title: Neonatal chemical sympathectomy attenuates fructose-induced hypertriglyceridemia and hypertension in rats.
abstract: Experiments were performed to determine the pathogenic contribution of the peripheral sympathetic nervous system to fructose-induced hypertriglyceridemia, hyperinsulinemia and hypertension in rats. Neonatal chemical sympathectomy was performed in neonatal Sprague-Dawley rats (1-week old) by administration of guanethidine (50 microg/g, i.p.) 5 times per week for consecutive 3 weeks and nerve-intact rats were served as controls. Both groups of rats were fed a fructose-enriched diet for 9 weeks. The systolic blood pressure (SBP) and body weight were measured weekly and arterial blood samples were taken weekly for determinations of plasma insulin, glucose and triglyceride levels. The results showed that fructose feeding for one week significantly increased SBP in intact rats and sympathectomized rats (116+/-1 to 119+/-1 mmHg and 116+/-1 to 120+/-1 mmHg, respectively). SBP further increased thereafter in both groups. However, the increased SBP levels were significantly higher in intact group than in sympathectomized group after 5 weeks of fructose feeding. Fructose feeding for one week concurrently produced hypertriglyceridemia that preceded the appearance of hyperinsulinemia in both groups. The elevated plasma triglyceride levels were significantly lower in sympathectomized rats than in intact rats after 3 weeks of fructose feeding, whereas the elevated plasma insulin concentrations were not different between groups throughout fructose feeding period. Plasma glucose concentrations of both groups were comparable and remained unchanged throughout the study. These data indicate that neonatal chemical sympathectomy attenuated, but did not prevent, fructose-induced elevations in blood pressure and plasma triglyceride levels, suggesting a partial dependency of fructose-induced hypertriglyceridemia and hypertension on the integrity of the peripheral sympathetic nervous system (SNS) in rats.
authors.affiliation: Department of Physiology and Biophysics, National Defense Medical Center, Taipei, Taiwan, ROC.
authors.forename: P S
authors.initials: PS
authors.lastname: Hsieh
authors.forename: W C
authors.initials: WC
authors.lastname: Huang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001786:Blood Glucose; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight; D005632:Fructose / Q000008:administration & dosage; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000628:therapy*; D015228:Hypertriglyceridemia / Q000139:chemically induced / Q000628:therapy*; D007328:Insulin / Q000097:blood; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013563:Sympathectomy, Chemical; D013564:Sympathetic Nervous System / Q000502:physiology*; D013566:Sympathomimetics / Q000494:pharmacology; D014439:Tyramine / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D007328:Insulin; D013566:Sympathomimetics; D010656:Phenylephrine; D005632:Fructose; D014439:Tyramine