title: Cardiovascular vagosympathetic activity in rats with ventromedial hypothalamic obesity.
abstract: OBJECTIVE
  Rats with ventromedial hypothalamic lesion (VMH) are massively obese with endogenous hyperinsulinemia, insulin resistance, low sympathetic activity, and high parasympathetic activity, which are likely to induce hypertension. The goal was to follow in this model the long-term hemodynamic changes and to investigate the role of autonomic nervous system and insulin resistance in these changes.
  
  
  METHODS
  Heart rate and blood pressure were monitored for 12 weeks after operation using a telemetric system in VMH and sham rats. Plasma catecholamines and heart beta-adrenoceptors were measured. Glucose tolerance was studied after an intravenous glucose injection and insulin sensitivity during a euglycemic hyperinsulinemic clamp test.
  
  
  RESULTS
  A marked bradycardia and only a mild increase in blood pressure occurred in VMH rats compared with sham animals. Response to autonomic-acting drugs showed an increase in heart vagal tone and responsiveness to a beta-agonist drug. Plasma catecholamine levels were markedly increased, and the density and affinity of heart beta-adrenoceptors were similar in VMH, sham, and control rats. Muscle glucose use was reduced by 1 week after operation in VMH animals.
  
  
  CONCLUSIONS
  These results show the following in this model of massively obese rats with sympathetic impairment: 1). adrenal medulla secretion is increased, probably as a result of hyperinsulinemia and increased vagal activity; 2). cardiac responsiveness to beta-agonist stimulation is increased; and 3). despite these changes and suspected resistance to the vasodilative effect of insulin, blood pressure does not increase. We conclude that high vagal activity may be protective against hypertension associated with obesity.
authors.affiliation: Laboratory of Nutrition and Metabolic Diseases, Paris-Nord University, Bondy, France. paul.valensi@jvr.ap-hop-paris.fr
authors.forename: Paul
authors.initials: P
authors.lastname: Valensi
authors.forename: Liliane
authors.initials: L
authors.lastname: Doaré
authors.forename: Gérard
authors.initials: G
authors.lastname: Perret
authors.forename: Renée
authors.initials: R
authors.lastname: Germack
authors.forename: Jacques
authors.initials: J
authors.lastname: Pariès
authors.forename: Didier
authors.initials: D
authors.lastname: Mesangeau
mesh_terms: D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure / Q000187:drug effects; D001835:Body Weight; D002319:Cardiovascular System / Q000294:innervation*; D004837:Epinephrine / Q000097:blood; D005260:Female; D015309:Glucose Clamp Technique; D005951:Glucose Tolerance Test; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics; D007033:Hypothalamus, Middle / Q000503:physiopathology* / Q000601:surgery*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D007545:Isoproterenol / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000097:blood; D009765:Obesity / Q000209:etiology / Q000503:physiopathology*; D010276:Parasympatholytics / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D011943:Receptors, Adrenergic, beta / Q000032:analysis; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D013566:Sympathomimetics / Q000494:pharmacology; D014630:Vagus Nerve / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D007328:Insulin; D010276:Parasympatholytics; D011943:Receptors, Adrenergic, beta; D013566:Sympathomimetics; D009599:Nitroprusside; D001285:Atropine; D007545:Isoproterenol; D009638:Norepinephrine; D004837:Epinephrine