title: Chronic stress improves the myocardial function without altering L-type Ca+2 channel activity in rats.
abstract: BACKGROUND
  Chronic stress is associated with cardiac remodeling; however the mechanisms have yet to be clarified.
  
  
  OBJECTIVE
  The purpose of this study was test the hypothesis that chronic stress promotes cardiac dysfunction associated to L-type calcium Ca2+ channel activity depression.
  
  
  METHODS
  Thirty-day-old male Wistar rats (70 - 100 g) were distributed into two groups: control (C) and chronic stress (St). The stress was consistently maintained at immobilization during 15 weeks, 5 times per week, 1h per day. The cardiac function was evaluated by left ventricular performance through echocardiography and by ventricular isolated papillary muscle. The myocardial papillary muscle activity was assessed at baseline conditions and with inotropic maneuvers such as: post-rest contraction and increases in extracellular Ca2+ concentration, in presence or absence of specific blockers L-type calcium channels.
  
  
  RESULTS
  The stress was characterized for adrenal glands hypertrophy, increase of systemic corticosterone level and arterial hypertension. The chronic stress provided left ventricular hypertrophy. The left ventricular and baseline myocardial function did not change with chronic stress. However, it improved the response of the papillary muscle in relation to positive inotropic stimulation. This function improvement was not associated with the L-type Ca2+ channel.
  
  
  CONCLUSIONS
  Chronic stress produced cardiac hypertrophy; however, in the study of papillary muscle, the positive inotropic maneuvers potentiated cardiac function in stressed rats, without involvement of L-type Ca2+ channel. Thus, the responsible mechanisms remain unclear with respect to Ca2+ influx alterations.
authors.affiliation: Department de Pharmacology, Institute of Bioscience, São Paulo State University (UNESP), Brazil. bruderthiago@usp.br
authors.forename: Thiago
authors.initials: T
authors.lastname: Bruder-Nascimento
authors.forename: Dijon Henrique Salome
authors.initials: DH
authors.lastname: Campos
authors.forename: André Soares
authors.initials: AS
authors.lastname: Leopoldo
authors.forename: Ana Paula
authors.initials: AP
authors.lastname: Lima-Leopoldo
authors.forename: Katashi
authors.initials: K
authors.lastname: Okoshi
authors.forename: Sandra
authors.initials: S
authors.lastname: Cordellini
authors.forename: Antônio Carlos
authors.initials: AC
authors.lastname: Cicogna
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D020746:Calcium Channels, L-Type / Q000502:physiology*; D002318:Cardiovascular Diseases / Q000503:physiopathology* / Q000523:psychology; D002908:Chronic Disease; D003345:Corticosterone / Q000097:blood; D004452:Echocardiography; D006321:Heart / Q000502:physiology*; D006973:Hypertension / Q000209:etiology; D008297:Male; D023421:Models, Animal; D051381:Rats; D017208:Rats, Wistar; D013315:Stress, Psychological / Q000150:complications / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D020746:Calcium Channels, L-Type; D003345:Corticosterone