Abstract
Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. The purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280–350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g⋅kg−1 b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. In sham rats, the HS infusion (3 M NaCl, 1.8 ml⋅kg−1 b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9±2.7 mmHg) and increases in the RBF and RVC (141±7.9% and 140±7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (−45±5.0% at 10 min after HS) throughout the experimental period. In the A2-lesioned rats, the HS infusion induced transient hypertension (6±1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133±5.2% and 134±6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115±3.1% at 10 min after HS). The extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.
Highlights
Several lines of evidence have found that acute or chronic hypernatremia engages several effector natriuretic mechanisms that remain active until the reestablishment of the plasma sodium concentration. [1,2,3,4,5,6,7,8]
In rats treated with bilateral nanoinjections of anti-DbHsaporin into the nucleus of the solitary tract (NTS) (n = 6), the number of Tyrosine hydroxylase (TH)-positive neurons caudal to the obex was reduced to approximately six cells per section
In A2-lesioned rats, hypernatremia failed to decrease renal sympathetic activity during the observation period. These results point out the involvement of A2 noradrenergic neurons in the autonomic responses that are induced by acute changes in the plasma sodium concentration, and the results highlight their involvement in the regulation of renal sympathetic nerve activity
Summary
Several lines of evidence have found that acute or chronic hypernatremia engages several effector natriuretic mechanisms that remain active until the reestablishment of the plasma sodium concentration. [1,2,3,4,5,6,7,8]. Previous studies have demonstrated that the intravenous infusion of hypertonic saline (HS) increases arterial blood pressure and renal vascular conductance and induces regionally distinct changes in the sympathetic nerve activity, such as increases in lumbar and decreases in renal and splanchnic nerve discharge [2,3,4,8,9]. It is generally accepted that the inhibition of renal sympathetic nerve activity (RSNA) is a key component of these adjustments as it can produce renal vasodilation, decrease renin secretion and reduce renal sodium reabsorption, all mechanisms that, either in isolation or synergistically, will lead to massive sodium loss. The central aspects of the neural pathways involved in the activation of these systems remain unclear. Duale et al [10] demonstrated that the silencing of A2 neurons affected water consumption and urine output
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