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Biomedical subjects

Kh M Markov

Publications and source records attributed to Kh M Markov.

At least 19 recordsLinked to original sources
PubMed1993

[The effect of endothelin-1 on vascular adrenoreactivity. The participation of G-proteins and protein kinase C in vascular constriction under the action of endothelin-1].

The experiments performed in endothelin-denuded preparations (the strips of thoracic aorta and perfused tail arteries) showed that: 1) ET-1 exerts dose-dependent and slowly developing contractions and in subthreshold doses it potentiates vasoconstriction reactions to stimulate sympathetic nerve endings or phenylephrine exposure. 2) ion F(-), that activates G-proteins in the cell membranes, at a dose of 2 microM increased about two times the ET-1-induced vasoconstriction. 3) the aortic strip incubation with the protein kinase C inhibitor staurosporin led to a 50% decrease in the contraction amplitude. Results suggest that G proteins and protein kinase C may participate in the development of ET-1 induced vascular smooth muscle contraction.

Animals↗
PubMed1993

[The role of extracellular calcium in the vasoconstriction evoked by endothelin-1].

Some mechanisms responsible for extracellular Ca++ entry into rat aortic smooth muscle cells were studied in response to endothelin-1 (ET-1). Isometric tension of de-endothelialized aortic strips was recorded. It was shown that the calcium-free medium or nifedipine blockade of calcium entry diminished responses to ET-1 to 20-30% of the control levels. Depolarization of the specimens with hyperpotassium solution also reduced constriction almost by 50%. When sodium ions were replaced by NMDG in the medium, a response to ET-1 showed a 50% reduction. The findings suggest that the potential-dependent calcium channels of the L-type are involved in cellular calcium entry, the opening of the channels depending upon the entry of Na+.

Animals↗
PubMed1993

[The effect of captopril on the arterial pressure, structural resistance and vascular reactivity of the kidney in rats with nephrogenic hypertension].

The angiotensin-converting enzyme inhibiting agent captopryl suppressed a moderate hypertension in rats with pyelonephritis and with ureteral obstruction, but not in rats with ureteral obstruction combined with the renal artery constriction. The suppression of the hypertension was accompanied by a reversion of structural alterations in the blood vessels.

Animals↗
PubMed1992

[The effect of endothelin-1 on Na+/H+ metabolism in vascular smooth muscle cells].

The effects of endothelin on intracellular pH (pHi) were examined in cultured rat vascular smooth muscle cells (VSMC) using the fluorescent probe BCECF. Endothelin induced biphasic changes in pHi: initial decrease followed by a subsequent increase above the basal level due to activation of the Na+/H+ exchange. The elevation of pHi was slow and sustained, but depended on the dose of endothelin: IC50 was about 3 x 10(-8) M. Na+/H+ exchange inhibition by EIPA (10(-7) M) or by equimolar replacement of external Na+ by choline abolished the pHi increase by enhancing the first phase of cytoplasm acidification. Effects of endothelin were compared with the action of protein kinase C (PK-C) activator phorbol 12-13 myristate ester (PMA). PMA induced a monophasic slow and sustained increase in pHi. The treatments of VSMC with H-7 and staurosporine (PK-C) inhibitors prevented the pHi response to endothelin and PMA. These results suggest that protein kinase C may play an important role in mediating the effects of endothelin on Na+/H+ exchange in VSMC.

Animals↗
PubMed1992

[Activation of Na/H exchange by thrombin in peritoneal mast cells].

Using the fluorescent probe, BCECF, the changes in intracellular pH (pHi) in rat peritoneal mast cells were studied. alpha-Thrombin (0.1 nM) induced biphasic changes in pHi which consisted in a temporary decrease in pH with its subsequent steady increase due to the Na/H exchange activation which was inhibited by EIPA and controlled by extracellular Na+. The biphasic changes in pHi induced by DIP-alpha-thrombin (0.1 pM-1 nM), a catalytically inactive form with an intact recognition site, were similar to those of alpha-thrombin, whereas beta/gamma-thrombin (10-1000 pM), a catalytically active form characterized by structural disturbances in the recognition site, was able to induce only the initial phase of acidification. The thrombin recognition site modulators, alpha 1-thymosin and heparin, blocked the ability of the enzyme to induce the alkalinization of pHi. Nigericin stimulated the Na/H-exchange in mast cells. The rate of the Na/H-exchange activation determined with nigericin, decreased with an increase in the alpha-thrombin dose from 0.1 pM up to 10 nM. Activation of protein kinase C (PKC) in mast cells by PMA used at 1 nM and 10 nM led to the alkalinization of the cytoplasm as a result of the Na/H-exchange activation blocked by EIPA. The PKC inhibitor, H-7, suppressed the pHi increase induced by both PMA and alpha-thrombin. The alpha-thrombin-induced acidification of the cytoplasm was completely blocked by SITS in Ca(2+)-free media, whereas in media with Ca2+ SITS inhibited the pHi decline. Acidification of the cytoplasm by thrombin seems to be due to both Ca2+ influx and activation of Cl- fluxes. It is concluded that the observed activation of the Na/H-exchange by thrombin is induced by a cascade of intracellular reactions involving PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

[Endogenous vasoactive factors in children with nephrotic syndrome].

In accordance with the results of examining 40 children with nephrotic and mixed glomerulonephritis, it has been established that in the pathogenesis of the nephrotic syndrome of paramount importance is imbalance of the output of renal prostanoids, manifesting in the predominance of the vasopressor and proaggregate fraction--thromboxane A2 and in the deficiency of its antagonist prostacyclin that exerts a protective action on glomerular filtration. Sodium and water retention in patients with the nephrotic syndrome favours an increase of the content of antidiuretic hormone and plasma renin activity.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

[Measuring of intracellular Ca2+ concentration in macrophages. Effects of platelet activation factor].

In experiments on mice resident and stimulated thioglycolate macrophages the changes in cytoplasmic Ca2+ concentration Ca2+ have been studied by the use of the fluorescent probe fura-2. PAF acether (10(-7) M) raised Ca2+ by 300-400 nM within 1 min only in the stimulated macrophages. In the resident cells this increase was much less. In the presence of 2mM EGTA, PAF raised Ca2+ to a lesser extent. This suggests that PAF causes influx of exogenous Ca2+ through the receptor-mediated channels as well as releasing Ca2+ from intracellular stores.

Animals↗
PubMed1989

[Prostacyclin-thromboxane balance and risk factors of ischemic heart disease].

The paper considers the significance of prostacyclin-thromboxane (PGI2/TxA2) balance for cardiovascular performance in health and in angina pectoris and myocardial infarction. The functional interaction between prostacyclin and thromboxane was examined in terms of a number of risk factors for coronary heart disease (CHD), such as ageing, atherosclerosis, arterial hypertension, diabetes mellitus, obesity, hypokinesia, smoking, alcoholism, sex differences, and predisposition to the disease. A unidirectional pattern of changes in the PGI2/TxA2 balance towards TxA2 was found in CHD and in the presence of all the aforementioned risk factors. The paper discusses possible mechanisms responsible for these changes, as well as their contribution to the pathogenesis and prevention of CHD.

Adult↗
PubMed1989

[Na+/H+ metabolic activity in the thrombocytes of spontaneously hypertensive rats].

The sodium-proton exchange was determined in platelets of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). The platelets were suspended in sodium propionate; the cytoplasmic acidification activated the exchanger and intracellular pH (the increasing) and volume of the platelets (the swelling) were registered. The activity of Na+/H+ exchange was inhibited by isopropyl amiloride. The platelets' volume and the exchange rate constant of SHR were increased on 30-40% as compared with those of WKY.

Animals↗
PubMed1989

[Effect of coronary arterial occlusion on prostacyclin biosynthesis in dogs of various ages].

In acute experiments in animals of different age, local myocardial ischemia was stimulated, and the pattern of change in prostacyclin biosynthesis by segments of ischemized and normal coronary arteries was studied. Prostacyclin biosynthesis by coronary arterial segments was much more intensive in young animals, as compared to adult ones. Ischemized arterial segments of pups were also shown to produce a much smaller quantity of prostacyclin, as compared to control animals and to adult levels. The demonstrated findings may be making an important pathogenetic contribution to ischemic heart damage.

Age Factors↗