Abstract
The alterations of the beta-adrenoceptor adenylyl cyclase are reviewed.
In failing myocardium, the down-regulation of beta 1-adrenoceptors
is accompanied by a decrease in steady state mRNA levels, as studied
with quantitative polymerase chain reactions in dilated and ischaemic
cardiomyopathy. The density of beta 2-adrenoceptors and beta 2-adrenoceptor
mRNA was unchanged in both pathological conditions compared to non-failing
myocardium. In addition to down-regulation of beta 1-receptor protein
and mRNA, an increased activity of the beta-adrenoceptor kinase (beta-ARK)
was observed. Correspondingly, quantification of beta-ARK mRNA by
a 5' and a middle portion PCR-product suggests that increased enzyme
activity could be due to increased transcription. In summary, decreased
steady state levels of beta 1-adrenoceptor mRNA could contribute
to reduced beta-adrenoceptor density in failing myocardium. The known
uncoupling of beta-adrenoceptors could be due to an increased mRNA
expression and activity of beta-ARK.
Users
Please
log in to take part in the discussion (add own reviews or comments).