The antiarrhythmic agent lidocaine reduces inward sodium current and i
ncreases outward potassium current. Described studies investigated the
effect of lidocaine on circulating and urinary levels of atrial natri
uretic peptides in an intact canine model. Surface electrocardiography
was monitored along with right ventricular, left ventricular and aort
ic pressures, and cardiac output. Plasma and urine atrial natriuretic
peptides were measured immediately before and five minutes after a fiv
e minute, 2 mg/min, intravenous lidocaine infusion. Long acting natriu
retic peptide (LANP), vessel dilator, and atrial natriuretic factor (A
NF) were monitored by RIA. There were no measured hemodynamic or cardi
omechanical changes noted after lidocaine infusion. Similarly, there w
as no change in plasma sodium or potassium, or urine sodium. There was
, however, an increase in urine potassium levels. Additionally, plasma
and urine LANP and ANF peptide levels were increased following lidoca
ine infusion, while plasma and urine concentrations of vessel dilator
were not changed. These data suggest that lidocaine increases plasma a
nd urine atrial natriuretic peptides by mechanisms other than cardiode
pression and/or vasodilatation.