Submitted on October 9, 2006
Accepted on December 23, 2006
Intracellular cAMP: the switch that triggers on Spontaneous Transient Outward Currents generation in freshly isolated myocytes from thoracic aorta
Sebastien Hayoz1, Jean-Louis Beny1, and Rostislav Bychkov2*
1 Zoology and Animal Biology, University of Geneva, Sciences III, Geneva, Geneva, Switzerland
2 Zoology and Animal Biology, University of Geneva, Sciences III, Geneva, Switzerland
* To whom correspondence should be addressed. E-mail: rostislav66{at}yahoo.com.
STOCs (Spontaneous Transient Outward Currents) have been reported in resistance and small arteries but have not yet been found in thoracic aorta. Do thoracic aorta myocytes possess cellular machinery that generates STOCs? It was found that majority of aortic myocytes do not generate STOCs. STOCs were generated in 8.7% of freshly isolated aortic myocytes. Myocytes that did not generate STOCs we have called "silent" myocytes and myocytes with STOCs have been called "active". STOCs recorded in "active" myocytes were voltage dependent and were inhibited by ryanodine, caffeine and charybdotoxin. Forskolin was reported to increase STOCs frequency in myocytes isolated from resistance arteries. Forskolin (10µM) triggered STOCs generation in 35.1% of "silent" aortic myocytes. In 36.8% percent of "silent" myocytes forskolin did not trigger STOCs but increased the amplitude of charybdotoxin sensitive outward-net current to 136.1±8.5% at 0 mV. Membrane permeable 8BrcAMP triggered STOCs generation in 38.7% of "silent" myocytes. Forskolin or 8BrcAMP-triggered STOCs were inhibited by charybdotoxin. 8BrcAMP also increased open probability of BKCa-channels in BAPTA-AM pretreated cells. Our data demonstrate that, in contrast to resistance arteries, STOCs are present just in minority of myocytes in the thoracic aorta. However, cellular machinery that generates STOCs can be "switched" on by cAMP. Such an inactive cellular mechanism could modulate the contractility of the thoracic aorta in response to physiological demand.
