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A Unitary Mechanism of Calcium Antagonist Drug Action '(Dihydropyridine/Nifedipine/Verapamil/Neuroleptic/Diltiazem) KENNETH M

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A Unitary Mechanism of Calcium Antagonist Drug Action '(Dihydropyridine/Nifedipine/Verapamil/Neuroleptic/Diltiazem) KENNETH M Proc. Nati Acad. Sci. USA Vol. 80, pp. 860-864, February 1983 Medical Sciences A unitary mechanism of calcium antagonist drug action '(dihydropyridine/nifedipine/verapamil/neuroleptic/diltiazem) KENNETH M. M. MURPHY, ROBERT J. GOULD, BRIAN L. LARGENT, AND SOLOMON H. SNYDER* Departments of Neuroscience, Pharmacology and Experimental Therapeutics, and Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, 72S North Wolfe Street, Baltimore, Maryland 21205 Contributed by Solomon H. Snyder, October 21, 1982 ABSTRACT [3H]Nitrendipine binding to drug receptor sites liquid scintillation counting were carried out as described (7). associated with calcium channels is allosterically regulated by a All experiments, performed in triplicate, were replicated at diverse group of calcium channel antagonists. Verapamil, D-600 least three times with similar results. (methoxyverapamit), tiapamil, lidoflazine, flunarizine, cinnari- Guinea pig ileum longitudinal muscles were prepared for zine, and prenylamine all reduce P3H]nitrendipine binding affin- recording as described by Rosenberger et aL (13) and incubated ity. By contrast, diltiazem, a benzothiazepine calcium channel an- in a modified Tyrode's buffer (14) at 370C with continuous aer- tagonist, enhances [3H]nitrendipine binding. All these drugeffects ation with 95% '02/5% CO2. Ileum longitudinal muscles were involve a single site allosterically linked to the [3H]nitrendipine incubated in this buffer for 30 min before Ca2"-dependent con- binding site. Inhibition of t3H]nitrendipine binding by prenyl- were as described Jim et aL amine, lidoflazine, or tiapamil is reversed by D-600and diltiazem, tractions recorded by (15). which alone respectively slightlyreduceorenhance H]mnitrendipine RESULTS binding. Diltiazem reverses the inhibition of [3H]nitrendipine binding by D-600. Our prediction that drugs allosterically regu- All dihydropyridine calcium antagonists evaluated inhibit lating P[H]nitrendipine binding should be calcium antagonists is [3H]nitrendipine.binding in a competitive fashion (6-10). Ver- confirmed by calcium antagonism in guinea pig ileum observed apamil inhibits [3H]nitrendipine binding (6-10), but Yamamura with the antihistamine dimethindene, the neuroleptics thiorida- and associates showed that this effect is not strictly competitive, zine and mesoridazine, and the anticholinergic biperiden. because verapamil cannot completely inhibit [3H]nitrendipine binding, the extent of inhibition of binding by verapamil de- Several distinct classes of organic calcium antagonist drugs are creases at increasing [3H]nitrendipine concentrations, and ver- important therapeutic agents in cardiovascular and numerous .apamil accelerates the dissociation of13H]nitrendipine from re- other medical conditions (1, 2). At leastfour classes ofstructures ceptor sites (9). Because diphenylalkylamines inhibit [3H]- are distinguished: the dihydropyridines exemplified by nifed- nitrendipine binding completely, it was suggested that these ipine (1-3), phenylalkylamines exemplified by verapamil (1- drugs act at the same receptor sites as dihydropyridines (11). 3), benzothiazepines such as diltiazem (1, 2, 4), and diphenylal- In our studies, the diphenylalkylamines prenylamine, flunari- kylamines such as prenylamine and lidoflazine (1, -2, 5). Re- zine, and lidoflazine and the phenylailylamine tiapamil max- ceptors for the drugs are labeled with [3H]nitrendipine (6-10), imally inhibit [3HInitrendipine.binding (Fig. 1). However, max- or [3H]nimodipine (10) and regulated in a physiological fashion imal inhibition of [3H]nitrendipine binding by these drugs by calcium (7). The apparent competitive inhibition of declines with increasing [3H]nitrendipine concentration be- [3H]nitrendipine binding by diphenylalkylamines has implied tween 0.1 and 3 nM (data not shown), suggesting a similarity effects at the same site as the dihydropyridines (11). Verapamil in the action ofthese agents and verapamil. We have confirmed and diltiazem respectively inhibit and stimulate [3H]nitrendipine this possibility in dissociation experiments (Fig. 2). As pre- binding allosterically, suggesting actions at different sites (9, viously reported (9), verapamil speeds the dissociation of 12). Here we show that the phenylalkylamine, diphenylalkyl- [3H]nitrendipine (data not shown), whereas the dihydropyri- amine, and benzothiazepine drugs,-in pharmacologically rele- dine nimodipine has no effect on the dissociation rate. Like vant concentrations, interact.at a single drug recognition site verapamil, the diphenylalkylamines lidoflazine and prenyl- allosterically linked to the dihydropyridine receptor. We pre- amine and the verapamil analog tiapamil accelerate [3H]- dict and confirm by bioassay previously unknown calcium an- n-itrendipine dissociation. Cinnarizine and flunarizine similar- tagonist activity for several drugs. ly increase the dissociation rate. Having established that the diphenylalkylamines influence MATERILS AND METHODS [3H]nitrendipine binding allosterically, we investigated whether Drugs were obtained from the following sources: nifedipine, the diphenylalkylamines and phenylalkylamines act at the same Pfizer; nimodipine, Miles; prenylamine, Hoechst-Roussel site. Ifso, then increasing concentrations ofD-600 (which max- Pharmaceuticals (Somerville, NJ); D-600 (gallopamil, methoxy- imally reduces [3H]nitrendipine binding only 20-30%) (Fig. 3) verapamil) and verapamil, Knoll Pharmaceutical (Whippany, should block the ability of a diphenylalkylamine to inhibit NJ); diltiazem, Marion Laboratories (Kansas City, MO) and [3H]nitrendipine binding, with a rightward shift in concentra- Tanabe (Osaka, Japan); desmethyl-cis-diltiazem and -trans-dil- tion-response curves. Indeed, increasing concentrations of D- tiazem, Tanabe; lidoflazine, flunarizine, and cinnarizine, Jans- 600 do produce rightward shifts in the concentration-response sen Pharmaceutical (Beerse, Belgium); and bepridil, McNeil curves for inhibition of [3H]nitrendipine binding by the di- Pharmaceutical (Spring House, PA). phenylalkylamines prenylamine, flunarizine, and lidoflazine Binding assays in guineapigbrain membranes, filtration, and (Fig. 1 a-c). Tiapamil, a phenylalkylamine closely similar in structure to verapamil and D-600 (16), produces the same max- The publication costs ofthis article were defrayed in part by page charge imal inhibition of [3H]nitrendipine binding elicited by the di- payment. This article must therefore be hereby marked "advertise- ment" in accordance with 18 U. S. C. §1734 solely to indicate this fact. * To whom reprint requests should be addressed. 860 Downloaded by guest on October 1, 2021 Medical Sciences: Murphy et aL Proc. NatL Acad. Sci. USA 80 (1983) 861 .5z 0I- 0 0 0 -logiflunafizine.J (M) ._ ._ I V0 c c 0 I z I C., IsoA S0 4 to- ; U'0 7l 6 5 4 7 6 -logilidoflazinel (M) -log [tiapamil I (M) FIG. 1. Inhibition of [3Hlnitrendipine binding by prenylamine, tiapamil, lidoflazine, and flunarizine: Interactions with D-600. Concentration- response curves for the inhibition of [3Hlnitrendipine binding were constructed for prenylamine (a), flunarizine (b), lidoflazine (c), and tiapamil (d) in the absence (e) or the presence of 2.5 nM (o), 25 nM (i), 250 nM (o), 2.5 pM (A), or 25 ptM (A) D-600. Concentration-response curves are the results of experiments that employed at least six concentrations of each drug assayed in triplicate with 0.25 nM [3Hlnitrendipine. Values are presented as a percent of control [3H]nitrendipine binding. phenylalkylamines (Fig. Id), and D-600 produces a rightward Because D-600 maximally reduces [3H]nitrendipine binding shift for tiapamil inhibition of [3Hjnitrendipine binding, re- less than the other diphenylalkylamines and phenylalkylamines flecting similar actions ofphenylalkylamines and diphenylalkyl- and assuming that the drugs act at the same site, D-600 should amines. The degree of rightward shift differs for -the drugs overcome inhibition of [3H]nitrendipine binding exerted by evaluated, being greatest with tia-pamil and least with.flunari- these other drugs. Accordingly, we examined the ability of D- zine. By contrast with these results, the concentration-response 600 to influence [3H]nitrendipine binding to membranes si- curve for inhibition of [3H]nitrendipine binding by nifedipine multaneously incubated with prenylamine, tiapamil, flunari- is not progressively shifted in the presence of increasing con- zine, or lidoflazine (Fig.. 3). In the absence of other drugs, D- centrations of D-600 (data not shown). 600 maximally reduces [3H]nitrendipine binding only about 25% with an ECG (50% effective concentration) ofabout 10 nM. By contrast, in the presence ofconcentrations ofprenylamine, tiapamil, flunarizine, or lidoflazine that give nearly maximal inhibition of [3H]nitrendipine binding, D-600 actually stimu- lates [3H]nitrendipine binding (Fig. 3). The percentage stim- ulation of [3H]nitrendipine binding by D-6(0 diminishes with too lower concentrations of the other drugs. [3H]Nitrendipine binding is restored by D-600 to the level ofbinding that occurs 0ml with maximally inhibitory concentrations of D-600 alone. As expected for drugs competing for the same site, D-600 is some- what less potent at enhancing [3H]nitrendipine binding in the presence of increasing concentrations of the other inhibitors (Fig. 3). Whereas diphenylalkylamines and phenylalkylamines inhibit 20. [3H]nitrendipine binding, diltiazem stimulates binding when evaluated in the absence ofother drugs (Fig. 4a) (12,
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