbit, a number of studies have reported the effects of angiotensin II (ANG II) on Na+ reabsorption by the proximal (PT) and dista l (DT) convoluted tubules of the kidney. The aim of the present study was t o examine the effect of ANG II on Ca2+ uptake by the luminal membranes of t he PT and DT of the rabbit. Incubation of PT and DT with 10(-12) M ANG II e nhanced the initial Ca2+ uptake in the two segments. Dose-response experime nts revealed, for Ca2+ as well as for Na+ transport, a biphasic action with a maximal effect at 10(-12) M. Ca2+ transport by the DT luminal membrane p resents a dual kinetic. ANG II action influenced the high-affinity Ca2+ cha nnel, increasing maximal velocity from 0.72 +/- 0.03 to 0.90 +/- 0.05 pmol. mug(-1).10 s(-1) (P < 0.05, n = 3) and leaving the Michaelis-Menten constan t unchanged. The effect of ANG II was abolished by losartan, suggesting tha t the hormone is acting through AT(1) receptors. In the PT, calphostin C in hibited the effect of the hormone. It is therefore probable that protein ki nase C is involved as a messenger. In the DT, however, neither Rp cAMP, cal phostin C, nor econazole (a phospholipase A inhibitor) influenced the hormo ne action. Therefore, the mechanisms involved in the hormone action remain undetermined. Finally, we questioned whether ANG II acts in the same DT seg ment as does parathyroid hormone on Ca2+ transport. The two hormones increa sed Ca2+ transport, but their actions were not additive, suggesting that th ey both influence the same channels in the same segment of the distal nephr on, i.e., the segment responsible for the high-affinity calcium channel.