ANP PROTECTS AGAINST REOXYGENATION-INDUCED HYPERCONTRACTURE IN ADULT CARDIOMYOCYTES

It was investigated whether atrial natriuretic peptide (ANP) or the re lated peptide urodilatin can be used for protecting cardiomyocytes aga inst reoxygenation-induced hypercontracture. Isolated ventricular card iomyocytes (from adult rats) were used as the experimental model. When the cells were submitted to substrate-free anoxia (185 min) and subse quent reoxygenation (30 min), the onset of reoxygenation provoked thei r hypercontracture. It was studied whether the temporary presence of A NP or urodilatin (I nM to I mu M) or 8-bromo-guanosine 3',5'-cyclic mo nophosphate (8-BrcGMP; 1 mu M to 1 mM) during the last 15 min of anoxi a and the first 15 min of reoxygenation prevented hypercontracture. It was found that ANP (1 mu M) prevented hypercontracture in 82 +/- 8% ( SD), urodilatin (1 mu M) in 80 +/- 9%, and 8-BrcGMP (1 mM) in 72 +/- 1 0% of the cells (n = 40 cells). When ANP (1 mu M) was added during the last 15 min of anoxia and the first 15 min of reoxygenation, the cell ular concentration of cGMP increased from 0.41 +/- 0.04 to 2.80 +/- 0. 81 pmol/mg protein (n = 6 cultures). The results show that the reoxyge nation-induced hypercontracture in cardiomyocytes can be attenuated by the temporary presence of the stimulators of particulate guanylate cy clase, ANP or urodilatin.