Abstract:
:To determine the effect of calcium-channel blockers on beta-adrenergic receptors, we studied the interactions of verapamil, diltiazem, and nifedipine with both human lymphocyte beta 2-adrenergic receptors and rat myocardial beta 1-adrenergic receptors by means of radioligand binding assays. We also determined the functional consequences of these interactions by measuring adenylate cyclase activity. Radioligand binding studies in vitro demonstrated a Ki of verapamil for the lymphocyte beta 2-receptor of 32 +/- 4 microM. Diltiazem and nifedipine were much less potent. In studies of adenylate cyclase activity, verapamil was shown to act as a competitive beta-receptor antagonist. Also, norverapamil, the active metabolite of verapamil, had the highest affinity for the beta-receptor of any of the calcium-channel blockers studied (Ki = 4.2 +/- 0.8 microM). After 1 week of verapamil administration in six normal subjects, isoproterenol-stimulated adenylate cyclase activity in lymphocytes was increased from 60 +/- 4% to 83 +/- 10% over basal activity (p less than .05). This was associated with an increase in lymphocyte beta-receptor affinity for agonist as represented by the decrease in the IC50 for isoproterenol inhibition of [125I] iodocyanopindolol binding from 240 +/- 20 to 170 +/- 10 nM (p less than .05). Additionally, plasma norepinephrine levels were reduced from 206 +/- 58 to 92 +/- 18 pg/ml with 1 week of verapamil treatment (p less than .05). Our data suggest that verapamil affects lymphocyte beta-receptors in vitro and with long-term administration regulates lymphocyte beta-receptor function either directly or indirectly via a reduction in plasma catecholamine levels.
journal_name
Circulationjournal_title
Circulationauthors
Feldman RD,Park GD,Lai CYdoi
10.1161/01.cir.72.3.547subject
Has Abstractpub_date
1985-09-01 00:00:00pages
547-54issue
3eissn
0009-7322issn
1524-4539journal_volume
72pub_type
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