Abstract

In salt‐sensitive hypertension, increases in cerebrospinal fluid (CSF) sodium activate the sympathetic nervous system (SNS) to raise arterial blood pressure (ABP). However, the sympathetic bed that mediates this hypertensive effect of CSF sodium is not known. The present study tested the contribution of the splanchnic sympathetic bed to central sodium‐induced hypertension. To confirm the participation of the SNS, male Sprague‐Dawley rats (280–350g) received intravenous (IV) infusion of terazosin (3 mg/day) plus atenolol (24 mg/day) or saline (6mL/day) followed by a 7‐day intracerebroventricular (ICV) infusion of 0.8M NaCl (0.5 ul/hr) via osmotic minipump. ICV infusion of NaCl in control rats significantly raised ABP from 98.5±2.0 mmHg to 107.0±1.8 mmHg at day 4 (Δ: 8.6±2.8 mmHg, P<0.05). In contrast, ICV NaCl infusion in SNS‐blocked rats failed to increase ABP from 87.4±2.9 mmHg vs 84.3±3.0 mmHg at day 4 (Δ: −2.6±1.2 mmHg). To determine the role of the splanchnic bed, celiac ganglionectomy was performed at least 1 week before ICV infusion of NaCl. ICV NaCl raised ABP from 98.5±2.0 mmHg to 107.0±1.8 mmHg (Δ: 8.6± 2.8mmHg). However, ICV infusion in rats receiving celiac ganglionectomy did not increase ABP from 86.3±3.6 mmHg to 85.8±36 (Δ: −0.1±0.7 mmHg). These results indicate that SNA, specifically splanchnic SNA, mediates central sodium‐induced hypertension.

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