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Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension
Journal article   Open access   Peer reviewed

Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension

Baojian Xue, Terry G Beltz, Yang Yu, Fang Guo, Celso E Gomez-Sanchez, Meredith Hay and Alan Kim Johnson
American journal of physiology. Heart and circulatory physiology, Vol.300(2), pp.H555-H564
02/2011
DOI: 10.1152/ajpheart.00847.2010
PMCID: PMC3044048
PMID: 21112947
url
https://doi.org/10.1152/ajpheart.00847.2010View
Published (Version of record) Open Access

Abstract

Many studies have implicated both angiotensin II (ANG II) and aldosterone (Aldo) in the pathogenesis of hypertension, the progression of renal injury, and cardiac remodeling after myocardial infarction. In several cases, ANG II and Aldo have been shown to have synergistic interactions in the periphery. In the present studies, we tested the hypothesis that ANG II and Aldo interact centrally in Aldo- and ANG II-induced hypertension in male rats. In rats with blood pressure (BP) and heart rate (HR) measured by DSI telemetry, intracerebroventricular (icv) infusions of the mineralocorticoid receptor (MR) antagonists spironolactone and RU28318 or the angiotensin type 1 receptor (AT 1 R) antagonist irbesartan significantly inhibited Aldo-induced hypertension. In ANG II-induced hypertension, icv infusion of RU28318 significantly reduced the increase in BP. Moreover, icv infusions of the reactive oxygen species (ROS) scavenger tempol or the NADPH oxidase inhibitor apocynin attenuated Aldo-induced hypertension. To confirm these effects of pharmacological antagonists, icv injections of either recombinant adeno-associated virus carrying siRNA silencers of AT 1a R (AT 1a R-siRNA) or MR (MR-siRNA) significantly attenuated the development of Aldo-induced hypertension. The immunohistochemical and Western blot analyses of AT 1a R-siRNA- or MR-siRNA-injected rats showed a marked reduction in the expression of AT 1 R or MR in the paraventricular nucleus compared with scrambled siRNA rats. When animals from all studies underwent ganglionic blockade with hexamethonium, there was a smaller reduction in the fall of BP in animals receiving icv AT 1 R or MR antagonists. These results suggest that ANG II and Aldo interact in the brain in a mutually cooperative manner such that the functional integrity of both brain AT 1 R and MR are necessary for hypertension to be induced by either systemic ANG II or Aldo. The pressor effects produced by systemic ANG II or Aldo involve increased central ROS and sympathetic outflow.
blood pressure Cardiovascular Neurohormonal Regulation sympathetic nervous system reactive oxygen species

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