The relationship between the kidney and genetic hypertension has been assessed in light of the changes seen in some kidney and cell functions during the phases preceding and accompanying the development of “genetic” types of hypertension in rats and humans. Comparison of the kidney function of normotensive subjects likely to develop hypertension with that of matched controls resistant to hypertension showed, in the former, a higher glomerular filtration rate (GFR), greater tubular reabsorption, larger 24-h urinary output, larger fraction of cardiac output to the kidney, and lower plasma renin activity. After the transplantation of a kidney from a subject in the hypertension-prone group, recipients had higher blood pressure and required more antihypertensive therapy than recipients of kidneys from the hypertension-resistant group. In humans this finding is not as clear as in rats. During the development of hypertension most of these differences in kidney function in the two groups of subjects tend to disappear. The changes in cell function, measured particularly in rats, were consistent with the organ function changes. Cell volume and sodium content were lower, while the transport rate across the cell membrane was faster in proximal tubular cells of rats with genetic hypertension than in the appropriate controls. This is in keeping with the concept of a primary increase in proximal tubular reabsorption leading, on the one hand, to an increase in GFR and renal blood flow and a decrease in renin and, on the other, to an increase in blood pressure. The same differences in proximal tubular cell function were found in the two groups of rats when their red blood cells (RBC) were compared. Genetic analysis and bone marrow transplantation studies showed that the RBC function of genetically hypertensive rats was primarily determined within their stem cells and was genetically linked to hypertension. In view of these two last findings and the similarities between red blood cells and proximal tubular cells, it is suggested that hypertension in rats may be caused by a genetic modification of the membranes of proximal tubular cells. In humans the same mechanisms might be present, but such a proposal remains highly hypothetical.
|Journal||Journal of Cardiovascular Pharmacology|
|Publication status||Published - 1984|
- Dahl strain
- Genetic hypertension
- Milan hypertensive strain
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine