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.

[The effect of tropoxin on the neurogenic and vasogenic inflammation of the dura mater vessels].

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.

[The effect of clofelin on the transudation of plasma proteins into the dura mater induced by stimulation of the trigeminal ganglion].

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.