AI Article Synopsis
- The thrombocyte membranes' ability to bind Ca(2+) remains unchanged initially after hydrocortisone administration, with no significant effect on arterial pressure observed.
- In cases of sustained increased arterial pressure due to repeated hydrocortisone doses, intracellular Ca2+ levels shift, decreasing at the outer membrane and increasing within the cell.
- This redistribution of Ca2+ may be related to hypertension mechanisms seen in both essential and steroid-induced forms, possibly involving the cell's adrenoreceptor mechanisms.
Article Abstract
The Ca(2+)-binding ability of the thrombocytes' membranes did not change within 30 min after administration of hydrocortisone when no significant changes of arterial pressure occur. In stable increase of arterial pressure evoked by thrice repeated administration of hydrocortisone, a redistribution of the intracellular Ca2+ occurs: its contents decreases at the external plasmatic membrane and increases in intracellular membranes. The hypertensive response seems to coincide with the redistribution. The same mechanisms of Ca2+ metabolism disorders seem to underlie both essential and steroid hypertension. The cell's adrenoreceptor mechanisms are probably involved in the process.
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