Source:http://linkedlifedata.com/resource/pubmed/id/16339825
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2006-4-10
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pubmed:abstractText |
The autocrine modulation of cardiac K(+) currents was compared in ventricular and atrial cells (V and A cells, respectively) from Type 1 diabetic rats. K(+) currents were measured by using whole cell voltage clamp. ANG II was measured by ELISA and immunofluorescent labeling. Oxidative stress was assessed by immunofluorescent labeling with dihydroethidium, a measure of superoxide ions. In V cells, K(+) currents are attenuated after activation of the renin-angiotensin system (RAS) and the resulting ANG II-mediated oxidative stress. In striking contrast, these currents are not attenuated in A cells. Inhibition of the angiotensin-converting enzyme (ACE) also has no effect, in contrast to current augmentation in V cells. ANG II levels are enhanced in V, but not in A, cells. However, the high basal ANG II levels in A cells suggest that in these cells, ANG II-mediated pathways are suppressed, rather than ANG II formation. Concordantly, superoxide ion levels are lower in diabetic A than in V cells. Several findings indicate that high atrial natriuretic peptide (ANP) levels in A cells inhibit RAS activation. In male diabetic V cells, in vitro ANP (300 nM-1 muM, >5 h) decreases oxidative stress and augments K(+) currents, but not when excess ANG II is present. ANP has no effect on ventricular K(+) currents when the RAS is not activated, as in control males, in diabetic males treated with ACE inhibitor and in diabetic females. In conclusion, the modulation of K(+) currents and oxidative stress is significantly different in A and V cells in diabetic rat hearts. The evidence suggests that this is largely due to inhibition of RAS activation and/or action by ANP in A cells. These results may underlie chamber-specific arrhythmogenic mechanisms.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
290
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1879-88
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16339825-Animals,
pubmed-meshheading:16339825-Autocrine Communication,
pubmed-meshheading:16339825-Cells, Cultured,
pubmed-meshheading:16339825-Diabetes Mellitus, Experimental,
pubmed-meshheading:16339825-Heart Atria,
pubmed-meshheading:16339825-Heart Ventricles,
pubmed-meshheading:16339825-Ion Channel Gating,
pubmed-meshheading:16339825-Male,
pubmed-meshheading:16339825-Membrane Potentials,
pubmed-meshheading:16339825-Myocytes, Cardiac,
pubmed-meshheading:16339825-Oxidative Stress,
pubmed-meshheading:16339825-Potassium,
pubmed-meshheading:16339825-Potassium Channels,
pubmed-meshheading:16339825-Rats,
pubmed-meshheading:16339825-Rats, Sprague-Dawley,
pubmed-meshheading:16339825-Renin-Angiotensin System,
pubmed-meshheading:16339825-Streptozocin
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pubmed:year |
2006
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pubmed:articleTitle |
Differential autocrine modulation of atrial and ventricular potassium currents and of oxidative stress in diabetic rats.
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pubmed:affiliation |
Department of Physiology and Biophysics, Health Sciences Centre, University of Calgary, Alberta, Canada T2N 4N1. shimoni@ucalgary.ca
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pubmed:publicationType |
Journal Article,
Comparative Study
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