Nonuniform sympathetic nerve responses to intravenous hypertonic saline infusion.

Peripheral hyperosmolality produced by the intravenous infusion of hypertonic saline (HTS) increases mean arterial blood pressure (MAP) in experimental animals. The mechanisms mediating the pressor response have not been fully ascertained, but likely involve vasopressin and/or activation of the sympathetic nervous system. The primary aim of this study was to determine if HTS infusion produces regionally uniform or nonuniform changes in sympathetic nerve discharge (SND). For this purpose we recorded renal, splanchnic and lumbar SND during intravenous HTS infusion (2.5 M NaCl, 10 microliters/100 g BW per min) in chloralose-anesthetized, Sprague-Dawley rats. In rats with intact arterial baroreceptors, HTS infusion significantly increased MAP (17 +/- 2 mmHg) and lumbar SND (29 +/- 13%) but reduced splanchnic (-52 +/- 7%) and renal SND (-33 +/- 8%). After sinoaortic denervation (SAD), HTS infusion significantly increased MAP (28 +/- 6 mmHg) and lumbar SND (27 +/- 9%) and decreased renal SND (-22 +/- 8%). The increase in lumbar SND occurred significantly sooner in SAD compared with baroreceptor-intact rats. In contrast, splanchnic SND remained unchanged from control levels during HTS infusion after SAD. These results demonstrate that HTS infusion produces regionally nonuniform changes in SND, and suggest that the pressor and lumbar sympathoexcitatory responses to HTS infusion are opposed by the arterial baroreceptors.