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Block of stretch‐activated atrial natriuretic peptide secretion by gadolinium in isolated rat atrium.
Author(s) -
Laine M,
Arjamaa O,
Vuolteenaho O,
Ruskoaho H,
Weckström M
Publication year - 1994
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1994.sp020383
Subject(s) - atrial natriuretic peptide , medicine , secretion , gadolinium , endocrinology , diltiazem , chemistry , atrium (architecture) , calcium , atrial fibrillation , organic chemistry
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.