Andreas Lückhoff

TL;DR: The initial rise in [Ca2+]i in response to receptor-binding agonists, caused by mobilization of Ca2+ from intracellular stores, activates K+ channels, thereby inducing hyperpolarization and providing the driving force for transmembrane Ca2- influx into endothelial cells and is thus an important signal for synthesis and release of EDRF.

TL;DR: EDRF production is directly controlled by extracellular Ca2+ during both receptor‐dependent and independent stimulation, and the results obtained during thimerosal stimulation indicate that there is not necessarily a tight coupling between the absolute level of [Ca2+]i and the amount of PGI2 released.

TL;DR: The results indicate that in a subgroup of patients with smooth coronary arteries angina can be caused by an abnormality of the endothelial function in the microcirculation.

TL;DR: The results characterize EDRF as a potent cyclic GMP- dependent antiaggregatory factor which may act synergistically in vivo with the cyclic AMP-dependent inhibitory effect of prostacyclin.

TL;DR: It is concluded that activation of purinergic receptors increases intracellular free calcium in endothelial cells, and that this increase is probably an essential trigger for synthesis of prostacyclin and the labile endothelium‐derived relaxant factor.