Calcium Transport in Synaptosomes and Subcellular Membrane Fractions of Brain Tissue in Spontaneously Hypertensive Rats

Abstract

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.

Hyperreactivity of platelets from spontaneously hypertensive rats. Role of external magnesium.

“…33 Our comparison of platelets from SHR and WKY suggests that this inhibitory mechanism would be less sensitive to external Mg 2+ in platelets from SHR than in those from WKY (respective optimal concentrations of Mg 2+ : 2 x 10" 3 M and 10-3 M) and therefore less active in SHR at physiological extracellular Mg 2+ concentrations. This suggestion agrees with the reduction in membrane Ca 2+ -ATPase activity measured in various tissues from SHR 20 ' 24 and with the modifications in cyclic AMP metabolism described in platelets from SHR.…”

“…This may result from an increased Ca 2+ permeability of the cell membrane, which may affect basal passive or thrombin-stimulated Ca 2+ influx. An increase in passive Ca 2+ influx was indeed observed in synaptosomes from SHR 20 and more recently in platelets from SHR.…”

Platelet membrane calmodulin-stimulated calcium-adenosine triphosphatase. Altered activity in essential hypertension.

“…"- 13 In these studies, a reduced V^ for calmodulin-stimulated calcium accumulation, with no alteration in the affinity of the calcium transporting system for calmodulin, was observed in hypertensive states. It was postulated that alterations in calcium pump activity are related to a defect of the calmodulinATPase interaction."…”

Losartan improved respiratory function and coenzyme Q content in brain mitochondria of young spontaneously hypertensive rats

“…They have shown increased Ca 2? accumulating capacity (Kravtsov et al 1983), decreased energy production (Doroshchuk et al 2004), and assembly defects in respiratory complexes in brain mitochondria of SHR (Lopez-Campistrous et al 2008). It was shown that superoxide mediates Ang II-influx of extracellular calcium in neural cells (Zimmerman et al 2005) and that sustained intra-mitochondrial elevation of Ca 2?…”