It has recently been proposed that
endothelin-1 (ET-1) is an important activator of
natriuretic peptide [atrial natriuretic peptide (
ANP) and the
brain natriuretic peptide (BNP)] release in the heart and may mediate
ANP and BNP deliberation to myocardial stretch and
ischemia. The close inter-relationship between ET-1 and
natriuretic peptide release was indicated mainly by the results of in vitro studies. In vivo, the local alterations of
ANP and BNP levels in the myocardial interstitium can be well characterized by the changes of their pericardial fluid concentrations. The effect of the intrapericardially administered ET-1 on
natriuretic peptide concentrations was studied on the in situ dog heart (n = 8). Control and three consecutive infusate samples were removed from the pericardial sac following ET-1 administration (150 pmol/kg) and parallel peripheral blood samples were taken to determine the
ANP and BNP concentrations (
enzyme-linked
immunosorbent assay). Standard hemodynamic parameters were recorded continuously. In our results the intrapericardial ET-1 increased pericardial
ANP but not BNP concentrations significantly (control versus ANPmax, 37 +/- 5 ng/mL versus 94 +/- 12 ng/mL; P < 0.02). ET-1 elicited significant ST elevations without changes of the hemodynamic values and the
natriuretic peptide levels in the arterial plasma samples. In conclusion, intrapericardial ET-1 effectively stimulated the myocardial
ANP release, which was reflected as elevation in the pericardial
ANP level. The results also support the hypothesis that important regulatory mechanisms might be activated from the pericardium.