• DOI:10.1152/AJPHEART.1991.261.3.H830
• Corpus ID: 34719649

Two mechanisms mediate relaxation by bradykinin of pig coronary artery: NO-dependent and -independent responses.

@article{Cowan1991TwoMM,
  title={Two mechanisms mediate relaxation by bradykinin of pig coronary artery: NO-dependent and -independent responses.},
  author={C L Cowan and Richard Alan Cohen},
  journal={The American journal of physiology},
  year={1991},
  volume={261 3 Pt 2},
  pages={
          H830-5
        }
}

• C. L. Cowan, R. Cohen
• Published 1 September 1991
• Biology
• The American journal of physiology

The role of nitric oxide and guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in the endothelium-dependent relaxation of the porcine coronary artery to bradykinin was investigated by comparing relaxation and cGMP accumulation in the presence or absence of NG-monomethyl-L-arginine (L-NMMA) and methylene blue. Rings were treated with indomethacin to eliminate the effects of prostaglandins. Relaxation to bradykinin of rings contracted with the thromboxane A2 mimetic U-46619 was not affected by L-NMMA and was only minimally inhibited by methylene blue. Rings contracted with elevated potassium (25 mM) also relaxed completely to bradykinin. However, L-NMMA or methylene blue effectively inhibited relaxation to bradykinin in rings contracted with potassium. cGMP accumulation was stimulated by bradykinin and inhibited by L-NMMA or methylene blue in rings contracted with either U-46619 or potassium. These results suggest that in the absence of nitric oxide-induced cGMP accumulation, a nonprostanoid mechanism exists that is capable of completely relaxing U-46619-contracted coronary artery. This mechanism is either inhibited in or unable to relax potassium-contracted rings. These results also demonstrate that nitric oxide mediates the bradykinin-induced cGMP accumulation that is largely responsible for the relaxation during contraction with potassium.