[Hypotensive activity and cerebroprotective properties of carvedilol in patients with arterial hypertension associated with type 2 diabetes mellitus].

Aim of the study was to elucidate peculiarities of influence of carvedilol on 24-hour blood pressure (BP) profiles and changes of parameters of cerebral perfusion in patients with arterial hypertension (AH) associated with type 2 diabetes mellitus. Investigations were performed in 30 patients with I-III degree AH associated with type 2 diabetes of compensation and subcompensation stages. At baseline and after 24 weeks of treatment with carvedilol we carried out 24-hour BP monitoring, single photon emission computer tomography of the brain, and assessed the state of carbohydrate and lipid metabolism. According to data of 24-hour BP monitoring marked lowering of BP parameters occurred under the influence of therapy. This was accompanied with 26% decrease of the number of hypoperfused sectors of the brain (chi2=6.04, =0.014). During adenosine test number of hypoperfused sectors decreased from 136 to 117 (chi2=2,10, =0,147) what evidenced for a tendency to improvement of reactivity of cerebral vessels in response to vasodilating influences. The preparation exerted favorable effect on metabolic parameters and lowering of level of postprandial glycemia in dynamics of treatment was statistically significant.

[Polymorphic markers of GNB3 (C825T), AGTR1 (A1166C) and ACE (A2350G and I/D) genes in patients with arterial hypertension combined with diabetes mellitus type 2]. / Polimorfnye markery genov GNB3(C825T), AGTR1(A1166C), and ACE(A2350G and I/D) u bol'nykh arterial'noi gipertoniei, sochetaiushcheisia s sakharnym diabetom tipa 2.

AIM: To elicit correlations of polymorphic markers of GNB3 (C825T), AGTR1 (A1166C), ACE (A2350G and I/D) genes with arterial pressure, left ventricular hypertrophy (LVH) and blood concentrations of proinflammatory cytokines in hypertensive patients with diabetes mellitus type 2 (DM2). MATERIAL AND METHODS: Clinical parameters (24-h arterial pressure profile, echocardiographic findings, immunoenzymes level) were studied in 89 hypertensive patients with DM2. These patients had different genotypes by the studied allele variants of the genes determined by polymerase chain reaction. RESULTS: Polymorphism of A1166C gene of type 1 vascular receptor of angiotensin II (AGTR1) contributes to formation of arterial hypertension (AH) signs diversity in DM2 patients. GNB3, a gene C825T polymorphic marker, showed a correlation with diastolic arterial pressure but this variant of the gene locus is not associated with LVH. However, G-allele of ACE gene contributes much to appearance of this pathological sign. Mean values of IL-1beta and TNF-alpha as well as the presence of LVH depended on genotypes by ACE gene (polymorphism I/D). CONCLUSION: Polymorphic markers of ACE and GNB3 candidate genes influence clinical diversity of pathological signs in DM2 patients through modification of AH and LVH severity and the level of proinflammatory cytokines.

[Effect of long-term antihypertensive therapy on vaso-regulating function of the brachial artery in patients with arterial hypertension associated with type 2 diabetes mellitus]. / Vliianie dlitel'noi antigipertensivnoi terapii na sostoianie vazoreguliruiushei funktsii plechevoi arterii u bol'nykh arteial'noi gipertoniei, assotsiirovannoi s sakharnym diabetom tipa 2.

AIM: To evaluate the impact of 6-month-to-one-year antihypertensive therapy on the vasoregulating junction of the brachial artery and predictors of its efficiency in 75 patients with stages I-II arterial hypertension associated with type 2 diabetes mellitus. MATERIALS AND METHODS: An open randomized study of parallel groups of patients receiving angiotensin-converting enzyme (ACE) inhibitors, calcium blockers (verapamil) and their combination and in those who did not take antihypertensive therapy examined endothelium-dependent vasodilation (EDVD) according to the data of ultrasound scanning and Doppler study of brachial arterial blood flow as compared with changes in metabolism and 24-hour blood pressure profile. RESULTS: A positive effect of verapamil on the baseline impaired EDVD is realized only in the presence of an adequate compensation of glycemia, at the normal blood level of cortisol, occurs in parallel with increased nonendothelium-dependent vasoreactivity, and associates with the magnitude of an antihypertensive effect. ACE inhibitors improve decreased EDVD irrespective of the degree of glycemic control, the blood level of cortisol without a clear correlation with the altered non-endothelium-dependent vasoreactivity and with the degree of an antihypertensive effect. Combined therapy with these agents causes decreases in baseline insulinemia and the athoregenicity index and it can improve impaired vasoreactivity even in case of incomplete antihypertensive therapeutic effect. CONCLUSION: The differences found in the effect of ACE inhibitors and verapamil on baseline decreased EDVD provide evidence for differential use of these drugs to correct impaired vasoreactivity in patients with AH associated with DM. The combined antihypertensive therapy fails to produce a positive impact if significant hypercholesterolemia (total blood cholesterol being more than 6.5 mmol/l) and stenosing peripheral atherosclerosis are present.