Calcium-antagonist receptors in the atrial tissue of patients with hypertrophic cardiomyopathy.

Calcium-antagonist receptors in the atrial tissue of patients with hypertrophic cardiomyopathy.
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DOI:
10.1056/nejm198903233201202
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发表时间:
1989-03
期刊:
The New England journal of medicine
影响因子:
--
通讯作者:
John A. Wagner;F. Sax;H. Weisman;J. Porterfield;C. Mcintosh;M. Weisfeldt;S. Snyder;S. Epstein
John A. Wagner;F. Sax;H. Weisman;J. Porterfield;C. Mcintosh;M. Weisfeldt;S. Snyder;S. Epstein
中科院分区:
其他
文献类型:
--
作者:
John A. Wagner;F. Sax;H. Weisman;J. Porterfield;C. Mcintosh;M. Weisfeldt;S. Snyder;S. Epstein

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肥厚型心肌病的特征是在没有任何明显原因的情况下左心室不扩张、肥大。左心室功能亢进的存在以及用β受体拮抗剂或钙拮抗剂治疗的患者所见的临床和症状改善表明肾上腺素能神经支配或细胞钙调节的可能作用。因此,我们测量了 16 名肥厚型心肌病患者和 19 名患有各种其他心脏疾病的患者心房肌中钙拮抗剂受体和 β-肾上腺素受体的密度。为了进行比较,我们还测量了电压敏感钠通道的数量。肥厚型心肌病患者的钙拮抗剂结合位点(以与心房组织结合的二氢吡啶的量来衡量)增加了 33%(肥厚型心肌病患者的平均[+/- SD]为 397 +/- 104 fmol 每毫克蛋白质,而其他心脏疾病患者为 299 +/- 108;P 小于 0.01)。电压敏感钠通道和 β 肾上腺素受体上石房蛤毒素结合位点的密度在两组中相同,但接受 β 受体拮抗剂的患者心房样本中 β 肾上腺素受体的密度较高(每毫克蛋白质 165 +/- 86 fmol [接受 β 受体阻滞剂的患者] vs. 85 +/- 60 [未接受 β 受体阻滞剂的患者];P 小于0.04)。肥厚型心肌病中钙拮抗剂受体数量的增加表明,通过电压敏感钙通道的异常钙通量可能在该疾病中发挥病理生理作用。
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.