Membrane Hyperpolarization in Hypoxic Vasorelaxation
Shortly after the discovery of endothelium-dependent relaxation of smooth muscle cells in blood vessels (1) it became apparent that endothelial cells also could generate vasoconstrictor signals (2). Both endothelium-dependent relaxation and contraction can be attributed to the release of vasoactive substances from the intimal cells that have been designated as an endothelium-dependent relaxing factor (EDRF) and endothelium-dependent contracting factor or EDCF (3). There is increasing evidence that endothelial cells can intervene in peripheral vascular regulation besides numerous other effector influences by balancing the production of EDRFs and EDCFs. It is known that in atherosclerosis, cerebral and coronary vasospasm, and hypertension, endothelial cells either lose their ability to produce EDRF or this substance is no longer able to control vascular tone. But the ability to secrete EDCF appears unperturbed or even augmented (4). Thus, the rationale for undertaking the present research should be considered within this context, namely, to estimate the role of these substances in local vascular control under physiological conditions and to analyze their interaction with the already known effectors. Thus, it can be demonstrated that not only endothelial cells but also smooth muscle cells possess peripheral chemoreceptors sensitive to changes in Po2.
KeywordsPlatinum Prostaglandin Noradrenaline Acetylcholine Indomethacin
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