The effects of experimental acute renal hypertension on sympathetic nerve activity to the kidney in the rat

Abstract

The reopening of the renal hilum after a period of complete renal ischaemia is followed by a hypertensive crisis (the experimental acute renal hypertension: EARH) which is due to the acute release of renin and endogenous angiotensin II formation. The present study was done to verify if the EARH is accompanied by simultaneous alterations in efferent sympathetic nerve activity to the kidney. The experiments were done on Sprague-Dawley spontaneously breathing rats (200-300 g) anaesthetized with nembutal (n=5). After excision of the left kidney, the renal nerves to the right kidney were exposed by a retroperitoneal approach and a single nerve strand was positioned on a bipolar hook electrode to record renal sympathetic postaganglionic nerve activity (RSNA). Threads were placed around the right renal artery and vein in order to produce a complete renal ischaemia. After three hours these ties could be loosened to reestablish blood flow to and from the kidney (functional right nephrectomy: FRN). RSNA, blood pressure, heart rate, rate of breathing and rectal temperature were continuously recorded. From the beginning of the experiment (time 0) to its end (time 300 min) the nerve strands were left untouched and their position on the electrode was unchanged. As previously reported with respect to control conditions RSNA decreased during three hours of FRN from 39.1 ±3 imp/sec at baseline, to 13.7 ±3 at the end of three hours of FRN period (Recordati, J Hypertens, 18: 1277, 2000). The present report describes what occurred at the reopening of the right renal hilum when a hypertensive crisis and tachycardia are observed. In four out of five rats this hypertension was accompanied by a 1-3 min continuous firing of the RSNA to a mean peak increase of 28.7 ±7 imp/sec at a time the mean systolic blood pressure had increased to 209.4 ±21 mmHg. RSNA subsequently recovered towards a spontaneous normal bursting discharge, while blood pressure persisted elevated. These results indicate that the increase in sympathetic activity at the reopening of the renal hilum is short-lasting and therefore may only be partially responsible for the observed persistent increase in blood pressure. The consistently observed excitation of RSNA may be due to a reflex excitatory effect upon stimulation of renal receptors or of nonrenal sympathetic afferents, or, more probably, from central and ganglionic excitation of sympathetic neurons by a substance released by the ischaemic kidney.