L-Arginine ameliorates effects of ischemia and reperfusion in isolated
cardiac myocytes.
Eur J Pharmacol, 476 (1-2):
45--54 (August 2003)Abstract
We determined effects of the nitric oxide (NO) precursor L-arginine,
on isolated guinea pig ventricular myocytes under normoxic conditions
and simulated ischemia and reperfusion. Currents and contractions
were recorded with voltage clamp and a video edge detector, respectively.
In normoxia, L-arginine (50-200 microM) had little effect on Ca2+
current, but significantly decreased contraction. Ischemia in the
absence of L-arginine reduced Ca2+ current and abolished contractions.
In reperfusion, the arrhythmogenic transient inward current was induced
and cells exhibited sustained contractile depression (stunning).
With L-arginine (100 microM) in ischemia, Ca2+ current did not decline
and recovery of contraction was potentiated in reperfusion. L-Arginine
had no effect on transient inward current. Inhibition of nitric oxide
synthase reversed effects of L-arginine on contractions but not Ca2+
current. Thus, NO contributes to beneficial effects of L-arginine
in reperfusion, although effects on I(Ca-L) are independent of NO.
Further, L-arginine effects differ under normoxic and ischemic conditions.
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