Mechanisms of renal sympathetic activation in renovascular hypertension

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Abstract

This review addresses the underlying mechanisms involved in the sympathoexcitation in renovascular hypertension. We focus on the importance of increased oxidative stress in the paraventricular nucleus of hypothalamus (PVN) and rostral ventrolateral medulla (RVLM) for the autonomic dysfunction associated with renovascular hypertension in the two-kidney, one-clip (2K-1C) model. We found in 2K-1C rats, 6 weeks after clipping, a significant increase in the mRNA and protein expression of the angiotensin II type 1 receptor within the RVLM and PVN. In addition, mRNA from NADPH oxidase subunits (p47phox and gp91phox) was greater in the RVLM and PVN of 2K-1C rats than in a sham-operated group. However, CuZn superoxide dismutase gene expression in these regions was not changed, suggesting that excessive production of reactive oxygen species overwhelms any endogenous antioxidant system in the RVLM and PVN in renovascular hypertension. In fact, acute administration of tempol or vitamin C (either i.v. or directly into the PVN or RVLM) caused a significant decrease in blood pressure and renal sympathetic nerve activity in 2K-1C rats, but not in control animals. Thus, we suggest that an increase in the activity of RVLM and PVN neurons triggered by angiotensin II and oxidative stress is a major mechanism involved in the maintenance of sympathoexcitation of the cardiovascular system in renovascular hypertension.

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