| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | American Journal of Physiology-Renal Physiology | ||||
| Verlag: | AMER PHYSIOLOGICAL SOC | ||||
| Ort der Veröffentlichung: | BETHESDA | ||||
| Band: | 287 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 3 | ||||
| Seitenbereich: | F427-F433 | ||||
| Datum: | 2004 | ||||
| Institutionen: | Biologie und Vorklinische Medizin > Institut für Physiologie > Prof. Dr. Armin Kurtz Biologie und Vorklinische Medizin > Institut für Physiologie > Prof. Dr. Frank Schweda | ||||
| Identifikationsnummer: |
| ||||
| Stichwörter / 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-Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik > 570 Biowissenschaften, Biologie | ||||
| Status: | Veröffentlicht | ||||
| Begutachtet: | Ja, diese Version wurde begutachtet | ||||
| An der Universität Regensburg entstanden: | Ja | ||||
| Dokumenten-ID: | 71312 |
Web of ScienceZusammenfassung
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 ...
Zusammenfassung
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.
Metadaten zuletzt geändert: 19 Dez 2024 15:11
Altmetric