Red blood cell abnormalities and spontaneous hypertension in the rat. A genetically determined link.

Abstract

The significance of the erythrocyte abnormalities described in rats and humans with spontaneous hypertension is far from clear. Two highly inbred strains of rats were studied to evaluate whether these abnormalities are primary and thus genetically related to hypertension. The Milan hypertensive strain (MHS) and its normotensive control strain (MNS) were used to carry out 2 types of experiments. In 2 groups of lethally irradiated (MHS .RTM. MNS) F1 hybrids, bone marrow from MHS or MNS was transplanted. The differences in red cell function between the recipients of bone marrow from MHS and recipients of bone marrow from MNS were similar to those existing between the parental donor MHS and MNS; Na+-K+ cotransport was increased (P < 0.02) and intracellular Na+ content (P < 0.05) and cell volume (P < 0.02) were decreased in MHS. The same pattern was observed when this experiment was repeated in different groups of F1 hybrids. In individuals of the segregating F2 population, obtained by crossing the (MHS .times. MNS) F1 hybrids, there was a positive correlation (P < 0.001) between the red blood cell Na+-K+ cotransport and the mean blood pressure. The erythrocyte abnormalities may well be genetically associated with the primary cause of spontaneous hypertension in rats. Because of the many similarities demonstrated when young prehypertensive MHS or humans prone to develop hypertension are compared with their respective controls, it is possible that the findings described here in rats are relevant to human essential hypertension.