Calcium channel blockers modulate gluco-corticoid receptors under hypovolemic shockстатьяТезисы
Статья опубликована в высокорейтинговом журнале
Информация о цитировании статьи получена из
Web of Science
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 1 апреля 2020 г.
Аннотация:The effects of calcium channel blockers on the functioning of cytosolic glucocorticoid receptors (GR) in hemorrhagic shock have been studied. The function of GR was studied in rat liver cytosol using radioligand methods with labelled steroid ligands possessing high spaciftc activities. The densities of types I and II GR as well as association and dissociation rate constants for ligand-receptor complexes were determined by Scatchard analysis. Blood corlicosterone levels were measured with the help of radioimmunoassay kits. It was found that compound A-l from the substituted pyrrole group (3 mg/kg) and nifedipin (Nf, 0.03 mglkg) activated the shock-induced function of type II GR, whereas verapamil (VP, 0.25 mglkg) inhibited it. A-i and Nf restored the biosynthetic activity of the liver under shock. Irrespective of the concentrations used (lo’*-I@’ M), these drugs did not influence the binding of the labelled ligand to type II receptors but produced pronounced dose-dependent effect on the function of type Ill receptors. Thus, Nf increased manyfold in the density of these receptors in rat liver cytosol, while Vp decreased it. Both Nf and Vp decreased elevated cortiwsterone concentrations in the blood which testifies to their antistressory effect. Compound A-l had no effect on the hormone concentration in the blood but increased the protein content in rat liver cytosol. The drugs under study affected differently the parameters of arterial pressure under shock, viz., Nf and A-l maintained AP at the subnormal level, while Vp enhanced hypotension and thus aggravated the post-hemorrhagic period. The ability of Vp to inhibit the function of GR which results in the inhibition of the glucocofticoid-dependent synthesis of the angiotensin-converting- enzyme in vascular endothelium cells is one of the reasons fat lowered AP.