Brain renin angiotensin system contributes to the salt-induced enhancement of hypertension in SHR.

The study was performed to determine whether the brain renin angiotensin system may contribute to the acceleration in hypertension following long-term salt loading in spontaneously hypertensive rats (SHR). Five weeks old SHR and normotensive Wistar-Kyoto (WKY) were given 1% NaCl solution or plain tap water as drinking for 7 weeks. The salt treatment exaggerated the development of hypertension in SHR, but did not change the blood pressure (BP) in WKY. The hypotensive actions of intracerebroventricular (ICV) captopril was greater in SHR treated with salt than in those without treatment, whereas ICV AII increased BP to a similar degree between salt and control SHR. In WKY, the effects of ICV captopril and AII were not altered by the salt loading. The increases in BP induced by ICV hypertonic saline were not different between the rats with and without saline drinking in either SHR or WKY. The intravenous (IV) hexamethonium led to a greater fall in BP in SHR treated with saline than in those without salt, while it tended to produce a smaller decrease in BP in WKY with salt overload than in those without loading. Both duration and magnitude of the depressor effects of IV captopril were reduced by the chronic saline treatment in SHR. The plasma renin concentration (PRC) in both SHR and WKY was significantly suppressed by the salt load. The present results suggest that long-term salt overload may result in the enhanced activity of brain renin angiotensin system, which could be responsible for the exaggerated development of hypertension in SHR. Our observations also provide further evidence that the central renin angiotensin system is independent of the peripheral system.