抄録
BACKGROUND: It has been proposed that atrial natriuretic peptide (ANP), which promotes renal NaCl excretion, is secreted when the heart dilates. However, it is not easy to determine whether this occurs with land animals, without measuring [Na+]o. The present work, therefore, has been carried out to examine the relation between [Na+]o and the cardiac function before stepping into the study of regulation of ANP secretion by [Na+]o. METHODS: Two types of preparations were subjected to experiments, 1) cultured cardiac myocytes obtained from fetal or new-born mice (to exclude effect of cardiac stretch), and 2) adult mouse whole-heart. Intracellular [Na+] or [Ca2+] of myocytes in culture was monitored with an image analyzer, and myocardial contraction with a video camera or a strain gauge. RESULTS & DISCUSSION: When [Na+]o was increased from a normal concentration (140 mM) to 165 or 190 mM, [Na+]i was raised and followed by an increase in [Ca2+]i. Concomitantly, myocardial contractility was decreased and arrhythmias were induced. Similar phenomena were observed when the myocardial tissue was exposed to an inhibitor of mitochondrial function (10 μM CCCP). These effects were mimicked by applying a Na+ ionophore (10 μM monensin) but not by increasing osmolarity of the solution with mannitol. The results indicate that myocardial function is perturbed by changing [Na+]o, and a possible target of increased Na+ is mitochondria. Such effect may be sufficient to lead to an alteration in the ANP secretion. [J Physiol Sci. 2008;58 Suppl:S175]
