1. 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.
2. 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.
3. 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).
4. Ca2+ uptake by mitochondria of hypertensive rats was increased, and the Ca2+ uptake by microsomes was decreased in these rats compared with controls.
5. 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.
6. The changes in the Ca2+-transporting and Ca2+-regulating systems of the synaptosomes of brain tissue in spontaneously hypertensive rats may be the basis for the increase of the intrasynaptosomal Ca2+ concentration and, in turn, for the alteration in the rate of neurotransmitter release.