Renal sympathoinhibition induced by hypernatremia: Involvement of A1 noradrenergic neurons

Several findings suggest that A1 noradrenergic neurons in the caudal ventrolateral medulla (CVLM) contribute to body fluid homeostasis and cardiovascular regulation. Recently we demonstrated that the renal vasodilation induced by infusion of hypertonic saline (HS) depends on the integrity of the A1 neurons. Here we determined the effect of lesions of these neurons on the inhibition of the renal sympathetic nerve activity (RSNA) induced by HS infusion. All experiments were performed in Wistar rats (280–350 g). A1 neurons were lesioned by microinjections of antidopamine-β-hydroxylase-saporin (6.3 ng in 60 nl) into the CVLM (n = 5), whereas sham rats received microinjections of free saporin (1.3 ng in 60 nl, n = 10). Two weeks later, rats were anesthetized (urethane 1.2 g/kg, iv), and instrumented for recording of arterial pressure and RSNA. In sham rats, HS infusion (3 M NaCl, 0.18 ml/100 g bw, iv) induced a transient (≤ 30 min) hypertension (peak at 10 min; 9 ± 5 mm Hg) and a fall in RSNA (− 32 ± 7% of baseline at 10 min). A1-lesions increased the duration of the pressor response induced by HS infusion (16 ± 2 mm Hg at 60 min) and abolished the fall in RSNA (− 6 ± 8% of baseline at 10 min). Catecholaminergic lesions extensions were confirmed by immunocytochemistry. Unilateral renal denervation reduced the renal vasodilatation induced by HS infusion (112 ± 7% in denervated rats versus 127 ± 4% in sham, 20 min after HS). These results suggest that A1 noradrenergic neurons are involved in the sympathoinhibition and consequent renal vasodilatation to acute changes in the extracellular fluid compartment.