Es. Piedrasrenteria et al., EFFECTS OF RELAXIN ON RAT ATRIAL MYOCYTES .1. INHIBITION OF I-TO VIA PKA-DEPENDENT PHOSPHORYLATION, American journal of physiology. Heart and circulatory physiology, 41(4), 1997, pp. 1791-1797
The peptide hormone relaxin has direct, positive inotropic and chronot
ropic effects on rat hearts in vivo and in vitro. Relaxin's effects on
the electrophysiological properties of single quiescent atrial cells
from normal rats were investigated with a whole cell patch clamp. Rela
xin had a significant inhibitory effect on outward potassium currents.
The outward potassium current consisted of a transient component (I-t
o) and a sustained component (I-S). The addition of 100 ng/ml of relax
in inhibited the peak I-to in a voltage-dependent manner (74% inhibiti
on at a membrane potential of -10 mV to 30% inhibition at +70 mV). The
time to reach peak I-to and the apparent time constant of inactivatio
n of I-to were increased by relaxin. Dialysis with the protein kinase
A inhibitor 5-24 amide (2 mu M) prevented relaxin's effects, suggestin
g an obligatory role for this kinase in the relaxin-dependent regulati
on of the potassium current.