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Biomedical subjects

V V Kolomiets

Publications and source records attributed to V V Kolomiets.

At least 19 recordsLinked to original sources
PubMed1999

[Treatment of mild and moderate hypertension with enalapril (multicenter study of enap and enap N in Ukraine)].

AIM: Assessment of efficiency and safety of enalapril (enap) and its combination with hydrochlorotiaside (enap-N). MATERIALS AND METHODS: 127 patients with mild and moderate blood hypertension entered an open non-comparative multicenter trial. 60 of them received enap (group 1), 67--enap N (group 2). Group 1 patients were given enap for 2 weeks in a dose 10 mg/day. If this dose was not adequate to normalize blood pressure, it was raised to 20-40 mg/day. Patients of group 2 received enap-N one tablet a day for 3 weeks. If the pressure persisted higher than 140/90 mm Hg, the treatment was continued for 3 weeks more in a dose of 2 tablets a day. RESULTS: Blood pressure lowered under 140/90 mm Hg in 40 patients of group 1 (66.7%). Systolic pressure dropped by 10 mm Hg minimum and diastolic by 5 mm minimum in 18 group 1 patients (30%). Enap-N reduced blood pressure under 140-90 mm Hg in 44 of 67 patients (65.7%). Systolic and diastolic pressure dropped, respectively, in 23(34.3%) patients. CONCLUSION: Enap and enap-N tablets were found highly effective and well tolerated. Side effects were caused by lowering of blood pressure.

Administration, Oral↗
PubMed1995

[The effect of calcium-regulating hormones on the renal transport of calcium in hypertension].

Enhanced and diminished calcemia following administration of parathormone and calcitonin in hypertensive patients, respectively, were found not to differ from relevant values in healthy subjects. Calciuretic effect of parathormone results from its action on the bone and renal calcium transport. Quantitatively, the effects on the bone and renal calcium transport. Quantitatively, the effects on the bone presenting as elevated calcemia and calcium filtration capacity, its excreted fraction and renal excretion prevail, being less pronounced in hypertensive patients. A direct renal effect of parathyroid hormone indicated by stimulation of calcium tubular reabsorption is weaker in hypertensive subjects. Calcitonin administration inhibits tubular calcium reabsorption in the less degree in hypertensive subjects. The disorders in calciuretic function of the kidney in hypertension are secondary to reduced kidney sensitivity to the action of calcium regulating hormones.

Adult↗
PubMed1990

[Calciuretic renal function in patients with essential hypertension].

Under the conditions of standard and customary calcium use, patients suffering from essential hypertension (EH) do not manifest any changes in calciuresis either at the expense of the glomerular or tubular mechanisms. After intravenous hypercalcemic injections EH patients demonstrate well-defined disorders in calciuretic renal function, caused by inadequate suppression of tubular reabsorption of calcium by parathyroid hormone (PTH). The hormonal-renal correlations in EH patients differ from those in normals. More pronounced alterations in the concentration of radioimmune PTH and calcitonin under acute hypercalcemia are not associated with an adequate increment of fractional excretion of calcium whereas the calciuretic effect of exogenous calcium-regulating hormones (CRH) realized at the tubular level is less remarkable. Therefore EH patients manifest changes not only in CRH secretion but also in the sensitivity to them of the renal tubules. White changing parathyroid regulation of calcium metabolism prolonged administration of calcium to EH patients enhances body capabilities of resisting acute alterations in calcemia because of normalization of calciuretic renal function, especially tubular calcium transport. In addition, it lowers arterial pressure and enables reduction of the dose of calcium antagonists used in the treatment of EH.

Adult↗
PubMed1990

[Regulation of calcium metabolism in hypertension].

In patients with hypertensive disease, the intravenous calcium tolerance test revealed a delayed elimination of loading hypercalcemia, which totally reflects the effectiveness mechanisms aimed at removing excessive calcium from the extracellular space. In hypertensives, renal calcium excretion was also delayed due to a lower suppression of calcium channel reabsorption. The patients showed a greater background concentration of parathyroid hormone (PTH) and during the calcium tolerance test a much lower PTH levels and higher calcitonin concentrations, though their homeostatic effects remained inadequate due to their diminished sensitivity of target organs. Thus, there was an increase in the activity of parathyroidal glands in patients with hypertensive disease.

Adult↗
PubMed1990

[The calcium concentration of the blood in arterial hypertension patients].

Determination of the concentration of ionized calcium in the blood of metallurgists and miners with arterial hypertension (AN) revealed a tendency to reduction of calcemia that was more pronounced in high arterial pressure and low consumption of calcium with food. A tendency to reduce calcemia by stimulating PTH secretion has a pathophysiological significance in the development of AH. A calcium-enriched diet may be of value in the prophylaxis of AH.

Adult↗
PubMed1988

[Effect of nifedipine on renal activity].

Sublingual administration of nifedipine (N) at a dose of 20 mg to 8 persons without cardiovascular and renal pathology and to 19 patients with congestive heart failure (CHF) increased renal excretion of sodium (by an average of 51.1-132.8%), water (by an average of 31.7-101.9%), potassium (by an average of 43.2-63.2%) and calcium (by an average of 118%). The natriuretic effect of N appeared in 20 min reaching its maximum in 45-60 min, being more noticeable in CHF. An increment of natriuresis resulted from a decrease in sodium tubular reabsorption (correlation factor--0.92) rather than from an increase in glomerular filtration (correlation factor +0.50). N suppressed sodium reabsorption in the proximal tubule (by an average of 34.1%) as well as in the segment, more distal of Henle's loop (by an average of 6.8%). N might suppress directly calcium-dependent mechanisms of sodium transtubular transport but it could also produce a mediated effect as a result of shifts of renal hemodynamics.

Diuresis↗