G. Lavilla et al., CARDIOVASCULAR AND RENAL EFFECTS OF LOW-DOSE ATRIAL-NATRIURETIC-PEPTIDE IN COMPENSATED CIRRHOSIS, The American journal of gastroenterology, 92(5), 1997, pp. 852-857
Patients with cirrhosis and ascites have high plasma levels of atrial
natriuretic peptide (ANP). Pharmacological doses of this hormone usual
ly worsen systemic hemodynamics of cirrhotic patients, We assessed whe
ther ANP influences cardiovascular homeostasis and renal function in p
atients with compensated cirrhosis at plasma levels comparable to thos
e observed in patients with cirrhosis and ascites. Methods: Radionucli
de angiocardiography was performed in eight compensated cirrhotic pati
ents during placebo (three periods of 15 min each) and ANP infusion (2
, 4, and 6 pmol/kg.min for 15 min each), together with appropriate blo
od and urine sampling, to evaluate left ventricular diastolic, systoli
c, and stroke volume, heart rate, cardiac output, arterial pressure, p
eripheral vascular resistance, creatinine clearance, urinary sodium ex
cretion, plasma renin activity, plasma aldosterone, norepinephrine and
hematocrit. Results: The infusion increased plasma ANP up to levels (
52.03 +/- 2.29 pmol/L) comparable with those observed in 35 patients w
ith ascites (46.42 +/- 1.57 pmol/ L). This increment was associated wi
th significant reductions in left ventricular end diastolic volume, st
roke volume, cardiac index (from 3.7 +/- 0.7 to 3.1 +/- 0.5 L/min.m(2)
, p < 0.85) and mean arterial pressure (from 96.7 +/- 6.5 to 88.5 +/-
9.5 mmHg, p < 0.05), while heart rate and hematocrit significantly inc
reased. Peripheral vascular resistance did not change. These hemodynam
ic effects occurred despite significant increases in plasma renin acti
vity and norepinephrine. ANP also induced increases in creatinine clea
rance, urinary sodium excretion, and fractional sodium excretion. Conc
lusions: Low-dose ANP affected cardiovascular homeostasis and renal so
dium handling in compensated cirrhosis, suggesting that this hormone m
ay be involved in the pathophysiology of systemic hemodynamic and rena
l functional abnormalities of cirrhosis.