title: Energy metabolism in BPH/2J genetically hypertensive mice.
abstract: Recent evidence indicates that genetic hypertension in BPH/2J mice is sympathetically mediated, but these mice also have lower body weight (BW) and elevated locomotor activity compared with BPN/3J normotensive mice, suggestive of metabolic abnormalities. The aim of the present study was to determine whether hypertension in BPH/2J mice is associated with metabolic differences. Whole-body metabolic and cardiovascular parameters were measured over 24 h by indirect calorimetry and radiotelemetry respectively, in conscious young (10-13 weeks) and older (22-23 weeks) BPH/2J, normotensive BPN/3J and C57Bl6 mice. Blood pressure (BP) was greater in BPH/2J compared with both normotensive strains at both ages (P<0.01). Metabolic rate was greater in young BPH/2J compared with BPN/3J mice (P<0.01) but similar to C57Bl6 mice indicating that high metabolic rate is not necessarily related to the hypertension per say. The slope of the BP-metabolic rate relationship was comparable between BPH/2J and normotensive mice when adjusted for activity (P>0.1) suggesting differences in this relationship are not responsible for hypertension. EchoMRI revealed that percentage body composition was comparable in BPN/3J and BPH/2J mice (P>0.1) and both strains gained weight similarly with age (P=0.3). Taken together, the present findings indicate that hypertension in BPH/2J mice does not appear to be related to altered energy metabolism.
authors.affiliation: 1] Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia [2] Department of Pharmacology, Monash University, Clayton, Victoria, Australia.
authors.forename: Kristy L
authors.initials: KL
authors.lastname: Jackson
authors.affiliation: Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
authors.forename: Thu-Phuc
authors.initials: TP
authors.lastname: Nguyen-Huu
authors.affiliation: Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia.
authors.forename: Pamela J
authors.initials: PJ
authors.lastname: Davern
authors.affiliation: 1] Neuropharmacology Laboratory, Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia [2] Department of Pharmacology, Monash University, Clayton, Victoria, Australia.
authors.forename: Geoffrey A
authors.initials: GA
authors.lastname: Head
mesh_terms: D000818:Animals; D001481:Basal Metabolism / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001823:Body Composition / Q000502:physiology*; D002153:Calorimetry, Indirect; D004734:Energy Metabolism / Q000235:genetics*; D006973:Hypertension / Q000235:genetics / Q000378:metabolism*; D008297:Male; D051379:Mice; D009043:Motor Activity / Q000502:physiology*