1. In chloralose-anaesthetized and artificially ventilated dogs, the carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (partial pressure of O2 (P(O2)) 43.8 +/- 2.4 mmHg, mean +/- S.E.M. n = 14) to stimulate the carotid chemoreceptors. The carotid sinus pressure was held constant at 142.0 +/- 2.8 mmHg. Measurements were made of renal and gracilis muscle blood flow by wrap-round electromagnetic flow probes placed around the renal and gracilis arteries, glomerular filtration rate by creatine clearance, urinary sodium excretion by flame photometry and solute excretion by osmometry. 2. In ten dogs, with intact cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced significant increases in aortic pressure (AoP) of 12.7 +/- 1.1 % (n = 10, P < 0-001), in glomerular filtration rate (GFR) of 14.7 +/- 4.1 % (P < 0.001), urine flow rate (V) of 16.5 +/- 3.5 % (P < 0.002), in urinary sodium excretion (U(Na)V) of 17.5 +/- 2.5 % (P < 0.005) and in urinary osmolar excretion (U(osm)V) of 13.2 +/- 2.2 % (P < 0.001), but a significant decrease in renal blood flow (RBF) of 5.8 +/- 1.8 % (P < 0.02). In six of these dogs in which gracilis muscle blood flow (MBF) was also recorded, carotid chemoreceptor stimulation caused significant increases in AoP of 12.8 +/- 1.4 % (n = 6, P < 0.001) and in MBF of 10.0 +/- 1.6 % (P < 0.002), and a small but significant decrease in RBF of 3.6 +/- 1.5 % (P < 0.02). 3. In fourteen dogs, with sectioned cervical vagosympathetic trunks, carotid chemoreceptor stimulation produced increases in AoP of 22.0 +/- 2.6 % (n = 14) P < 0.001), in GFR of 36.9 +/- 4.2 % (P < 0.001), in V of 30.1 +/- 4.4 % (P < 0.001), in U(Na)V of 31.4 +/- 5-3 % (P < 0.001), and in U(osm)V of 25.7 +/- 5.8 % (P < 0.001). However, it produced a greater decrease in RBF of 10.5 +/- 1.9 % (P < 0.001). In ten of these dogs, where MBF was recorded, carotid chemoreceptor stimulation caused greater increase in AoP of 22.4 +/- 3.0 % (n = 10, P < 0.001) and in MBF of 32.8 +/- 3.7 % (P < 0.001), and a greater decrease in RBF of 9.8 +/- 1.9 % (P < 0.001). 4. In fourteen dogs, with sectioned vagosympathetic trunks and controlled AoP, carotid chemoreceptor stimulation caused significant decreases in RBF of 19.1 +/- 1-6 % (n = 14, P < 0.001), in GFR of 17.7 +/- 2-2 % (P < 0-001), in V of 23.4 +/- 2.5 % (P < 0.001), in U(Na)V of 22.0 +/- 2.4 % (P < 0.001) and in U(osm)V of 16.7 +/- 2.1 % (P < 0.001). In ten of these dogs, in which MBF was measured, carotid chemoreceptor stimulation produced a large decrease (a reverse effect) in MBF of 18.8 +/- 2.1 % (n = 10, P < 0.001) and in a further decrease in RBF of 19.7 +/- 2.0 % (P < 0.001). 5. It is concluded that the primary effects of carotid chemoreceptor stimulation are a reduction in both muscle and renal blood flow, antinatriuresis and antidiuresis. The MBF, GFR, V, U(Na)V, UosmV, and not the RBF, are increased passively by a concomitant increase in arterial pressure in response to carotic chemoreceptor stimulation.
