P170Peripheral and coronary vasodilator response in chronic weary heart

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Aim: in vitro evaluation of the isolated aorta rings and coronary reactivity of isovolimic heart in fluorine induced on rat heart defeat (FHD).

Material and methods: The control and FHD (water with NaF 0,3% during 7 weeks,) isolated aorta rings and isovolumic heart were perfused by Krebs solution. The phenylephrine induced aorta constrictor plateau relaxation ratio has been assayed on acetylcholine (Ach) or Ang 1-7 action (10-8-10-6 M). Coronary functional reserve was determined upon action of Ach, Ang 1-7, bradykinin (Br), adenosine (Ad), hydrogen peroxide (H2O2) or sildenafil (Sd) in concentration range of 10-7-10-4 M. Also Ang II constrictor effect was estimated in association with Ang 1-7 or A779 (mas receptor antagonist) administration.

Results: Ach induced aorta relaxation was in FHD significantly lower by 19-26%. However Ang 1-7 action led to a similar to control aorta relaxation in all concentrations. Remarkably, increased Ang II induced aorta constriction in FHD was blunted by Ang 1-7 premedication or augmented by A779 premedication in analogous to control values. Endothelium dependent coronary flow rise was significantly lesser in FHD during Ach, Br or Ad action by 13-24%. Importantly to note that Ang 1-7, H2O2 or Sd didn't shift coronary reserve in FHD comparably to control pattern. More than that H2O2 and Sd induced even a higher coronary flow elevation rate in concentration of 10-4 M by 4,7-6,7%. Heart perfusion with A799 more conspicuously boosted Ang II induced coronary constriction, and Ang 1-7 more evidently limited coronary flow fall in FHD.

Conclusions: (1) The endothelium dependent peripheral vascular and coronary dilation in FHD is compromised, but Ang 1-7 vasorelaxing action mediated by mas receptor is not altered. (2) The mas receptor inhibition or activation more conspicuously modified Ang II action in coronaries of FHD vs control suggesting compensatory role of mas receptor in coronary reserve regulation. (3) Phosphodiesterase-5 expression and mechanism of hyperpolarization appear as benefic tools of coronary dilation in FHD associated with endothelium dysfunction.

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