In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 293, No. 6 ( 2007-12), p. H3643-H3649
Abstract:
ATP-sensitive K + (K ATP ) channels are essential for maintaining the cellular homeostasis against metabolic stress. Myocardial remodeling in various pathologies may alter this adaptive response to such stress. It was reported that transmural electrophysiological heterogeneity exists in ventricular myocardium. Therefore, we hypothesized that the K ATP channel properties might be altered in hypertrophied myocytes from endocardium. To test this hypothesis, we determined the K ATP channel currents using the perforated patch-clamp technique, open cell-attached patches, and excised inside-out patches in both endocardial and epicardial myocytes isolated from hypertrophied [spontaneous hypertensive rats (SHR)] vs. normal [Wistar-Kyoto rats (WKY)] left ventricle. In endocardial cells, K ATP channel currents ( I K,ATP ), produced by 2 mM CN − and no glucose at 0 mV, were significantly smaller ( P 〈 0.01), and time required to reach peak currents after onset of K ATP channel opening (Time onset to peak ) was significantly longer (319 ± 46 vs. 177 ± 37 s, P = 0.01) in the SHR group ( n = 9) than the WKY group ( n = 13). However, in epicardial cells, there were no differences in I K,ATP and Time onset to peak between the groups (SHR, n = 12; WKY, n = 12). The concentration-open probability-response curves obtained during the exposure of open cells and excised patches to exogenous ATP revealed the impaired K ATP channel activation in endocardial myocytes from SHR. In conclusion, K ATP channel activation under metabolic stress was impaired in endocardial cells from rat hypertrophied left ventricle. The deficit of endocardial K ATP channels to decreased intracellular ATP might contribute to the maladaptive response of hypertrophied hearts to ischemia.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.01357.2006
Language:
English
Publisher:
American Physiological Society
Publication Date:
2007
detail.hit.zdb_id:
1477308-9
SSG:
12
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