Chemical sympathectomy completely abolished the pressor effect of chronic L-NAME (SBP 116.6 vs 174.3 mm Hg) and restored baroreflex sensitivity and heart rate variability.
Does chemical sympathectomy prevent hemodynamic and autonomic dysfunction in rats with chronic nitric oxide deficiency?
Chemical sympathectomy prevents hypertension and restores baroreflex sensitivity and heart rate variability in rats with chronic nitric oxide deficiency, suggesting sympathetic overactivity is the principal mechanism of L-NAME-induced hypertension.
Absolute Event Rate: 116.6% vs 174.3%
p-value: p=<0.05
Nitric oxide (NO) plays a crucial role not only in regulation of blood pressure but also in maintenance of cardiac autonomic tone and its deficiency induced hypertension is accompanied by cardiac autonomic dysfunction. However, underlying mechanisms are not clearly defined. We hypothesized that sympathetic activation mediates hemodynamic and cardiac autonomic changes consequent to deficient NO synthesis. We used chemical sympathectomy by 6-hydroxydopamine to examine the influence of sympathetic innervation on baroreflex sensitivity (BRS) and heart rate variability (HRV) of chronic N(G)-nitro-L-arginine methyl ester (L-NAME) treated adult Wistar rats. BRS was determined from heart rate responses to changes in systolic arterial pressure achieved by intravenous administration of phenylephrine and sodium nitroprusside. Time and frequency domain measures of HRV were calculated from 5-min electrocardiogram recordings. Chronic L-NAME administration (50 mg/kg per day for 7 days orally through gavage) in control rats produced significant elevation of blood pressure, tachycardia, attenuation of BRS for bradycardia and tachycardia reflex and fall in time as well as frequency domain parameters of HRV. Sympathectomy completely abolished the pressor as well as tachycardic effect of chronic L-NAME. In addition, BRS and HRV improved after removal of sympathetic influence in chronic L-NAME treated rats. These results support the concept that an exaggerated sympathetic activity is the principal mechanism of chronic L-NAME hypertension and associated autonomic dysfunction.
Chaswal et al. (Sun,) conducted a other in Chronic nitric oxide deficiency (L-NAME induced hypertension) (n=40). Chemical sympathectomy (6-hydroxydopamine) vs. Vehicle (intact sympathetic nervous system) was evaluated on Systolic blood pressure (mm Hg) after 7 days of L-NAME treatment (p=<0.05). Chemical sympathectomy completely abolished the pressor effect of chronic L-NAME (SBP 116.6 vs 174.3 mm Hg) and restored baroreflex sensitivity and heart rate variability.
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