The altered function and hemodynamic characteristics of the kidney or kidneys of the experimental hypertensive animals reported here may participate in the etiology and/or maintenance of the hypertensive state. A depression of GFR and enhanced sodium reabsorption in the SHR owing to hemodynamic, membrane permeability, and neural influences appear to be important in this form of experimental hypertension. In Goldblatt hypertension the renin-angiotensin system causes both vasoconstriction and increased proximal fluid reabsorption in the contralateral kidney of the two-kidney, one-clip Goldblatt hypertensive rat and dog. These factors could lead to the establishment of a long-term pressor influence in these animals. Protein in the diet has been clearly shown to worsen the glomerular lesions seen in several forms of experimental hypertension - those caused by reduced renal mass, DOCA-salt, and constriction of the renal artery. However, only in the DOCA-salt model does protein seem to accentuate the increase in blood pressure. On the other hand, glomerular damage seen in these hypertension models is also partly a function of the increased pressure. In the salt-sensitive Dahl rat with glomerulonephritis, sodium through its hypertensive effect contributes to renal damage. In these rats glomerular injury is aggravated by high dietary protein but is not prevented by protein restriction.
|Original language||English (US)|
|Number of pages||4|
|State||Published - Dec 1 1986|
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