[Molecular bases of arterial hypertension induced by cadmium].
In order to establish at subcellular level the biochemical role of cadmium in the etiology of arterial hypertension, we studied the effect of this metal on some mitochondrial functions. The results showed that cadmium inhibits calcium uptake as well as stimulates calcium release in kidney mitochondria. By the same token Cd2+ inhibits the ADP and ATP exchange-reaction and also inhibits succinate oxidation. From these results it is proposed that C d2+ interacts with--SH groups that are important for energy--linked reactions and calcium transport; the above produces metabolic modifications that may result in hypertensive disease.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002104:Cadmium / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism; D004229:Dithiothreitol / Q000494:pharmacology; D004285:Dogs; D006973:Hypertension / Q000139:chemically induced / Q000378:metabolism*; D008931:Mitochondria, Muscle / Q000187:drug effects* / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D013385:Succinate Dehydrogenase / Q000037:antagonists & inhibitors
D002104:Cadmium; D000244:Adenosine Diphosphate; D013385:Succinate Dehydrogenase; D002118:Calcium; D004229:Dithiothreitol
Bases moleculares de la hipertensión arterial inducida por cadmio.