Response by Danser and van den Meiracker to letter by Zhou and Zhou regarding article, "Hypertension: Renin-angiotensin-aldosterone system alterations"

In Response:
Zhou and Zhou raise the interesting possibility that renin– angiotensin–aldosterone system (RAAS) alterations are a consequence of excretory organ insufficiency. Indeed, a lower sweat rate, as occurs in blacks, might induce sodium retention, thereby reducing renin release. The latter concept is well known and discussed in our review. Zhou and Zhou additionally suggest that excretory organ insufficiency reduces aldosterone removal, thereby potentially increasing the aldosterone/renin ratio. When comparing renin and aldosterone levels in blacks and whites, we did not find evidence for this concept: the aldosterone/renin ratios were identical in both the groups. Clearly, blacks display an overall reduction in RAAS activity, and whether this is entirely because of excretory organ insufficiency remains to be investigated. Given this diminished RAAS contribution, it is not surprising that hypertensive blacks display blunted responses to ACE inhibitors, as acknowledged by Zhou and Zhou. Finally, they suggest that RAAS alterations are not the cause of essential hypertension. We fully agree: in fact, the cause of essential hypertension is unknown, and RAAS alterations are at most one of many possible causes. Yet, the overwhelming success of RAAS blockers in hypertension at least supports the idea that alterations in this system are a major player.