Effects of salt and water depletion on the early phase of hypertension in Goldblatt two-kidney hypertensive dogs.
1. Hypertension was induced in dogs by partial occlusion of one renal artery, the opposite kidney remaining intact, and the changes in blood pressure, plasma renin activity, aldosterone and prostaglandin E (PGE) were monitored. 2. Two days after induction of hypertension, the retained sodium and water were removed by haemodialysis and the animals were then maintained on a low dietary intake of sodium for the following 7 days. 3. Removal of the accumulated sodium and water had no immediate effect on blood pressure, but during the ensuring 7 days there was a small decrease in blood pressure, which again increased after re-institution of a normal sodium intake. 4. Plasma renin activity and aldosterone increased during development of hypertension and remained elevated during the period of sodium restriction. 5. Sodium and water retained during the development of hypertension was not responsible for the elevated blood pressure. 6. The concentration of PGE in arterial plasma and renal venous plasma from the unclamped kidney were unchanged during the study, although we have previously shown that in the absence of sodium depletion, PGE rises. 7. PGE released from the kidney may be important in mediating the excretion of sodium and water that is retained during the development of renal hypertension.
D000450:Aldosterone / Q000097:blood; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D004039:Diet, Sodium-Restricted; D004285:Dogs; D005260:Female; D006339:Heart Rate; D006400:Hematocrit; D006977:Hypertension, Renal / Q000378:metabolism*; D006978:Hypertension, Renovascular / Q000378:metabolism* / Q000503:physiopathology; D011458:Prostaglandins E / Q000097:blood; D006435:Renal Dialysis; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism*; D014867:Water / Q000378:metabolism*
D011458:Prostaglandins E; D014867:Water; D000450:Aldosterone; D012964:Sodium; D012083:Renin