title: Calcium-antagonist receptors in the atrial tissue of patients with hypertrophic cardiomyopathy.
abstract: Hypertrophic cardiomyopathy is characterized by a nondilated, hypertrophied left ventricle in the absence of any overt cause. A possible role of adrenergic innervation or of cellular calcium regulation is suggested by the presence of hyperdynamic left ventricular function and by the clinical and symptomatic improvement seen in patients treated with beta-receptor antagonists or calcium antagonists. Therefore, we measured the density of calcium-antagonist receptors and beta-adrenoceptors in the atrial myocardium of 16 patients with hypertrophic cardiomyopathy and 19 patients with various other cardiac disorders. For comparison, we also measured the number of voltage-sensitive sodium channels. Calcium-antagonist binding sites, measured as the amount of dihydropyridine bound to atrial tissue, were increased by 33 percent in patients with hypertrophic cardiomyopathy (mean [+/- SD], 397 +/- 104 fmol per milligram of protein in patients with hypertrophic cardiomyopathy, as compared with 299 +/- 108 in patients with other cardiac disorders; P less than 0.01). The densities of saxitoxin-binding sites on voltage-sensitive sodium channels and beta-adrenoceptors were the same in the two groups, although the density of beta-adrenoceptors was higher in atrial samples from patients receiving beta-receptor antagonists (165 +/- 86 fmol per milligram of protein [patients receiving beta-blockers] vs. 85 +/- 60 [patients not receiving beta-blockers]; P less than 0.04). The increase in the number of calcium-antagonist receptors in hypertrophic cardiomyopathy suggests that abnormal calcium fluxes through voltage-sensitive calcium channels may play a pathophysiologic part in the disease.
authors.affiliation: Department of Neuroscience, Johns Hopkins Medical Institutions, Baltimore, MD.
authors.forename: J A
authors.initials: JA
authors.lastname: Wagner
authors.forename: F L
authors.initials: FL
authors.lastname: Sax
authors.forename: H F
authors.initials: HF
authors.lastname: Weisman
authors.forename: J
authors.initials: J
authors.lastname: Porterfield
authors.forename: C
authors.initials: C
authors.lastname: McIntosh
authors.forename: M L
authors.initials: ML
authors.lastname: Weisfeldt
authors.forename: S H
authors.initials: SH
authors.lastname: Snyder
authors.forename: S E
authors.initials: SE
authors.lastname: Epstein
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002121:Calcium Channel Blockers / Q000378:metabolism; D015220:Calcium Channels / Q000502:physiology; D002312:Cardiomyopathy, Hypertrophic / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D002648:Child; D005260:Female; D006325:Heart Atria / Q000032:analysis; D006331:Heart Diseases / Q000378:metabolism; D006346:Heart Septum / Q000032:analysis; D006439:Hemodynamics; D006801:Humans; D020120:Iodocyanopindolol; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000032:analysis*; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000032:analysis; D011978:Receptors, Nicotinic / Q000032:analysis*; D012530:Saxitoxin / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D015220:Calcium Channels; D011943:Receptors, Adrenergic, beta; D011978:Receptors, Nicotinic; D012530:Saxitoxin; D020120:Iodocyanopindolol; D010869:Pindolol