1. We have previously shown that normotensive rabbits with a genetic impairment in arterial baroreflex sensitivity showed a delayed sodium excretion and failed to increase their renal blood flow in response to a saline infusion that did not alter blood pressure. These renal haemodynamic and excretory abnormalities were abolished by renal denervation. The present study determined the sensitivity of the cardiopulmonary baroreceptors and the renal response to a mild saline infusion in normotensive rabbits varying widely in their arterial baroreflex sensitivity.

2. Sensitivity of cardiopulmonary baroreceptors was assessed from the slope of the relationship of the change in both blood pressure and heart rate and the dose of phenylbiguanide, a stimulator of vagal afferents.

3. The change in renal blood flow and lithium and sodium excretion was measured in response to saline, infused at a rate of 0.11 ml·min-1·kg-1 into the ear vein. Urine was collected via a urethral catheter and renal blood flow was measured by para-aminohippurate clearance.

4. A significant correlation was found between the magnitude of the gain of the cardiac arterial baroreflex and the sensitivity of the cardiopulmonary baroreceptor response to phenylbiguanide. The latter was significantly correlated to renal blood flow and lithium clearance 60–90 min after the start of the saline infusion.

5. It was also found that in some normotensive rabbits there was a blunting of cardiovascular regulation as indicated by a reduced sensitivity of cardiopulmonary and arterial baroreceptors. This may explain their abnormal haemodynamic and natriuretic response to salt.

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