Splenorenal reflex modulates renal blood flow in the rat.

Abstract

We have previously shown that the splenorenal reflex controls renin release through splenic afferent and renal sympathetic nerves. We proposed that this reflex would also affect renal blood flow (RBF). RBF was measured in male Long Evans rats using transit-time flow probes. There were no significant differences between any of the experimental groups with respect to baseline values of RBF (8.9 +/- 0.4 ml min(-1), n= 25) or mean arterial pressure (MAP, 98.7 +/- 2.5 mmHg, n= 25). Splenic venous pressure was selectively raised (from 7.9 +/- 0.6 to 21.6 +/- 0.3 mmHg, n= 25) in anaesthetized rats by partial ligation of the splenic vein. This caused an immediate fall in RBF (-2.1 +/- 0.2 ml min(-1), n= 7) and in MAP (-12.4 +/- 2.8 mmHg, n= 7). The fall in RBF, but not the fall in blood pressure, was attenuated by renal denervation (DeltaRBF: - 0.7 +/- 0.1 ml min(-1), n= 6), splenic denervation (DeltaRBF: -0.8 +/- 0.1 ml min(-1), n= 6) and close renal arterial injection of the alpha1-adrenergic blocker phenoxybenzamine (12.5 microg; DeltaRBF: -0.8 +/- 0.1 ml min(-1), n= 6). Renal conductance fell only in the intact control group, i.e. the residual fall in RBF in the denervated and phenoxybenzamine-treated animals could be attributed to the fall in MAP. We also showed that splenic vein occlusion increased both splenic afferent (from 3.0 +/- 0.3 to 6.6 +/- 0.6 spikes s(-1), n= 5) and renal efferent (from 24.8 +/- 2.0 to 50.2 +/- 4.9 spikes s(-1), n= 9) nerve activity. We conclude that obstruction to splenic venous outflow, such as would occur in portal hypertension, initiates increased splenic afferent nerve activity and renal vasoconstriction through the splenorenal reflex, as well as a fall in blood pressure. We propose that this contributes to the renal and cardiovascular dysfunction observed in portal hypertension.