The effect of varying renal artery pressure between 160 and 40 mm Hg on renal blood flow and renin release was studied in seven conscious foxhounds under beta-adrenergic blockade receiving a normal sodium diet (4.1 mmol/kg/day). Pressure was either increased by bilateral common carotid occlusion or reduced in steps and maintained constant by a control-system using an inflatable renal artery cuff. Carotid occlusion itself had no influence on renal blood flow and renin release when renal artery pressure was kept constant and the beta-receptors in the kidney were blocked. Between 160 mm Hg and resting pressure there was no change in renal blood flow; between resting blood pressure and the lower limit of autoregulation (average 63.9 mm Hg) renal blood flow increased slightly (average 7%) indicating a high efficiency of renal blood flow autoregulation. The relationship between renal artery pressure and renin release could be approximated by two linear sections: a low sensitivity to a pressure change (average slope: -0.69 +/- 0.26 ng AI/min/mm Hg) was found above a threshold pressure (average: 89.8 +/- 3.3 mm Hg) and a high sensitivity to a pressure change (average slope: -64.4 +/- 20.8 ng AI/min/mm Hg) was observed between threshold pressure and 60 mm Hg. There was no further increase of renin release between 60 and 40 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
We studied the effect of bilateral common carotid occlusion (implanted pneumatic cuffs) on renal blood flow (electromagnetic flowmeter) and renal function (implanted ureteral catheter) in nine chronically instrumented, conscious dogs on a high sodium diet (14 mmol/kg body weight per day). By means of suprarenal aortic constriction (pneumatic cuff) the influence of renal perfusion pressure was investigated. There was no change in renal blood flow or glomerular filtration rate (inulin clearance) with either reflexly increasing (+49.6%) or constant renal perfusion pressure. Carotid occlusion caused an increase of urine output by 80.5% and of sodium excretion by 85.3% due to a fall in fractional sodium reabsorption (-0.9%) when renal perfusion pressure was allowed to rise. Neither an increase of diuresis or sodium excretion nor an antinatriuresis was observed when renal perfusion pressure was kept constant during carotid occlusion. We conclude that, in conscious dogs at rest, the moderate sympathetic activation associated with carotid occlusion is too small to induce renal sympathetic vasoconstriction or antinatriuresis. The "carotid sinus polyuria" is a pressure-diuresis.
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