title: Rats selectively bred for differences in aerobic capacity have similar hypertensive responses to chronic intermittent hypoxia.
abstract: Exposure to chronic intermittent hypoxia (CIH) is an animal model that mimics the repetitive bouts of hypoxemia experienced by humans with sleep apnea. Rats exposed to CIH develop hypertension that depends on the activation of sympathetic nerve activity (SNA). Since obesity and metabolic syndrome have been linked to neurogenic hypertension and sleep apnea, and because sleep apnea can adversely affect aerobic exercise capacity, we tested the hypothesis that rats bred for selection of low aerobic capacity running (LCR) would have a greater hypertensive response to CIH than rats bred for high aerobic capacity running (HCR). Blockade of ganglionic transmission was performed to compare the contribution of SNA to the maintenance of resting mean arterial pressure (MAP). Next, hypertensive responses to 7 days of CIH were compared across LCR and HCR rats (14-16 mo old). Finally, the contribution of the hypothalamic paraventricular nucleus (PVN) to the maintenance of SNA and hypertension after CIH was determined and compared across groups. Although LCR rats were less active and had greater body weights than HCR rats, resting MAP, the contribution of ongoing SNA to the maintenance of MAP, and hypertensive responses to CIH were similar between groups. Contrary to our hypothesis, chemical inhibition of the PVN with muscimol (1 mmol/100 nl) caused a larger fall of MAP in HCR rats than in LCR rats. We conclude that LCR rats do not have resting hypertension or an exaggerated hypertensive response to CIH. Interestingly, the maintenance of CIH hypertension in LCR rats compared with HCR rats appears less reliant on ongoing PVN neuronal activity.
authors.affiliation: Department of Pharmaceutical Sciences, Feik School of Pharmacy, University of the Incarnate Word, San Antonio, TX 78209, USA. sharpe@uiwtx.edu
authors.forename: Amanda L
authors.initials: AL
authors.lastname: Sharpe
authors.forename: Mary Ann
authors.initials: MA
authors.lastname: Andrade
authors.forename: Myrna
authors.initials: M
authors.lastname: Herrera-Rosales
authors.forename: Steven L
authors.initials: SL
authors.lastname: Britton
authors.forename: Lauren G
authors.initials: LG
authors.lastname: Koch
authors.forename: Glenn M
authors.initials: GM
authors.lastname: Toney
mesh_terms: D000818:Animals; D062186:Arterial Pressure / Q000187:drug effects / Q000235:genetics; D001835:Body Weight; D002908:Chronic Disease; D004195:Disease Models, Animal; D017079:Exercise Tolerance / Q000235:genetics; D058785:GABA-A Receptor Agonists / Q000494:pharmacology; D005730:Ganglionic Blockers / Q000494:pharmacology; D005838:Genotype; D006339:Heart Rate; D006973:Hypertension / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology; D000860:Hypoxia / Q000150:complications* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D009043:Motor Activity; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000503:physiopathology; D010641:Phenotype; D051381:Rats; D011919:Rats, Inbred Strains; D013045:Species Specificity; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology; D013997:Time Factors
chemical_list: D058785:GABA-A Receptor Agonists; D005730:Ganglionic Blockers
keywords: metabolic syndrome; obesity; paraventricular nucleus; sympathetic nerve activity