Release of renin in hypertensive rats

¹ Research Division, Cleveland Clinic Foundation; and the Frank E. Bunts Institute, Cleveland, Ohio

A method for perfusing rat's kidneys is described in which renal release of pressor substances (renin?) was measured by grafting a kidney on to a 24-hour nephrectomized recipient. Normal kidneys provoked a sharp and sustained rise in blood pressure. Kidneys that had undergone compensatory hypertrophy behaved as normal kidneys as long as the animals received tap water to drink; when 1% saline was substituted, pressor activity decreased gradually and finally disappeared usually around the 3rd week. DCA injection (2 mg/day) enhanced the salt effect so that no pressor activity could be demonstrated after the 4th day of treatment. Kidneys from rats with post-DCA or adrenal regeneration hypertension did not release pressor material. Unilateral renal infarction associated with contralateral nephrectomy caused initially a decrease in renin release followed by disappearance in both the rats that developed hypertension and in some that remained normotensive. Since absence of pressor activity in the renal venous effluent as determined by this method is not necessarily associated with development of hypertension, it is possible that this change represents primarily a response to renal injury, sodium excess and/or high blood pressure.

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