title: Food restriction attenuates the blood pressure response to paraventricular hypothalamic nuclei lesions in aortic coarctation hypertension.
abstract: Chronic food restriction reduces blood pressure (BP) and sympathetic support of BP in aortic coarctation hypertension. The purpose of this study was to test the hypothesis that chronic food restriction would reduce sympathetic support of BP mediated by the paraventricular hypothalamic nuclei (PVN). Hypertension was induced in male Sprague-Dawley rats (n=40) by suprarenal aortic coarctation. Rats were assigned to either an ad libitum fed (AL) group or a food restricted (FR) group that received 60% of the food consumed by AL for 3 weeks. One week prior to data collection, catheters were implanted in the left carotid artery and right jugular vein. BP was measured for 2 days prior to, and 7 days after rats in AL and FR groups received either bilateral electrolytic lesions of the PVN (PVNx) or sham lesions (SHAM). Prior to either PVNx or SHAM, FR rats had significantly lower BP (AL=152+/-5; FR=113+/-2 mmHg), less of a depressor response to ganglionic blockade (AL=-58+/-4; FR=-35+/-2 mmHg), and lower plasma norepinephrine levels (AL=758+/-71; FR=380+/-23 pg/ml) compared to AL. PVNx reduced BP in both AL and FR rats (AL-PVNx=105+/-6 mmHg, FR-PVNx=101+/-3 mmHg). PVNx also lowered the depressor response to ganglionic blockade (AL-PVNx=-28+/-5 mmHg, FR-PVNx=-29+/-4 mmHg) and plasma norepinephrine levels (AL-PVNx=372+/-74 pg/ml, FR-PVNx=248+/-31 pg/ml). FR decreased the magnitude of the reductions in resting BP and in sympathetic activity in response to PVNx. These results indicate that intact PVN are required for maintenance of aortic coarctation hypertension, and implicate the PVN as a site involved in BP reductions produced by chronic food restriction.
authors.affiliation: Department of Nutrition, Food and Movement Sciences, and the Program in Neuroscience, Florida State University, Tallahassee, FL 32306-4340, USA.
authors.forename: J M
authors.initials: JM
authors.lastname: VanNess
authors.forename: R M
authors.initials: RM
authors.lastname: Casto
authors.forename: J E
authors.initials: JE
authors.lastname: DeMaria
authors.forename: J M
authors.initials: JM
authors.lastname: Overton
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D001017:Aortic Coarctation / Q000503:physiopathology*; D001285:Atropine / Q000494:pharmacology; D001786:Blood Glucose; D001794:Blood Pressure / Q000502:physiology*; D001835:Body Weight / Q000502:physiology; D002149:Energy Intake; D005508:Food Deprivation / Q000502:physiology; D005730:Ganglionic Blockers / Q000494:pharmacology; D018738:Hexamethonium / Q000494:pharmacology; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000097:blood; D010276:Parasympatholytics / Q000494:pharmacology; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology* / Q000601:surgery; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000502:physiology*
chemical_list: D000316:Adrenergic alpha-Agonists; D001786:Blood Glucose; D005730:Ganglionic Blockers; D010276:Parasympatholytics; D010656:Phenylephrine; D018738:Hexamethonium; D001285:Atropine; D009638:Norepinephrine