Profiling of cardiac beta-adrenoceptor subtypes in the cardiac left ventricle of rats with metabolic syndrome: Comparison with streptozotocin-induced diabetic rats


Okatan E. N., TUNCAY E., Hafez G., Turan B.

CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, cilt.93, sa.7, ss.517-525, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 93 Sayı: 7
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1139/cjpp-2014-0507
  • Dergi Adı: CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.517-525
  • Anahtar Kelimeler: sympathetic stimulation, high-sucrose diet, type 1 diabetes, cardiac dysfunction, intracellular calcium homeostasis, INTRACELLULAR CA2+, OXIDATIVE STRESS, WEIGHT-GAIN, SHORT-TERM, STIMULATION, ALTERNANS, SELENIUM, HEART, BETA(3)-ADRENOCEPTORS, CARDIOMYOPATHY
  • Ankara Üniversitesi Adresli: Evet

Özet

Little is known about metabolic syndrome (MetS)-associated cardiomyopathy, especially in relation to the role and contribution of beta-adrenoceptor (beta-AR) subtypes. Therefore, we examined the roles of beta-AR subtypes in the cardiac function of rats with MetS (MetS group) and compared it with that of rats with streptozotocin (STZ)-induced diabetes (STZ group). Compared with the normal control rats, the protein levels of cardiac beta(1)-and beta(2)-AR in the MetS group were significantly decreased and with no changes in their mRNA levels, whereas the protein levels of beta(3)-AR were similar to those of the controls. However, as shown previously, the protein levels of cardiac beta(1)-and beta(2)-AR in the STZ group were decreased, whereas the beta(3)-AR levels were significantly increased by comparison with the controls. Additionally, the mRNA levels of beta(2)-and beta(3)-AR were increased, but beta(1)-AR mRNA was decreased in the STZ group. Furthermore, left ventricular developed pressure responses to beta(3)-AR agonist BRL37344 were increased in the STZ group but not in the MetS group, whereas for both groups, the responses to noradrenaline were not different from those of the controls. However, the response to stimulation with high concentrations of fenoterol was depressed in the MetS group, compared with the controls, but not in the STZ group. Consequently, our data suggest that the contribution of the beta-AR system to cardiac dysfunction in the rats with MetS is not the same as that in the STZ group, although they have similar cardiac dysfunction with similar ultrastructural changes to the myocardium.