Reactivity of the Mesenteric Vessels to Norepinephrine in Rats Treated with Co-protoporphyrin IX or Sn-protoporphyrin IX

Background. Heme oxygenase (HO) catalyzes the conversion of heme to biliverdin with the release of iron and carbon monoxide. Various HO-1 modification factors are known, but blood vessel reactivity to them has not been established. Objectives. To evaluate the impact of Co-protoporphyrin IX (a HO-1 inducer) and Sn-protoporphyrin IX (a HO-1 inhibitor) on the reactivity of rats' isolated mesenteric blood vessels. Material and Methods. Male Buffalo rats weighing 155 to 185 g were given Co-protoporphyrin IX (CoPPIX) or Sn-protoporphyrin IX (SnPPIX) intraperitoneally at a dosage of 1.5 mg/kg b.w. Control rats were given 0.9% NaCl solution. The rats were anesthetized with ketaminum (300 mg/kg intramuscularly) and the superior mesenteric artery was isolated, cannulated and removed with its small resistance vessels. Results. The reactivity of mesenteric vessels to norepinephrine (NE) given in doses from 0.1 to 5.0 mu g did not differ significantly in the rats treated with porphyrins and in the controls. However, the NE50 dose estimated for the SnPPIX- and CoPPIX-treated rats was lower in comparison to the controls (p < 0.02 and p < 0.01, respectively). The mesenteric vessels from the SnPPIX- treated rats showed an increased response to NE50 in comparison to the controls (p < 0.001). Also, L-omega-NOARG (1.0 mu g/ml/min) infused into the mesenteric arteries from the SnPPIX- treated rats induced higher perfusion pressure (p < 0.05). NE injected after L-omega-NOARG infusion caused similar changes in perfusion pressure in all preparations. The reactivity of the mesenteric bed to an injection of NE50 after infusions of acetylcholine (0.5 mu g/ml/min) or propranolol (0.3 mu g/ml/min) was also similar in all groups of rats. Conclusions. The study showed an increased response of the mesenteric artery wall to the vasoconstrictor action of norepinephrine in rats treated with a heme oxygenase-1 inhibitor. Decreased production of carbon monoxide is at least partially responsible for this altered response (Adv Clin Exp Med 2010, 19, 5, 555-561).