Comments on Point:Counterpoint: The dominant contributor to systemic hypertension: Chronic activation of the sympathetic nervous system vs. Activation of the intrarenal renin-angiotensin system. Intrarenal angiotensin II generation as a hypertensinogenic mechanism.

摘要

The importance of alterations in the renin-angiotensin system (RAS) in human hypertension has long been supported by the effectiveness of angiotensin-converting enzyme (ACE) inhibitors and ATI receptor blockers to reduce blood pressure and slow the associated organ damage (3). However, as mentioned by Esler et al. (2), often human hypertensive patients lack consistent signs of systemic RAS activation (1). How can we reconcile such discrepancy? We would argue that the answer resides in alterations of tissue-specific RAS like the one in the kidneys. In support of this, recent clinical studies suggest that urinary angiotensinogen is increased in hypertensive subjects (6). If that holds true, blocking the enzymes responsible for intrarenal ANG II generation, like ACE, should therefore reduce blood pressure levels. On the other hand, enhancing intrarenal ACE activity should cause hypertension. We have generated evidence in favor of both cases.