In male Sprague-Dawley rats, renal artery constriction in the presence of an inact contralateral kidney induced sodium retention (for 2-3 wk), moderate potassium loss,elevation of blood volume (BV), and an increase in water turnover. It is suggestedthat renal artery constriction activates the renin-angiotensin-aldosterone system, resulting in disordered regulation of salt and water balance and in blood pressure (BP) elevation. Subsequently, sodium balance was reestablished in one group of hypertensive rats. The previously retained sodium was kept in the body, and BV and reninactivity remained elevated. In a second group of animals, a malignant course of hypertension developed: BP surpassed a critical level of about 180 mmHg; sodium, potassium, and water were lost; BV declined; renin activity was further stimulated; and in the contralateral kidney malignant nephrosclerosis occurred. It is assumed that pressure diuresis and natriuresis induce a vicious circle: the increasing renin activity may maintain or further increase BP level, therby inducing further salt and water loss, etc.; high BP levels and high renin activities induce vascular damage and deterioration of renal function.
The chloride channel Bestrophin‐1 acts in the Malpighian tubule and hindgut of
Drosophila melanogaster
to maintain salt and water balance
