Effect of magnesium supplementation on blood pressure and vascular reactivity in nitric oxide synthase inhibition-induced hypertension model.


BASRALI F., Kocer G., KARADAMAR P. U., ULKER S. N., SATI L., ÖZEN N., ...Daha Fazla

Clinical and experimental hypertension (New York, N.Y. : 1993), cilt.37, sa.8, ss.633-42, 2015 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 37 Sayı: 8
  • Basım Tarihi: 2015
  • Doi Numarası: 10.3109/10641963.2015.1036063
  • Dergi Adı: Clinical and experimental hypertension (New York, N.Y. : 1993)
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.633-42
  • Anahtar Kelimeler: Hypertension, blood pressure, nitric oxide, magnesium, vascular tonus, CHRONIC NOS INHIBITION, RESISTANCE ARTERIES, DEOXYCORTICOSTERONE ACETATE, ORAL MAGNESIUM, MINERAL SALT, RATS, CALCIUM, EXERCISE, ENDOTHELIN-1, MECHANISMS
  • Akdeniz Üniversitesi Adresli: Evet

Özet

The aim of this study was to assess the effect of oral magnesium supplementation (Mg-supp) on blood pressure (BP) and possible mechanism in nitric oxide synthase (NOS) inhibition-induced hypertension model. Hypertension and/or Mg-supp were created by N-nitro-l-arginine methyl ester (25mg/kg/day by drinking water) and magnesium-oxide (0.8% by diet) for 6 weeks. Systolic BP was measured weekly by tail-cuff method. The effects of hypertension and/or Mg-supp in thoracic aorta and third branch of mesenteric artery constriction and relaxation responses were evaluated. NOS-inhibition produced a gradually developing hypertension and the magnitude of the BP was significantly attenuated after five weeks of Mg-supp. The increased phenylephrine-induced contractile and decreased acetylcholine (ACh)-induced dilation responses were found in both artery segments of hypertensive groups. Mg-supp was restored ACh-relaxation response in both arterial segments and also Phe-constriction response in thoracic aorta but not in mesenteric arteries. The contributions of NO, prostaglandins and K+ channels to the dilator response of ACh were similar in the aorta of all the groups. The contribution of the NO to the ACh-mediated relaxation response of mesenteric arteries was suppressed in hypertensive rats, whereas this was corrected by Mg-supp. The flow-mediated dilation response of mesenteric arteries in hypertensive rats failed and could not be corrected by Mg-supp. Whereas, vascular eNOS protein and magnesium levels were not changed and plasma nitrite levels were reduced in hypertensive rats. The results of this study showed that Mg-supp lowered the arterial BP in NOS-inhibition induced hypertension model by restoring the agonist-induced relaxation response of the arteries.