Effects of combined carotid chemoreceptor and atrial receptor stimulation on renal blood flow in anaesthetized dogs.

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In dogs anaesthetized with chloralose and artificially ventilated, carotid chemoreceptors were stimulated by changing the perfusate of the vascularly isolated carotid bifurcations from arterial to venous blood. Left atrial receptors were stimulated by distending balloons in two pulmonary vein-left atrial junctions and in this left atrial appendage. The left renal blood flow was measured by an electromagnetic flow meter at a constant systemic (renal) arterial pressure in preparations in which heart rate changes were prevented by administration of propranolol hydrochloride (0.5 mg kg-1) and atropine sulphate (0.4 mg kg-1). Muscular movement was prevented by gallamine triethiodide (0.2 mg kg-1). Stimulation of left atrial receptors resulted in a significant increase (P less than 0.001) in renal blood flow of 5.6 +/- 0.88 ml min-1 100 g-1 renal mass from a control of 223 ml min-1 100 g-1 renal mass. The responses were abolished by cooling the cervical vagus nerves to 6-8 degrees C. Stimulation of carotid chemoreceptors, by perfusion of the carotid bifurcations by venous blood, caused a decrease in renal blood flow of 20 +/- 6.9 ml min-1 100 g-1 renal mass from 224 ml min-1 100 g-1 renal mass. Stimulation of left atrial receptors during venous perfusion of carotid chemoreceptors resulted in an increase in renal blood flow of 10.9 +/- 1.82 ml min-1 100 g-1 renal mass from 208 ml min-1 100 g-1 renal mass. These results show that atrial receptors and chemoreceptors can interact in their effects on renal blood flow.

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