Dietary selenium and vitamin E intakes alter beta-adrenergic response of L-type Ca-current and beta-adrenoceptor-adenylate cyclase coupling in rat heart

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Sayar K., Ugur M., GÜRDAL H., ONARAN H. O., Hotomaroglu O., Turan B.

JOURNAL OF NUTRITION, cilt.130, sa.4, ss.733-740, 2000 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 130 Sayı: 4
  • Basım Tarihi: 2000
  • Doi Numarası: 10.1093/jn/130.4.733
  • Dergi Adı: JOURNAL OF NUTRITION
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.733-740
  • Anahtar Kelimeler: trace element, selenium, vitamin E, receptor-adenylate cyclase coupling, rat cardiac myoctes, LIPID-PEROXIDATION, KESHAN DISEASE, RECEPTORS, ANTIOXIDANTS, DEFICIENT, REDUCTASE, BINDING, TISSUES, PLASMA, CHINA
  • Ankara Üniversitesi Adresli: Evet

Özet

Previously we have shown that both insufficient (combined with vitamin E deficiency) and excess intake of selenium (Se) impairs isoproterenol (ISO)-induced contractions of rat papillary muscle. In the present study, we used patch-clamp and biochemical techniques to investigate mechanisms of this effect in rats fed a Se-and vitamin E-deficient, a Se-excess or a normal diet. Whole-cell configuration of patch-clamp technique was used to investigate L-type Ca2+ currents (1(Ca,L)) and their regulation by beta-adrenergic receptor stimulation in enzymatically isolated single rat ventricular myocytes. Alteration of Se and vitamin E intake did not affect peak I-Ca.L, but the threshold potential of activation was significantly different among groups. Maximal I-Ca,I-L responses to ISO were depressed in both experimental groups, but the EC50 values were not affected. In the Se-deficient group, basal, ISO- or forskolin-induced adenylate cyclase (AC) activity, measured in cardiac membrane preparations, was reduced when compared to the control, whereas 5' guanylyimidodphosphate (GppNHp) stimulated activity was unaffected. Decreased beta-adrenoceptor density and reduced GppNHp-induced affinity shift in ISO binding were also observed in the deficient group. No such differences were present in the excess group. These results suggest that combined Se and vitamin E deficiency interferes with beta-adrenoceptor-AG coupling, whereas excess intake of Se does not affect it. Thus, in the deficient group, the impairment of I-Ca responses to ISO may be a result of a defect in beta-adrenoceptor-AC pathway. Impairment of I-ca response in the excess group, however, appears to have a different underlying mechanism.