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

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SAYAR K., UĞUR 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
  • Lokman Hekim Üniversitesi Adresli: Hayır

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 (I(Ca,L)) and their regulation by β- 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.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 β-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 β-adrenoceptor-AC 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 β-adrenoceptor-AC pathway. Impairment of I(Ca) response in the excess group, however, appears to have a different underlying mechanism.