Does enhanced respiratory-sympathetic coupling contribute to peripheral neural mechanisms of angiotensin II-salt hypertension?
Hypertension caused by chronic infusion of angiotensin II (Ang II) in experimental animals is likely to be mediated, at least in part, by an elevation of ongoing sympathetic nerve activity (SNA). However, the contribution of SNA relative to non-neural mechanisms in mediating Ang II-induced hypertension is an area of intense debate and remains unresolved. We hypothesize that sympathoexcitatory actions of Ang II are directly related to the level of dietary salt intake. To test this hypothesis, chronically instrumented rats were placed on a 0.1 (low), 0.4 (normal) or 2.0% NaCl diet (high) and, following a control period, administered Ang II (150 ng kg(1) min(1), s.c.) for 10-14 days. The hypertensive response to Ang II was greatest in rats on the high-salt diet (Ang II-salt hypertension), which was associated with increased ‘whole body’ sympathetic activity as measured by noradrenaline spillover and ganglionic blockade. Indirect and direct measures of organ-specific SNA revealed a distinc
