1. The rate of calcium transport and calmodulin distribution in the erythrocytes of patients with essential hypertension were studied. In erythrocyte membranes subjected to calmodulin depletion by treatment with EGTA, both the affinity of the calcium pump for Ca 2+ and its maximal activity were the same in normotensive and hypertensive patients. 2. The addition of exogenous calmodulin to calmodulin-stripped membranes from erythrocytes of patients with essential hypertension resulted in a smaller increase of the maximal activity of the calcium pump and its affinity for Ca 2+ . The addition of calmodulin to erythrocyte membranes obtained without EGTA treatment resulted in a smaller increase of the maximal activity of the calcium pump only. 3. There were no significant differences of calmodulin distribution (cytoplasmic concentration and size of the membrane-bound pool) between the erythrocytes of normotensive and hypertensive patients. 4. It is suggested that alterations in the calcium pump activity of the erythrocyte membranes of patients with essential hypertension are related to the alteration of interaction between calmodulin and Mg 2+ , Ca 2+ -ATPase.
1. The uptake of Na + and Ca 2+ by synaptosomes and uptake of Ca 2+ 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 Ca 2+ 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. Ca 2+ uptake by mitochondria of hypertensive rats was increased, and the Ca 2+ uptake by microsomes was decreased in these rats compared with controls. 5. The increment of the maximal Ca 2+ 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 Ca 2+ -transporting systems of the plasma membrane are an important part of the widespread membrane defect observed in spontaneous hypertension. 6. The changes in the Ca 2+ -transporting and Ca 2+ -regulating systems of the synaptosomes of brain tissue in spontaneously hypertensive rats may be the basis for the increase of the intrasynaptosomal Ca 2+ concentration and, in turn, for the alteration in the rate of neurotransmitter release.