Es. Piedrasrenteria et al., EFFECTS OF RELAXIN ON RAT ATRIAL MYOCYTES .2. INCREASED CALCIUM INFLUX DERIVED FROM ACTION-POTENTIAL PROLONGATION, American journal of physiology. Heart and circulatory physiology, 41(4), 1997, pp. 1798-1803
Relaxin produces positive inotropic and chronotropic effects in rat he
arts. The effect of relaxin on the action potential duration (APD) of
single quiescent rat atrial cells was investigated with a whole cell p
atch clamp. Relaxin induced a significant, dose-dependent prolongation
of the APD. This effect was maximal at 200 ng/ml (nominal concentrati
on of 33.6 nM), which caused, on average, a 57% increase in the time t
aken to reach 90% repolarization. The effect of relaxin was blocked by
the protein kinase A inhibitor 5-24 amide, indicating that its effect
is mediated by an adenosine 3',5'-cyclic monophosphate-dependent mech
anism. The increased APD induced by relaxin caused an enhanced entranc
e of calcium, with the charge carried through voltage-activated calciu
m channels increased by similar to 25%. This increase was not due to a
direct modulation of calcium currents (20); rather, it was a conseque
nce of the longer period of cellular depolarization. Our findings that
relaxin increased the APD and therefore increased the calcium influx
in atrial myocytes could explain the positive inotropic effects induce
d by relaxin in atrial preparations.