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It is well known that the secretion of atrial natriuretic peptide (ANP) is dependent on the atrial stretch. It has been claimed in this laboratory that the secretion of ANP occurs with a reduction in atrial distension. It was shown in the present experiment that the secretion of immunoreactive (ir) ANP occurs coincidently with a translocation of extracellular space marker (3-H)-inulin in the isolated perfused rabbit atria. Translocation of extracellular space fluid was observed with a reduction in atrial distension. The secretion of irANP into the atrial lumen occurs less than 15 sec of the reduction in atrial distension. It is therefore suggested that the incremental response of irANP secretion to the reduction in atrial distension is a sequential mechanism of ANP secretion, in which first is the release of ANP from the atrial myocytes into the extracellular space and then second is the translocation of ANP with extracellular space fluid into the atrial lumen with a reduction in atrial distension.

An easy and convenient isolated atrial perfusion technique was developed. The effect of stretch of the atrial subpericardial myocytes was investigated in the inside-out perfused rabbit atria. Graded distension of the inverted atria was induced by changing the elevation of the atrial catheter tip. Intra-luminal volume expansion resulted in an increase in release of immunoreactive atrial natriuretic peptides (irANPs). The response was volume, or pressure dependent. Distension-induced release of irANPs occurred at the reduction of the distension. IrANPs in epicardial perfusate showed both high and low molecular weights. The major peak of irANP was observed at the corresponding fraction to the rat ANP-(1-28) in the Sephadex G-50 gel chromatography. The data suggest that the epicardial release of irANP is stretch-induced response and that the release may be involved in the regulation of cardiac function.