PubMed · 6104197
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J M Cruickshank. 1980-06-28. Beta-blocking agents.. https://doi.org/10.1016/s0140-6736(80)92677-x
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BACKGROUND: Postsynaptic alpha 1 adrenoceptor blockers are considered suitable drugs for modern vasodilatatory treatment of chronic heart failure. Therefore new analogues of these substances with more favourable characteristics than those of their main representative, prazosin are sought. The objective of the present work was to evaluate the therapeutic effect and tolerance of the original alpha 1-adrenoceptor blocker metazosin developed in the Research Institute for Pharmacy and Biochemistry (VUFB). METHODS AND RESULTS: In a multicentre clinical trial metazosin (tablets à 10 mg), 10-20 mg/day, were added to standard treatment of 56 patients of both sexes suffering from chronic congestive heart failure, for a period of eight weeks. The administration of metazosin led to rapid improvement of subjective complaints (in particular dyspnoea) as well as objective symptoms of peripheral congestion, to a significant (p < 0.05) regression of X-ray signs of pulmonary congestion and a slight (but statistically significant--p < 0.05) increase of the ejection fraction and cardiac output. After two months treatment the functional degree of severity of insufficiency according to the NYHA classification decreased from 2.7 to 2.2. Metazosin did not induce tachycardia and was well tolerated by the patients. CONCLUSIONS: Metazosin (Kenosin) tablets is a suitable supporting drug in the comprehensive treatment of chronic cardiac failure, in particular if refractory to treatment.
Activation of alpha 1-adrenoceptors in rat hypothalamic ventromedial nucleus can excite neurons and facilitate female sexual behavior. To identify the alpha 1-adrenoceptor subtype(s) involved, the alpha 1B-adrenoceptor-specific antagonist chloroethylclonidine (100 microM) and/or the alpha 1A-adrenoceptor-selective antagonist 5-methyl urapidil (1 or 2.5 microM) or WB-4101 (0.1-10 microM) were applied to a recording chamber bathing the hypothalamic slice containing the ventromedial nucleus. In all the neurons tested, both types of antagonists blocked, often completely, excitatory responses to nonselective alpha 1-adrenoceptor agonists. Since the doses used were unlikely to make these antagonists nonselective, the results suggest that activation of both alpha 1A- and alpha 1B-adrenoceptor subtypes was necessary for alpha 1-adrenoceptor agonists to evoke an excitation, or that with the present application method--injection into the continuously perfused chamber--chloroethylclonidine did not act specifically. In preincubation (at 37 degrees C for 90 min) where it was reported to act by specific alkylation, chloroethylclonidine (100 microM) but not the vehicle abolished the excitation evoked by an alpha 1-adrenoceptor agonist, but not that by carbachol or other excitants. Also, either in bath application or incubation, chloroethylclonidine worked equally efficiently on slices from ovariectomized rats, that reportedly contain few alpha 1B-adrenoceptors, and from those treated with estrogen which induces alpha 1B-adrenoceptors selectively, suggesting that alpha 1B-adrenoceptor was necessary even when in low abundance.(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of lidocaine on alpha 1-adrenoceptors in cultured neonatal rat ventricular cardiocytes was studied by binding assay. When the cells were cultured in the presence of lidocaine, the binding of (+/-)-beta-([125I]iodo-4-hydroxyphenyl)-ethyl-aminomethyl-tetralone to the cells increased in a concentration- and time-dependent manner. The effect was due to an increase in maximum binding but not due to a change in the dissociation constant for the ligand. The increased number of alpha 1-adrenoceptors returned to the control level after culturing the cells without lidocaine. The stimulating effect on the number of alpha 1-adrenoceptors of lidocaine was also observed in the presence of norepinephrine. Other class I antiarrhythmic drugs such as procainamide. disopyramide, mexiletine and flecainide increased the number of alpha 1-adrenoceptors in the cells. These results suggest that cardiac responsiveness mediated by alpha 1-adrenoceptors is increased by class I antiarrhythmic drugs.