Inhibition of atrial receptor-induced renal responses by stimulation of carotid baroreceptors in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The receptors at three pulmonary vein-atrial junctions and in the left atrial appendage were stimulated by distension of small balloons. The carotid sinuses were vascularly isolated and perfused with arterial blood. A volume reservoir was connected to the aorta via the common carotid and femoral arteries to keep the mean aortic pressure constant (78.8 +/- 2.9 mmHg at low and 87.1 +/- 4.3 mmHg at high carotid sinus pressure, CSP). Propranolol and atropine were infused (i.v.) at 17 and 13 micrograms kg-1 min-1 respectively in order to block beta-adrenergic and cholinergic receptor activities. The renal blood flow was measured by an electromagnetic flow meter (wrap-round probe), glomerular filtration rate by creatinine clearance, urinary sodium excretion by flame photometry and osmolar excretion by osmometry. 2. In twelve tests in eight dogs, stimulation of the left atrial receptors for 13 min, at a mean CSP of 68.6 +/- 2.3 mmHg, resulted in significant increases in renal blood flow from 216 +/- 20.0 to 230 +/- 22.1 ml min-1 (100 g renal mass)-1 (P less than 0.005), glomerular filtration rate from 33.9 +/- 3.2 to 42.1 +/- 4.1 ml min-1 100 g-1 (P less than 0.005), filtration fraction from 0.23 +/- 0.02 to 0.26 +/- 0.02 (P less than 0.005), urine flow rate from 0.21 +/- 0.03 to 0.26 +/- 0.03 ml min-1 100 g-1 (P less than 0.001), sodium excretion from 12.9 +/- 4.0 to 16.4 +/- 4.8 mumol min-1 100 g-1 (P less than 0.01), osmolar excretion from 196 +/- 27.8 to 246 +/- 32.9 muosmol min-1 100 g-1 (P less than 0.005), whilst free water clearance decreased from -0.39 +/- 0.07 to -0.50 +/- 0.09 ml min-1 100 g-1 (P less than 0.005). However, the fractional excretion of sodium did not change. 3. In nine tests in seven dogs, stimulation of the left atrial receptors at a constantly high CSP (161 +/- 11.3 mmHg) did not produce significant change in any of the renal variables. 4. The results show that high level excitation of carotid baroreceptors can completely inhibit the reflex renal haemodynamic and functional responses to atrial receptor stimulation.