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Ter Arkh. 2002;74(12):38-41.
[Tonocardin in complex treatment of diabetes mellitus concurrent with hypertension]

[Article in Russian]

Balabolkin MI, Khasanova ER, Trukhina TV, Kreminskaia VM.

AIM: To examine the effect of the alpha 1-adrenoblocker tonocardin (doxazosin) on the course of arterial hypertension (AH) and on carbohydrate and lipid metabolism and insulin resistance in patients with type 2 diabetes mellitus (DM) concurrent with AH. MATERIALS AND METHODS: 18 patients with type 2 DM concurrent with AH, treated with tonocardin for at least 12 weeks were examined; the fasting glycemia, the levels of blood glycosylated hemoglobin, serum total cholesterol and triglycerides, and the degree of insulin resistance (intravenous insulin load or insulin tolerance test and the insulin resistance index estimated by the HOMA method) were determined. RESULTS: Tonocardin treatment lowered systolic BP (from 159 +/- 19.83 to 136.57 +/- 17.43 mm Hg; by 14.5%), diastolic BP (from 93.38 +/- 12.98 to 79.12 +/- 11.69 mm Hg; by 15.28%), fasting glycemia (from 9.32 +/- 1.61 to 7.05 +/- 1.51 mmole/l; by 24.36%), glycosylated hemoglobin Ai (from 9.63 +/- 1.86 to 8.59 +/- 0.98%; by 10.8%), total cholesterol (from 6.09 +/- 0.57 to 5.4 +/- 0.4 mmole/l; by 11.4%), triglycerides (from 2.11 +/- 0.57 to 1.88 +/- 0.52 mmole/l; by 11%), glycemia after 30-min insulin load (from 9.32 +/- 1.61 to 5.77 +/- 1.57; by 39% and from 7.05 +/- 1.51 to 4.2 +/- 1.25 mmole/l; by 44% at the beginning and end of the follow-up, respectively), insulin resistance index (from 9.87 +/- 2.45 to 6.57 +/- 1.99; by 33.5%). CONCLUSION: The findings suggest that tonocardin exerts an antihypertensive effect and positively affects carbohydrate and lipid metabolisms, and diminishes insulin resistance in patients with type 2 DM concurrent with AH.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12577838&dopt=Abstract

yeal.net

AIM: To establish new methods for the chiral separation and preparation of three new drugs, alfuzosin, terazosin and doxazosin. METHODS: By optimizing factors which affect the chiral separation, modifier of solvent, chiral additive, pH of mobile phase, modifier of organic base and stationary phase, the optimum condition for chiral separation were selected. The preparation of enantiomers was carried out on semi-preparative reverse phase column (7.8 mm x 250 mm C4 5 microns). Acetonitrile-water modified by the addition of carboxymethyl-beta-cyclodextrin (2%-5%, w/v) was applied as chiral mobile phase. RESULTS: The enantiomers of three new drugs were base-line-separated and milligram-scale samples of enantiomer were obtained. CONCLUSION: The newly established method can be used in research and development of the enantiomers of three new drugs.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12579804&dopt=Abstract




Gen Pharmacol. 1999 Jul;33(1):99-105.
Characterization of postjunctional alpha-adrenoceptors in the pithed mouse.

McCafferty GP, Naselsky DP, Hieble JP.

SmithKline Beecham Pharmaceuticals, King of Prussia, PA 19406, USA.

The adrenoceptor subtypes responsible for the pressor response to alpha1- and alpha2-adrenoceptor agonists have not yet been established, although gene knockout experiments in the mouse have provided evidence for a role of the alpha1B- and alpha2B-adrenoceptor. We have evaluated the blood pressure response to selective activation of postjunctional alpha1- and alpha2-adrenoceptors in the pithed mouse. The pressor response to phenylephrine was sensitive to blockade by terazosin, a selective alpha1-adrenoceptor antagonist, but insensitive to rauwolscine, an antagonist at alpha2-adrenoceptors. Phentolamine, a nonselective alpha-adrenoceptor antagonist, blocked the response to either phenylephrine or the selective alpha2-adrenoceptor agonist B-HT 933, whereas rauwolscine blocked only B-HT 933. A dose of terazosin effective against phenylephrine had no effect on B-HT 933; however, the B-HT 933 response was antagonized when the terazosin dose was increased tenfold. A high dose of doxazosin, an alpha1-adrenoceptor antagonist having no affinity for the alpha2B adrenoceptor, blocked the response to phenylephrine but not B-HT 933. Comparison of the potencies of these antagonists against the pressor response to phenylephrine with their affinities for recombinant alpha1-adrenoceptor subtypes suggests that this response is mediated by either alpha1B- or alpha1D-adrenoceptors. The alpha2B-adrenoceptor subtype is likely to take part in the response to B-HT 933. The ability of certain quinazoline alpha1-adrenoceptor antagonists to block the alpha2B adrenoceptor may contribute to their activity as antihypertensive agents.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10428022&dopt=Abstract












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