Effect of 24-week treatment with telmisartan on myocardial structure and function: relationship to insertion/deletion polymorphism of the angiotensin-converting enzyme gene.

The aim of the present study was to assess the effect of treatment with the angiotensin II receptor blocker telmisartan for 24 weeks on myocardial structure and function in patients with essential hypertension, and the relationship between this effect and the structural polymorphism of the angiotensin-converting enzyme (ACE) gene. Thirty-five patients with essential hypertension and left ventricular hypertrophy (LVH) without other associated morbidity were included in an open-label, non-comparative study. The patients were treated with telmisartan 40-80 mg once daily. In the final analysis, there were 29 patients who received the full course of treatment and were evaluated echocardiographically before and after treatment by the same blinded investigator, and myocardial structure and function were analysed. The myocardial mass of the left ventricle was determined in M-mode. Assessment of diastolic function of transmitral blood flow was performed using pulsed Doppler echocardiography. All patients were genotyped for insertion/deletion (I/D) polymorphism of the ACE gene. Telmisartan produced a significant reduction in left ventricular mass index from 140.4 +/- 48.6 to 128.7 +/- 40.6 g/m2 that was accompanied by an improvement in characteristics of diastolic function. The decrease in LVH was more significant in the ID genotype group than in the II and DD groups. Thus, prolonged treatment with telmisartan is accompanied by an improvement in myocardial structure, expressed as a reduction in left ventricular mass and function that is more marked in patients with ID genotype of the ACE gene.

[The effect of tropoxin on the neurogenic and vasogenic inflammation of the dura mater vessels]. / Vliianie tropoksina na neirogennoe i vazogennoe vospalenie sosudov tverdoi mozgovoi obolochki.

Subchronic administration of tropoxin (in doses of 7.5 and 10 mg/kg) caused dose-dependent blocking of 131I-albumin plasma transudation from the dura mater vessels, induced by electrical stimulation of the trigeminal ganglion and intravenous infusion of the agonist of 5-HT2B/2C receptors metachlorophenylpiperazine. The antimigraine agent metisergid produced a similar effect. A single injection of metisergid and tropoxin did not block albumin transudation. A 3 mg/kg dose of mianserin prevented the blocking effect of tropoxin and metisergid on plasma exudation into the dura mater. It is suggested that the mechanism of the tropoxin antimigraine effect is realized through the presynaptic 5-HT1 receptors of afferent endings of the trigeminal nerve and the postsynaptic 5-HT2B/2C receptors of the dura mater vessels.

[The effect of clofelin on the transudation of plasma proteins into the dura mater induced by stimulation of the trigeminal ganglion]. / Vliianie klofelina na propotevanie belkov plazmy v tverduiu mozgovuiu obolochku, vyzvannoe stimuliatsiei troinichnogo gangliia.

Intravenous administration of clofelin blocks transudation of 131I-albumin into the dura mater of rats in electrical stimulation of the trigeminal ganglion. Preliminary injection of the alpha-adrenoblocker yohimbine and the antagonist of serotonin receptors 5-NT1 mianserin completely removes the blocking effect of clofelin. Naloxon and the alpha 1-adrenoblocker prazosin had no effect on the degree of expression of albumin transudation and the clophelin effect. The role of the adrenergic system, the presynaptic alpha 2-adrenoceptors in particular, in functioning of the trigeminovascular system and the development of neurogenic inflammation in the dura mater is discussed.