Demerath, Theo and Staffel, Janina and Schreiber, Andrea and Valletta, Daniela and Schweda, Frank (2014) Natriuretic peptides buffer renin-dependent hypertension. AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 306 (12). F1489-F1498. ISSN 1931-857X, 1522-1466
Full text not available from this repository. (Request a copy)Abstract
The renin-angiotensin-aldosterone system and cardiac natriuretic peptides [atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)] are opposing control mechanisms for arterial blood pressure. Accordingly, an inverse relationship between plasma renin concentration (PRC) and ANP exists in most circumstances. However, PRC and ANP levels are both elevated in renovascular hypertension. Because ANP can directly suppress renin release, we used ANP knockout (ANP(-/-)) mice to investigate whether high ANP levels attenuate the increase in PRC in response to renal hypoperfusion, thus buffering renovascular hypertension. ANP(-/-) mice were hypertensive and had reduced PRC compared with that in wild-type ANP(+/+) mice under control conditions. Unilateral renal artery stenosis (2-kidney, 1-clip) for 1 wk induced similar increases in blood pressure and PRC in both genotypes. Unexpectedly, plasma BNP concentrations in ANP(-/-) mice significantly increased in response to two-kidney, one-clip treatment, potentially compensating for the lack of ANP. In fact, in mice lacking guanylyl cyclase A (GC-A(-/-) mice), which is the common receptor for both ANP and BNP, renovascular hypertension was markedly augmented compared with that in wild-type GC-A(+/+) mice. However, the higher blood pressure in GC-A(-/-) mice was not caused by disinhibition of the renin system because PRC and renal renin synthesis were significantly lower in GC-A(-/-) mice than in GC-A(+/+) mice. Thus, natriuretic peptides buffer renal vascular hypertension via renin-independent effects, such as vasorelaxation. The latter possibility is supported by experiments in isolated perfused mouse kidneys, in which physiological concentrations of ANP and BNP elicited renal vasodilatation and attenuated renal vasoconstriction in response to angiotensin II.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CYCLASE-A RECEPTOR; BLOOD-PRESSURE; MICE LACKING; RENOVASCULAR HYPERTENSION; JUXTAGLOMERULAR CELLS; CARDIAC-HYPERTROPHY; CHRONIC INFUSION; TRANSGENIC MICE; HEART-FAILURE; RATS; renin; atrial natriuretic peptide; B-type natriuretic peptide; hypertension; guanylyl cyclase A |
| Subjects: | 500 Science > 570 Life sciences |
| Divisions: | Biology, Preclinical Medicine > Institut für Physiologie Biology, Preclinical Medicine > Institut für Physiologie > Prof. Dr. Frank Schweda |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 16 Sep 2019 11:07 |
| Last Modified: | 16 Sep 2019 11:07 |
| URI: | https://pred.uni-regensburg.de/id/eprint/10020 |
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