Role of cardiac sympathetic nerves in blood pressure regulation

Stellate ganglionectomy (SGx) was used to assess the contribution of cardiac sympathetic nerves to neurogenic hypertension in deoxycorticosterone (DOCA)-salt treated rats. Experiments were conducted in two substrains of Sprague-Dawley (SD) rats since previous studies reported bradycardia in Charles River-SD (CR-SD) rats and tachycardia in SASCO-SD (SA-SD) rats with DOCA treatment suggesting different underlying neural mechanisms. Uninephrectomized male rats underwent SGx or SHAM surgery and were instrumented for telemetric monitoring of mean arterial pressure (MAP) and heart rate (HR). After recovery, 0.9% saline solution and DOCA (50 mg) were administered. Baseline MAP (Days 0-5 average) after SGx in CR-SD rats (96 ± 2 mm Hg; n = 7) was not significantly different (p = 0.08) than CR-SD SHAM rats (103 ± 3 mm Hg; n = 9); however, there was a significantly lower HR during the baseline period (377 ± 7 vs. 432 ± 7 bpm, p < 0.05) in SGx rats. In SA-SD rats baseline MAP was not different between SGx and SHAM rats and HR was lower in SGx rats (428 ± 8 vs. 371 ± 5 bpm, p < 0.05). After DOCA treatment in both substrains, MAP and HR were elevated similarly in SHAM and SGx groups showing minimal impact in both groups of SGx on hypertension development. However, overall MAP in SA-SD SHAM rats reached a significantly higher level (155 ± 10 mm Hg vs 135 ± 5 mm Hg, p < 0.05) than that observed in CR-SD SHAM rats demonstrating that the magnitude of hypertensive response to DOCA-salt treatment varies between substrains. In conclusion, removal of cardiac sympathetic nerves did not alter the development or maintenance of DOCA-salt hypertension in SD rats.