Diminished cardiovascular responsiveness to vagal stimulation in obese rats.
Obese rats maintained on a high-fat diet since weaning were studied to determine whether parasympathetic deficiencies contribute to the cardiovascular malfunction in obesity. Elevations in tail-cuff systolic pressures and plasma insulin indicated that obese rats had borderline hypertension and hyperinsulinemia. Reflex bradycardia produced by angiotensin or phenylephrine in conscious obese rats was less than that in age-matched controls. However, reflex responses elicited by phenylephrine or sodium nitroprusside when the same rats were later anesthetized did not differ between groups. Impairment of afferent or central components of the baroreflex arc was considered unlikely, because depressor, bradycardic, and sympathoinhibitory responses to electrical stimulation of aortic depressor afferents were similar in both rat groups. By contrast, efferent parasympathetic mediation was probably reduced, since depressor and bradycardic responses to electrical stimulation of vagal nerve efferents were significantly smaller in obese than in control rats. Collectively our findings suggest that cardiovascular and baroreflex malfunction in obese rats may result from an autonomic imbalance involving diminished parasympathetic activity.
Buñag
R D
RD
Department of Pharmacology, College of Health Sciences and Hospital, University of Kansas Medical Center, Kansas City 66103.
Krizsan
D
D
Itoh
H
H
D000758:Anesthesia; D000818:Animals; D002319:Cardiovascular System / Q000503:physiopathology*; D004558:Electric Stimulation; D006339:Heart Rate; D006973:Hypertension / Q000209:etiology; D007328:Insulin / Q000097:blood; D008297:Male; D009765:Obesity / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex; D014630:Vagus Nerve / Q000503:physiopathology*
D007328:Insulin