Do resistance vessel abnormalities contribute to the elevated blood pressure of spontaneously-hypertensive rats? A review of some of the evidence.

This review summarizes some of the evidence pointing to the existence of vascular abnormalities in the spontaneously hypertensive rat (SHR) and the extent to which such abnormalities could be responsible for the elevated blood pressure in this animal. Compared with its genetic normotensive control, the Wistar-Kyoto rat (WKY), the adult SHR has an increased total peripheral resistance (TPR). Many factors appear to contribute to the increased TPR, including an active rarefication of the vascular bed and a general constriction of the vasculature. There is evidence that the general constriction is due to structural differences in the resistance vessels, to abnormally high activation levels (i.e. increased sympathetic nerve activity), and to abnormal excitation-contracting coupling within the vasculature itself (i.e. increased noradrenaline sensitivity of the vascular smooth muscle cells). Age studies and studies of the effects of antihypertensive treatment suggest that both structural and excitation-contraction abnormalities may be present before the onset of hypertension.