Calcium transport in synaptosomes and subcellular membrane fractions of brain tissue in spontaneously hypertensive rats.
The uptake of Na+ and Ca2+ by synaptosomes and uptake of Ca2+ by the mitochondria and microsomes of brain tissue of rats with spontaneous hypertension (SH rats) and normotensive Kyoto-Wistar rats (WKY rats) were studied with an isotope-exchange method. By means of inhibitor analysis it has been shown that calcium influx into the synaptosomes during depolarization of their plasma membrane takes place only through the potential-dependent channels in both groups of animals. Basal Ca2+ uptake by the synaptosomes of hypertensive rats was increased, apparently by partial depolarization of the synaptosome membrane caused by the increased membrane permeability to Na+ (basal Na+ uptake by synaptosomes was found to be increased in hypertensive rats). Ca2+ uptake by mitochondria of hypertensive rats was increased, and the Ca2+ uptake by microsomes was decreased in these rats compared with controls. The increment of the maximal Ca2+ transport rate in microsomes after the addition of calmodulin was decreased in spontaneously hypertensive rats compared with normotensive animals. Thus alterations in the interaction of calmodulin with the Ca2+-transporting systems of the plasma membrane are an important part of the widespread membrane defect observed in spontaneous hypertension.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001921:Brain / Q000378:metabolism* / Q000648:ultrastructure; D002118:Calcium / Q000378:metabolism*; D002147:Calmodulin / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D006973:Hypertension / Q000378:metabolism*; D066298:In Vitro Techniques; D007425:Intracellular Membranes / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D013574:Synaptosomes / Q000378:metabolism
D002147:Calmodulin; D012964:Sodium; D002118:Calcium