Kaczmarczyk G, Marx M, Lee K, Mohnhaupt R, Reinhardt H W, Ehlers R
J Physiol (Paris). 1984;79(6):491-5.
Renal effects of A II, retention of sodium and water, may be mediated by the stimulation of aldosterone secretion and/or by direct effects of A II on the kidneys. An attempt was made to differentiate between these two possibilities.
Conscious, female beagle dogs were used. The dogs were kept under standardized conditions (metabolic cage, daily sodium intake 4.5 mmol X kg-1 bw, chronically implanted arterial and venous catheters, i.v. hormone substitution after adrenalectomy by a portable pump). A II was infused i.v. over a period of 60 min after 60 min control. (Rate: 1, 4, 20 or 200 ng X min-1 X kg-1 bw).
Mean arterial blood pressure (MABP) increased with 20 and 200 ng A II X min-1 X kg-1 bw by an average of 34 mm Hg and 65 mm Hg resp. before and after adrenalectomy. Before adrenalectomy: sodium and water excretion decreased always at 4 and 20 ng A II X min-1 X kg-1 bw, whereas a rate of 200 ng A II X min-1 X kg-1 bw had different effects on renal sodium and water excretion. After adrenalectomy: sodium and water excretion decreased at 4 ng A II X min-1 X kg-1 bw. Whereas a rate of 20 and 200 ng. -As no marked alterations of the glomerular filtration rate occurred, sodium retention observed was mainly due to tubular effects of A II. Plasma aldosterone concentration increased at 4, 20 and 200 ng A II X min-1 X kg-1 bw in the intact dogs.(ABSTRACT TRUNCATED AT 250 WORDS)