Natriuretic peptides maintain sodium homoeostasis during chronic volume loading post-myocardial infarction in sheep

The impaired ability to excrete sodium is a key feature of established congestive heart failure and is also apparent in asymptomatic left ventricular (LV) impairment. However, few studies have examined responses to chronic volume loading immediately post-myocardial infarction (MI). Experimental MI was induced in six sheep by thrombogenic coil coronary artery occlusion, and resulted in significant LV dysfunction with reduced LV ejection fraction (P = 0.001) and subsequent remodelling (increased LV volumes, P = 0.015). Chronic volume loading with 2, 3 and 4litres/day intravenous saline (each for 7 days) showed no evidence of renal sodium or volume retention in sheep with experimental MI compared with six normal control sheep. Plasma levels of brain natriuretic peptide (BNP), N-terminal pro-BNP and cGMP (all P<0.05) were higher in the MI group compared with normal control sheep. There were no differences in haemodynamics, body mass or renin–aldosterone levels between groups. This study provides evidence that natriuretic peptides play a pivotal role in preserving volume/electrolyte balance in the early stages of post-MI cardiac dysfunction.