While resting mammalian ventricular myocardium does not usually exhibit pacemaker like activity, under certain conditions spontaneous localized release of Ca2+ from sarcoplasmic reticulum (SR) results in an increase in myoplasmic (Ca2+) (Cai) which cause miniature inward currents resulting in oscillations of membrane potential. At the normal resting membrane potential in cardiac myocytes this is insufficient to induce an action potential. However, when spontaneous SR Ca2+ release occurs simultaneously at more than a single locus, i.e. when these loci are """"""""synchronized,"""""""" the resultant sarcolemmal depolarization is augmented to levels that are sometimes sufficient to produce a spontaneous action potential and contraction. Thus, multiple areas of localized spontaneous Ca2+ release within ventricular cardiac cells, if """"""""synchronized"""""""" is a mechanism for abnormal automaticity in these cells and can produce a """"""""heart beat in reverse.""""""""

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Intramural Research (Z01)
Project #
1Z01AG000240-03
Application #
3821461
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
3
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Aging
Department
Type
DUNS #
City
State
Country
United States
Zip Code
Wang, Mingyi; Lakatta, Edward G (2009) The salted artery and angiotensin II signaling: a deadly duo in arterial disease. J Hypertens 27:19-21
Lin, Li; Park, Sungha; Lakatta, Edward G (2009) RAGE signaling in inflammation and arterial aging. Front Biosci (Landmark Ed) 14:1403-13