| Item type: | Article | ||||
|---|---|---|---|---|---|
| Journal or Publication Title: | American Journal of Physiology-Renal Physiology | ||||
| Publisher: | AMER PHYSIOLOGICAL SOC | ||||
| Place of Publication: | BETHESDA | ||||
| Volume: | 287 | ||||
| Number of Issue or Book Chapter: | 3 | ||||
| Page Range: | F427-F433 | ||||
| Date: | 2004 | ||||
| Institutions: | Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Armin Kurtz Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Frank Schweda | ||||
| Identification Number: |
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| Keywords: | RENAL CORTICAL SLICES; MACULA DENSA; BLOOD-PRESSURE; RENOVASCULAR HYPERTENSION; ACE-INHIBITION; MICE LACKING; RAT-KIDNEY; CYCLOOXYGENASE-2; SECRETION; EXPRESSION; renin secretion; renal vascular resistance; bumetanide; isolated; perfused mouse kidney | ||||
| Dewey Decimal Classification: | 500 Science > 570 Life sciences | ||||
| Status: | Published | ||||
| Refereed: | Yes, this version has been refereed | ||||
| Created at the University of Regensburg: | Yes | ||||
| Item ID: | 71312 |
Web of ScienceAbstract
PGE(2) is a potent stimulator of renin release. So far, the contribution of each of the four PGE(2) receptor subtypes (EP(1) - EP(4)) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP(1)(-/-), EP(2)(-/-), EP(3)(-/-), EP(4)(-/-), and wild-type mice. PGE(2) concentration ...
Abstract
PGE(2) is a potent stimulator of renin release. So far, the contribution of each of the four PGE(2) receptor subtypes (EP(1) - EP(4)) in the regulation of renin release has not been characterized. Therefore, we investigated the effects PGE2 on renin secretion rates (RSR) from isolated, perfused kidneys of EP(1)(-/-), EP(2)(-/-), EP(3)(-/-), EP(4)(-/-), and wild-type mice. PGE(2) concentration dependently stimulated RSR from kidneys of all four knockout strains with a threshold concentration of 1 nM in EP(1)(-/-), EP(2)(-/-), EP(3)(-/-), and wild-type mice, whereas the threshold concentration was shifted to 10 nM in EP(4)(-/-) mice. Moreover, the maximum stimulation of RSR by PGE(2) at 1 muM was significantly reduced in EP(4)(-/-) (12.8-fold of control) and EP(2)(-/-) (15.9-fold) compared with wild-type (20.7-fold), EP(1)(-/-) (23.8-fold), and EP(3)(-/-) (20.1-fold). In contrast, stimulation of RSR by either the loop diuretic bumetanide or the beta-adrenoceptor agonist isoproterenol was similar in all strains. PGE2 exerted a dual effect on renal vascular tone, inducing vasodilatation at low concentrations ( 1 nmol/) and vasoconstriction at higher concentrations ( 100 nmol/) in kidneys of wild-type mice. In kidneys of EP(2)(-/-) as well as EP(4)(-/-) mice, vasodilatation at low PGE(2) concentrations was prevented, whereas vasoconstriction at higher concentrations was augmented. In contrast, the vasodilatatory component was pronounced in kidneys of EP(1) and EP(3) knockout mice, whereas in both genotypes the vasoconstriction at higher PGE(2) concentrations was markedly blunted. Our data provide evidence that PGE(2) stimulates renin release via activation of EP(2) and EP(4) receptors, whereas EP(1) and EP(3) receptors appear to be without functional relevance in juxtaglomerular cells. In contrast, all four receptor subtypes are involved in the control of renal vascular tone, EP(1) and EP(3) receptors increasing, and EP(2) as well as EP(4) receptors, decreasing it.
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