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Chemical sympathectomy restores baroreceptor-heart rate reflex and heart rate variability in rats with chronic nitric oxide deficiency.
Physiol Res. 2015; 64(4):459-66.PR

Abstract

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.

Authors+Show Affiliations

Department of Physiology, Vardhaman Mahavir Medical College & Safdarjung Hospital, New Delhi, India, Department of Physiology, Hamdard Institute of Medical Sciences & Research, Jamia Hamdard, New Delhi, India. vpciphysiology@yahoo.com.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

25470513

Citation

Chaswal, M, et al. "Chemical Sympathectomy Restores Baroreceptor-heart Rate Reflex and Heart Rate Variability in Rats With Chronic Nitric Oxide Deficiency." Physiological Research, vol. 64, no. 4, 2015, pp. 459-66.
Chaswal M, Das S, Prasad J, et al. Chemical sympathectomy restores baroreceptor-heart rate reflex and heart rate variability in rats with chronic nitric oxide deficiency. Physiol Res. 2015;64(4):459-66.
Chaswal, M., Das, S., Prasad, J., Katyal, A., & Fahim, M. (2015). Chemical sympathectomy restores baroreceptor-heart rate reflex and heart rate variability in rats with chronic nitric oxide deficiency. Physiological Research, 64(4), 459-66.
Chaswal M, et al. Chemical Sympathectomy Restores Baroreceptor-heart Rate Reflex and Heart Rate Variability in Rats With Chronic Nitric Oxide Deficiency. Physiol Res. 2015;64(4):459-66. PubMed PMID: 25470513.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Chemical sympathectomy restores baroreceptor-heart rate reflex and heart rate variability in rats with chronic nitric oxide deficiency. AU - Chaswal,M, AU - Das,S, AU - Prasad,J, AU - Katyal,A, AU - Fahim,M, Y1 - 2014/12/03/ PY - 2014/12/4/entrez PY - 2014/12/4/pubmed PY - 2016/5/20/medline SP - 459 EP - 66 JF - Physiological research JO - Physiol Res VL - 64 IS - 4 N2 - 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. SN - 1802-9973 UR - https://www.unboundmedicine.com/medline/citation/25470513/Chemical_sympathectomy_restores_baroreceptor_heart_rate_reflex_and_heart_rate_variability_in_rats_with_chronic_nitric_oxide_deficiency_ L2 - http://www.biomed.cas.cz/physiolres/pdf/64/64_459.pdf DB - PRIME DP - Unbound Medicine ER -