Effects of vasoactive drugs on the natriuresis of nephrotic rats
Okay, Y.; Ruiz, G.; Marcondes, M.
Brazilian Journal of Medical and Biological Research 17(1): 93-99
1984
ISSN/ISBN: 0100-879X PMID: 6478099 Document Number: 230590
Seven nephrotic rats with edema, massive proteinuria and reduced glomerular filtration rate and filtration fraction were compared with ten normal rats. The experiment consisted of three consecutive periods: C, control; Ach, in which acetylcholine (40-60 ng/min) was continuously infused directly into the left renal artery; and Ach-AN-NA, in which angiotensin II (AN, 0.025 ng/min) + noradrenaline (NA, 0.25 micrograms/min) was systemically infused to elevate blood pressure, without interrupting acetylcholine infusion. Mean arterial pressure (MAP) and renal function parameters were measured. In both groups, MAP remained unchanged from C to Ach (P greater than 0.05) and was increased (P less than 0.05) from Ach to Ach-AN-NA (136 +/- 3.3 to 148 +/- 2.9 mmHg in normal animals, and 132 +/- 5.8 to 148 +/- 4.9 mmHg in nephrotic animals). In the normal group, intrarenal acetylcholine infusion increased (P less than 0.05) natriuresis from 3.75 to 7.93 microEq min-1 kd-1 kg BW-1 and a further, but transitory, increment up to 10.20 microEq min-1 kd-1 kg BW-1 was observed (P less than 0.05) when MAP was elevated. These natriuretic changes occurred without alterations of glomerular filtration rate (P greater than 0.05). Therefore, as previously reported in the literature, normal rats were responsive to intrarenal infusion of acetylcholine (vasodilator) followed by increased blood pressure, a condition known as pressure natriuresis. However, no natriuretic response was observed in the nephrotic group either to intrarenal acetylcholine infusion or to blood pressure elevation. We assume that nephrotic rats are insensitive to pressure natriuresis.