Renal mechanisms and calcium in the pathogenesis of a type of genetic hypertension.
Results concerning kidney and red blood cell (RBC) function of Milan hypertensive rats (MHS), and of their age- and body weight-matched normotensive controls (MNS), are summarized. Our data suggest a biochemical and physiological link between RBC abnormalities and the renal mechanisms causing hypertension in MHS, and therefore the possibility of using the former as a tool for studying the genetic biochemical mechanisms of hypertension. In particular, the following results are discussed: a positive correlation between blood pressure and RBC Na+-K+ cotransport found in the F2 generation, obtained by crossing F1 (MHS X MNS) hybrids; bone marrow transplantation from MHS and MNS into F1 hybrids, causing a parallel change in recipient RBC characteristics; and similarities between erythrocytes and renal tubular cells in Na+ content, cell volume, and Na+ transport. Ca2+ ATPase or Ca2+ pump at Vmax are lower in MHS renal tubular cells and MHS erythrocytes than in MNS cells. Moreover, isolated kidneys of MHS and MNS, perfused in vitro with media at different Ca2+ concentrations, showed that the function of MNS kidney remained stable over a range of Ca2+ from 0.75 to 1.25 mM, while the function of MS kidney deteriorated at a Ca2+ concentration of 1.25 mM.
D000328:Adult; D000368:Aged; D002118:Calcium / Q000502:physiology*; D002352:Carrier Proteins / Q000378:metabolism; D004905:Erythrocyte Aging; D004911:Erythrocyte Volume; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics* / Q000503:physiopathology; D007668:Kidney / Q000503:physiopathology*; D008875:Middle Aged; D028021:Sodium-Potassium-Chloride Symporters
D002352:Carrier Proteins; D028021:Sodium-Potassium-Chloride Symporters; D002118:Calcium