title: [Membrane-physiologic reaction of arteriosclerotic coronary vessels to hypoxia in man].
abstract: Human coronary arteries were taken from heart transplant patients. Arteriosclerotic arteries were more depolarized and constricted over the whole PO2 range between 535 and 0 mmHg. During oxygen deficiency, control preparations showed a maximal hyperpolarization of delta V = 10.9 mV and a maximal relaxation of delta T = 0.466 g. Arteriosclerotic arteries, however, became hyperpolarized by merely delta V = 7.1 mV and relaxed by delta T = 0.258 g. In normal coronary arteries, indomethacin reduced the hypoxic hyperpolarization and dilatation at 30 mmHg PO2 by about 51%. The reduction was 26% in arteriosclerotic vessels. The complete removal of the endothelium caused a 49% (74%) restriction of dilatory vascular reactivity. The relationship was quite similar for a carbogen Krebs solution. The hyperpolarizing and dilatory contribution by prostacyclin was 32% in normal and 12% in arteriosclerotic coronary arteries. The remainder could be attributed to the basal release of the endothelial dilator endothelium-derived hyperpolarizing factor (EDHF). Thus it may be concluded that in arteriosclerotic blood vessels, prostacyclin (PGI2) synthesis and release are predominantly diminished. Finally, we found that the ratio PGI2/EDHF in the voltage and tension changes strongly shifted to the PGI2 side with a declining oxygen concentration. This is true for normal and arteriosclerotic vessels. In accordance with the activation curve for vascular smooth muscle, the hyperpolarization leads to relaxation via a closure of Ca2+ channels. Hyperpolarization of 2.5 mV reduces the tension developed by one-half. Minimal changes in cell polarization cause large changes in tissue perfusion.
authors.affiliation: Institut für Physiologie der Freien Universität Berlin.
authors.forename: G
authors.initials: G
authors.lastname: Siegel
mesh_terms: D000818:Animals; D001685:Biological Factors / Q000502:physiology; D015220:Calcium Channels / Q000502:physiology; D015687:Cell Hypoxia / Q000502:physiology*; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000503:physiopathology*; D046508:Culture Techniques; D004285:Dogs; D004730:Endothelium, Vascular / Q000503:physiopathology; D011464:Epoprostenol / Q000502:physiology; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D001685:Biological Factors; D015220:Calcium Channels; D007473:Ion Channels; C067410:endothelium-dependent hyperpolarization factor; D011464:Epoprostenol