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1 Department of Physiology, Faculty of Medicine, University of Porto, Porto, Portugal
* To whom correspondence should be addressed. E-mail: amoreira{at}med.up.pt.
ET-1 acts on ETA and ETB receptors. The later include ETB1 (endothelial) and ETB2 (muscular) subtypes, which mediate opposite effects on vascular tone. This study investigated, in rabbit papillary muscles (n=84), the myocardial effects of ETB stimulation. ET-1 (10-9 M) was given in absence or presence of BQ-123 (ETA antagonist). Effects of IRL- 1620 (ETB1 agonist, 10-10-10-6M) or Sarafotoxin-S6c (ETB agonist, 10-10-10-6M) were evaluated in muscles with: intact or damaged endocardial endothelium (EE); intact EE, in presence of NG-Nitro-L-Arginine (L-NA); and intact EE, in presence of Indomethacin (INDO). Sarafotoxin-S6c effects were also studied in presence of BQ-788 (ETB2 antagonist). ET-1 alone increased 64±18% active tension (AT), but decreased it by 4±2% in presence of BQ-123. In muscles with intact EE, Sarafotoxin-S6c alone did not significantly alter myocardial performance. Sarafotoxin-S6c (10-6M) increased, however, AT by 120± 27%, when EE was damaged, and by 39±8% or 23±6%, in presence of L-NA or INDO, respectively. In presence of BQ-788, Sarafotoxin-S6c decreased AT (21±3% at 10-6M) in muscles with intact EE, effect that was abolished when EE was damaged. IRL-1620 also decreased AT (22±3% at 10-6M) in muscles with intact EE, effect that was abolished when EE was damaged or in presence of L-NA or INDO. In conclusion, ETB-mediated negative inotropic effect is presumably due to ETB1 stimulation, requires an intact EE and is mediated by NO and prostaglandins; while, ETB mediated positive inotropic effect, observed when EE was damaged, or NO and prostaglandins synthesis inhibited is presumably due to ETB2 stimulation.
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