atrial-natriuretic-factor and nickel-chloride

1. Isolated superfused rat atrial preparations were used to study the mechanism of stretch-induced atrial natriuretic peptide (ANP) secretion. The stretch of the atrial myocytes was induced by raising the intra-atrial pressure. The secretion rates were analysed by measuring ANP concentrations from the superfusate fractions by radioimmunoassay. 2. The effect of gadolinium, a blocker of stretch-activated ion channels, on stretch-induced and basal ANP secretion was investigated by superfusing the atrial preparation with 5, 20 or 80 microM GdCl3. Gadolinium decreased stretch-induced ANP secretion in a dose-dependent manner, but did not affect basal secretion. 3. Because high concentrations of gadolinium may block voltage-gated calcium channels, we tested whether the selective blockers of L-type (diltiazem) and T-type (NiCl2) calcium channels affect the stretch-stimulated ANP release. Neither diltiazem at 3 microM nor NiCl2 at 50 microM affected stretch-induced ANP release in paced atrial preparation. 4. Gadolinium, but not diltiazem, also inhibited stretch-stimulated ANP secretion in non-paced, quiescent atria. 5. The findings that ANP release is inhibited by Gd3+, but not by diltiazem or NiCl2, and that the stretch-induced secretion in quiescent atria is also inhibited by Gd3+, suggest that stretch-activated ion channels are involved in the regulation of stretch-induced ANP release.

Topics: Animals; Atrial Natriuretic Factor; Cardiac Pacing, Artificial; Diltiazem; Gadolinium; Heart Atria; In Vitro Techniques; Male; Myocardial Contraction; Myocardium; Nickel; Rats; Rats, Sprague-Dawley