Abstract:
:Exposure of cultured heart muscle cells to noradrenaline led to a decrease in the effects of isoproterenol and prostaglandin E1 on cAMP formation and contraction velocity. However, heterologous desensitization, as measured by prostaglandin E1 stimulation, only occurred at higher noradrenaline concentrations than homologous desensitization (isoproterenol stimulation). As the defects of the adenylate cyclase system in heart failure are attributed to noradrenaline-induced desensitization, it is concluded from the results that, in comparison to the subsensitivity to beta-adrenoceptor agonists in failing human hearts, a decrease in the responsiveness to other receptor-dependent adenylate cyclase stimulators should also occur but only at higher degrees of heart failure.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Reithmann C,Werdan Kdoi
10.1016/0014-2999(88)90370-6subject
Has Abstractpub_date
1988-09-01 00:00:00pages
99-104issue
1eissn
0014-2999issn
1879-0712pii
0014-2999(88)90370-6journal_volume
154pub_type
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
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journal_title:European journal of pharmacology
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