Hypoxia exposure and B‐type natriuretic peptide release from Langendorff heart of rats

Aim We studied whether available oxygen without induced mechanical stretch regulates the release of the biologically active B‐type natriuretic peptide (BNP) from Langendorff heart. Methods Rat hearts were isolated and perfused with a physiological Krebs–Henseleit solution at a constant hydrostatic pressure in Langendorff set‐up. The basal O2level of perfusate (24.4 ± 0.04 mg L−1) was gradually lowered to 3.0 ± 0.01 mg L−1over 20 min using N2gas (n = 7).BNPand O2level were measured from coronary flow. During control perfusions (n = 5), the O2concentration was kept at 26.6 ± 0.3 mg L−1. Results A low oxygen concentration in the perfusate was associated with a significant increase inBNPrelease (F = 40.4,P < 0.001). Heart rate decreased when the oxygen concentration in the perfusate reached 9.1 ± 0.02 mg L−1and continued to fall in lower oxygen concentrations (F = 14.8, P < 0.001). There was also a significant but inverse correlation betweenBNPand oxygen in the coronary flow (R2 = 0.27,P < 0.001). Conclusion In the spontaneously beating Langendorff rat heart, a decreasing concentration of oxygen in the ingoing perfusion increased the secretion ofBNP. The effect of oxygen was independent of mechanical stretch of the heart as it occurred even when the heart rate decreased but the pressure conditions remained constant. The difference in the oxygen capacitance of blood and Krebs–Henseleit solution appears to be a major factor affecting secretion ofBNP, which is correlated with the oxygen tension of myocardial cells and affected both by the oxygen concentration and capacitance of solution perfusing the heart and by the coronary flow.