Regional vascular resistance and haemodynamics in the spontaneously hypertensive rat: the effects of bradykinin.

To identify those vascular beds that contribute to the elevated peripheral resistance (TPR) seen in spontaneously hypertensive rats (SHR) as compared to Wistar-Kyoto rats (WKY), the distribution of cardiac output, organ blood flow, and regional vascular resistance were measured using radiolabelled microspheres. WKY and SHR had similar heart rates, cardiac outputs, and cardiac stroke volumes, whereas SHR had significantly elevated TPR. This increased TPR was the cumulative effect of significant elevations in vascular resistance in the brain, testes, epididymides, gastrointestinal tract, pancreas/mesentery, skin, kidneys, and skeletal muscle. Only in the renal and skeletal muscle vasculature was this elevation in resistance associated with reduced blood flow. Haemodynamic responses to bradykinin [thought to act through a release of endothelium-derived relaxing factor (EDRF)] were similar in both WKY and SHR with the exception of the liver where no reduction of hepatic arterial resistance was seen in the SHR. We suggest that the increase in resistance in the renal and skeletal muscle vasculature is due to active vasoconstriction in these beds. This vasoconstriction diverts a significant proportion of the cardiac output through other vascular beds, especially the brain, liver, and coronary circulation. This will result in increased shear-stress and consequent damage to endothelial cells.