title: Changes in hemodynamic and neurohumoral control cause cardiac damage in one-kidney, one-clip hypertensive mice.
abstract: Sympathovagal balance and baroreflex control of heart rate (HR) were evaluated during the development (1 and 4 wk) of one-kidney, one-clip (1K1C) hypertension in conscious mice. The development of cardiac hypertrophy and fibrosis was also examined. Overall variability of systolic arterial pressure (AP) and HR in the time domain and baroreflex sensitivity were calculated from basal recordings. Methyl atropine and propranolol allowed the evaluation of the sympathovagal balance to the heart and the intrinsic HR. Staining of renal ANG II in the kidney and plasma renin activity (PRA) were also evaluated. One and four weeks after clipping, the mice were hypertensive and tachycardic, and they exhibited elevated sympathetic and reduced vagal tone. The intrinsic HR was elevated only 1 wk after clipping. Systolic AP variability was elevated, while HR variability and baroreflex sensitivity were reduced 1 and 4 wk after clipping. Renal ANG II staining and PRA were elevated only 1 wk after clipping. Concentric cardiac hypertrophy was observed at 1 and 4 wk, while cardiac fibrosis was observed only at 4 wk after clipping. In conclusion, these data further support previous findings in the literature and provide new features of neurohumoral changes during the development of 1K1C hypertension in mice. In addition, the 1K1C hypertensive model in mice can be an important tool for studies evaluating the role of specific genes relating to dependent and nondependent ANG II hypertension in transgenic mice.
authors.affiliation: Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Av. Bandeirantes, 3900, 14049-900 - Ribeirão Preto, SP, Brazil.
authors.forename: Giulianna R
authors.initials: GR
authors.lastname: Borges
authors.forename: Helio C
authors.initials: HC
authors.lastname: Salgado
authors.forename: Carlos Alberto A
authors.initials: CA
authors.lastname: Silva
authors.forename: Marcos A
authors.initials: MA
authors.lastname: Rossi
authors.forename: Cibele M
authors.initials: CM
authors.lastname: Prado
authors.forename: Rubens
authors.initials: R
authors.lastname: Fazan
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D003250:Constriction; D004195:Disease Models, Animal; D005355:Fibrosis; D006339:Heart Rate; D006439:Hemodynamics / Q000187:drug effects; D006978:Hypertension, Renovascular / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D007672:Kidney Cortex / Q000378:metabolism; D008297:Male; D051379:Mice; D018727:Muscarinic Antagonists / Q000494:pharmacology; D012077:Renal Artery / Q000601:surgery; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D013997:Time Factors; D014630:Vagus Nerve / Q000187:drug effects / Q000503:physiopathology*
chemical_list: D000319:Adrenergic beta-Antagonists; D018727:Muscarinic Antagonists; D000804:Angiotensin II; D012083:Renin