| Dokumentenart: | Artikel | ||||
|---|---|---|---|---|---|
| Titel eines Journals oder einer Zeitschrift: | American Journal of Physiology-Renal Physiology | ||||
| Verlag: | AMER PHYSIOLOGICAL SOC | ||||
| Ort der Veröffentlichung: | BETHESDA | ||||
| Band: | 302 | ||||
| Nummer des Zeitschriftenheftes oder des Kapitels: | 10 | ||||
| Seitenbereich: | F1278-F1285 | ||||
| Datum: | 2012 | ||||
| Institutionen: | Biologie und Vorklinische Medizin > Institut für Physiologie > Prof. Dr. Armin Kurtz | ||||
| Identifikationsnummer: |
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| Stichwörter / Keywords: | BETA-RECEPTOR BLOCKADE; ANGIOTENSIN SYSTEM; RAT-KIDNEY; AT(1A) RECEPTOR; NITRIC-OXIDE; MACULA DENSA; DIETARY SALT; CYCLOOXYGENASE-2 EXPRESSION; ALDOSTERONE SYNTHASE; CAPILLARY-PRESSURE; AT(1a) knockout | ||||
| 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: | 63774 |
Web of ScienceZusammenfassung
Machura K, Neubauer B, Steppan D, Kettl R, Gro beta A, Kurtz A. Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney. Am J Physiol Renal Physiol 302: F1278-F1285, 2012. First published February 22, 2012; doi:10.1152/ajprenal.00688.2011.-The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined ...
Zusammenfassung
Machura K, Neubauer B, Steppan D, Kettl R, Gro beta A, Kurtz A. Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney. Am J Physiol Renal Physiol 302: F1278-F1285, 2012. First published February 22, 2012; doi:10.1152/ajprenal.00688.2011.-The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. We used wild-type (WT) mice and mice lacking angiotensin II type 1a receptors (AT(1a)-/-) displaying an enhanced salt sensitivity to renin expression. In WT kidneys, we found renin-expressing cells at the ends of all afferent arterioles. A low-salt diet (0.02%) led to a moderate twofold increase in renin-expressing cells along afferent arterioles. In AT(1a)-/- mice, lowering of salt content led to a 12-fold increase in renin expression. Here, the renin-expressing cells were distributed along the preglomerular vascular tree in a typical distal-to-proximal distribution gradient which was most prominent at high salt intake and was obliterated at low salt intake by the appearance of renin-expressing cells in proximal parts of the preglomerular vasculature. While lowering of salt intake produced only a small drop in blood pressure in WT mice, the marked reduction of systolic blood pressure in AT(1a)-/- mice was accompanied by the disappearance of the distribution gradient from afferent arterioles to arcuate arteries. Unilateral renal artery stenosis in AT(1a)-/- mice on a normal salt intake produced a similar distribution pattern of renin-expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS inhibitor N-nitro-L-arginine methyl ester or of the adrenergic agonist phenylephrine in AT(1a)-/- mice kept on low salt intake produced a similar distribution pattern of renin-producing cells as did normal salt intake alone. These findings suggest that changes in preglomerular blood pressure may be an important mediator of the influence of salt intake on the number and distribution of renin-producing cells in the kidney.
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