0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: not found
      • Article: not found

      Differential effects of hydroxocobalamin on NO-mediated relaxations in rat aorta and anococcygeus muscle

      , ,
      British Journal of Pharmacology
      Wiley

      Read this article at

      ScienceOpenPublisher
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Related collections

          Most cited references6

          • Record: found
          • Abstract: found
          • Article: not found

          Endothelium-derived relaxing factor from pulmonary artery and vein possesses pharmacologic and chemical properties identical to those of nitric oxide radical.

          The objective of this study was to elucidate the close similarity in properties between endothelium-derived relaxing factor (EDRF) and nitric oxide radical (NO). Whenever possible, a comparison was also made between arterial and venous EDRF. In vascular relaxation experiments, acetylcholine and bradykinin were used as endothelium-dependent relaxants of isolated rings of bovine intrapulmonary artery and vein, respectively, and NO was used to relax endothelium-denuded rings. Oxyhemoglobin produced virtually identical concentration-dependent inhibitory effects on both endothelium-dependent and NO-elicited relaxation. Oxyhemoglobin and oxymyoglobin lowered cyclic guanosine monophosphate (cGMP) levels, increased tone in unrubbed artery and vein, and abolished the marked accumulation of vascular cGMP caused both by endothelium-dependent relaxants and by NO. The marked inhibitory effects of oxyhemoglobin on arterial and venous relaxant responses and cGMP accumulation as well as its contractile effects were abolished or reversed by carbon monoxide. These observations indicate that EDRF and NO possess identical properties in their interactions with oxyhemoproteins. Both EDRF from artery and vein and NO activated purified soluble guanylate cyclase by heme-dependent mechanisms, thereby revealing an additional similarity in heme interactions. Spectrophotometric analysis disclosed that the characteristic shift in the Soret peak for hemoglobin produced by NO was also produced by an endothelium-derived factor released from washed aortic endothelial cells by acetylcholine or A23187. Pyrogallol, via the action of superoxide anion, markedly inhibited the spectral shifts, relaxant effects, and cGMP accumulating actions produced by both EDRF and NO. Superoxide dismutase enhanced the relaxant and cGMP accumulating effects of both EDRF and NO. Thus, EDRF and NO are inactivated by superoxide in a closely similar manner. We conclude, therefore, that EDRF from artery and vein is either NO or a chemically related radical species.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Nitrergic transmission: nitric oxide as a mediator of non-adrenergic, non-cholinergic neuro-effector transmission.

            1. The possibility that transmission at some non-adrenergic, non-cholinergic (NANC) neuro-effector junctions is mediated by nitric oxide (NO) arose from the discoveries that NO mediated the effects of nitrovasodilator drugs and that endothelium-derived relaxing factor (EDRF) was NO or a NO-yielding substance. 2. NO donated by nitrovasodilator drugs or formed by endothelial cells activates soluble guanylate cyclase in smooth muscle and the consequent increase in cyclic guanosine monophosphate (cGMP) results in relaxation. The relaxations produced by stimulation of some NANC nerves are also due to a rise in cGMP. 3. The biosynthesis of NO by oxidation of a terminal guanidino nitrogen of L-arginine is inhibited by some NG-substituted analogues of L-arginine. These substances block EDRF formation by NO synthase and endothelium-dependent vasodilatation, and the blockade is overcome by L-arginine 4. NANC relaxations in some tissues are blocked by NG-substituted analogues of L-arginine and restored by L-arginine. Other agents that affect endothelium-dependent vasodilator responses produce corresponding changes in responses to stimulation of these NANC nerves. Such observations indicate that transmission is mediated by NO: we have termed this mode of transmission nitrergic. 5. There is evidence for nitrergic innervation of smooth muscle in the gastrointestinal tract, genito-urinary system, trachea and some blood vessels (penile and cerebral arteries). 6. The recognition of a mediator role for NO in neurotransmission calls for reconsideration of previously accepted generalizations about mechanisms of transmission. 7. Studies on nitrergic transmission will provide new insights into physiological control mechanisms and pathophysiological processes and may lead to new therapeutic developments.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              EVIDENCE FOR A ROLE OF NITRIC OXIDE IN THE NEUROTRANSMITTER SYSTEM MEDIATING RELAXATION OF THE RAT ANOCOCCYGEUS MUSCLEC

              C Li, M Rand (1989)
                Bookmark

                Author and article information

                Journal
                British Journal of Pharmacology
                Wiley
                00071188
                January 1993
                January 1993
                July 19 2012
                : 108
                : 1
                : 3-5
                Article
                10.1111/j.1476-5381.1993.tb13429.x
                77831a07-a72a-442d-a86f-2162bedd07c7
                © 2012

                http://doi.wiley.com/10.1002/tdm_license_1.1

                History

                Comments

                Comment on this article