Atp-sensitive potassium channels regulate stimulated anf secretion
in isolated rat heart.
Xu, Tie, Jin-Hua Jiao, Richard A. Pence, and Alex J. Baertschi.
Department of Molecular Physiology and Biological Physics,
University of Virginia Health Sciences Center, Charlottesville,
Virginia 22908
APStracts 3:0302H, 1996.
Perfused hearts (n=127) were exposed to acute hypoxia (10%O2, 12 or
20min) or left atrial stretch (increase in atrial pressure) in the
presence/absence of 100 [mu]moles/L KATP-channel blocker
(tolbutamide) or openers (pinacidil, diazoxide). Hypoxia alone
elicited a prolonged ANF release peaking at 74% over baseline
(P<0.01); with tolbutamide, ANF secretion peaked at 132% over
baseline (P<0.01). Both pinacidil or diazoxide abolished the ANF
response to hypoxia (P<0.01). Atrial stretch alone (1mm Hg)
transiently (2min) increased ANF by 56% (P<0.05); with
tolbutamide, ANF increased transiently by 124% and showed a prolonged
increase of 52% (P<0.05). With tolbutamide, graded stretch
(0.52.3 mmHg) induced a bell-shaped transient (2 min) increase of ANF
release [-3% at 0.5 mmHg, 124% (P<0.05) at 1.0 mmHg, 80%
(P<0.05) at 1.48 mmHg and 14% at 2.22 mmHg], and a saturating
prolonged ANF response. Lower doses (30 [mu]moles/L) of tolbutamide
increased the ANF response non-significantly, and had no effect at 1
[mu]moles/L. Pinacidil abolished the stretch-induced ANF release.
These results suggest that KATP-channels are extremely potent
modulators of stimulated ANF secretion.
Received 6 February 1996; accepted in final form 18 June 1996.
APS Manuscript Number H113-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996