Chronic central administration of ANG II combined with high sodium intake induces a specific model of low-renin, volume-expanded hypertension in experimental animals.
Caution against clinical translation; leaves open central ANG II mechanisms in human low-renin hypertension.
The acute administration of ANG II into the brain of experimental animals produces transient pressor effects, a marked increase in drinking, release of the antidiuretic hormone, increase in total peripheral resistance, a diuretic and natriuretic effect and an increase in sympathetic outflow. The chronic administration of ANG II into a cerebrolateral ventricle produces sustained pressor effects only if 0.9% sodium chloride solution is used as the drinking fluid. The hypertension is due to an increase in total peripheral resistance which appears to be due to an increase in intrinsic tone of vascular smooth muscle. In addition there was enhanced responsiveness of the vasculature to norepinephrine and ANG II and a decrease in reflex vasodilatation of the hind limb of ANG II treated dogs. The chronic elevation of ANG II in the CSF plus an increase in NaCl intake produces a low renin, sodium dependent, expanded volume hypertension. Data are presented suggesting that this model of hypertension is induced by the central release of an inhibitor of the Na+,K+-Pump.
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Joseph P. Buckley (1988) studied this question.
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