1. A possible interaction between an osmotic stimulus and brain angiotensin II was studied in anaesthetized dogs by measuring the changes in arterial pressure, heart rate and renal sympathetic nerve activity during a brain ventricular injection of hypertonic NaCl solution before and after pretreatment with either captopril or [Sar1, Ile8]angiotensin II.
2. Mild pressor responses accompanied by a reflex decrease in renal sympathetic nerve activity were a characteristic before pretreatment, but after baroreceptor denervation the cardiovascular response to hypertonic NaCl solution doubled and the activity increased. These changes were prevented by intravenous pretreatment with hexamethonium chloride.
3. Brain ventricular injection of captopril slightly augmented pressor and tachycardia effects of hypertonic NaCl solution.
4. Blockade of central angiotensin II receptors with [Sar1, Ile8]angiotensin II was without effect.
5. It is concluded that central administration of hypertonic NaCl solution in baroreceptor-denervated dogs produces marked pressor responses due to increased sympathetic nerve activity via mechanisms not related to the brain renin-angiotensin system.
