title: Ouabain-induced hypertension enhances left ventricular contractility in rats.
abstract: Chronic ouabain treatment produces hypertension acting on the central nervous system and at vascular levels. However, cardiac effects in this model of hypertension are still poorly understood. Hence, the effects of hypertension induced by chronic ouabain administration ( approximately 8 microg day(-1), s.c.) for 5 weeks on the cardiac function were studied in Wistar rats. Ouabain induces hypertension but not myocardial hypertrophy. Awake ouabain-treated rats present an increment of the left ventricular systolic pressure and of the maximum positive and negative dP/dt. Isolated papillary muscles from ouabain-treated rats present an increment in isometric force, and this effect was present even when inotropic interventions (external Ca(2+) increment and increased heart rate) were performed. However, the sarcoplasmic reticulum activity and the SERCA-2 protein expression did not change. On the other hand, the activity of myosin ATPase increased without changes in myosin heavy chain protein expression. In addition, the expression of alpha(1) and alpha(2) isoforms of Na(+), K(+)-ATPase also increased in the left ventricle from ouabain-hypertensive rats. The present results showed positive inotropic and lusitropic effects in hearts from awake ouabain-treated rats, which are associated with an increment of the isometric force development and of the activity of myosin ATPase and expression of catalytic subunits of the Na(+), K(+)-ATPase.
authors.affiliation: Department of Physiological and Biophysical Sciences, ICB, University of Sao Paulo, Sao Paulo, SP, Brazil. lrossoni@icb.usp.br <lrossoni@icb.usp.br>
authors.forename: Luciana V
authors.initials: LV
authors.lastname: Rossoni
authors.forename: Fabiano E
authors.initials: FE
authors.lastname: Xavier
authors.forename: Cleci M
authors.initials: CM
authors.lastname: Moreira
authors.forename: Diego
authors.initials: D
authors.lastname: Falcochio
authors.forename: Angélica M
authors.initials: AM
authors.lastname: Amanso
authors.forename: Carolina U
authors.initials: CU
authors.lastname: Tanoue
authors.forename: Carla R O
authors.initials: CR
authors.lastname: Carvalho
authors.forename: Dalton V
authors.initials: DV
authors.lastname: Vassallo
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D002316:Cardiotonic Agents / Q000633:toxicity*; D006352:Heart Ventricles / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced* / Q000201:enzymology; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects*; D018995:Myosin Heavy Chains / Q000378:metabolism; D009218:Myosins / Q000378:metabolism; D010042:Ouabain / Q000633:toxicity*; D010210:Papillary Muscles / Q000187:drug effects / Q000502:physiology; D020033:Protein Isoforms / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012519:Sarcoplasmic Reticulum / Q000201:enzymology; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D016276:Ventricular Function; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D002316:Cardiotonic Agents; D020033:Protein Isoforms; D010042:Ouabain; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D018995:Myosin Heavy Chains; D009218:Myosins; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase