Information de reference pour ce titreAccession Number: | 00003012-199910010-00008.
|
Author: | Hein, Travis W.; Kuo, Lih
|
Institution: | From the Department of Medical Physiology, Cardiovascular Research Institute, Texas A&M University System Health Science Center, College Station, Tex.
|
Title: | cAMP-Independent Dilation of Coronary Arterioles to Adenosine: Role of Nitric Oxide, G Proteins, and KATP Channels.[Miscellaneous Article]
|
Source: | Circulation Research. 85(7):634-642, October 1, 1999.
|
Abstract: | Adenosine is known to play an important role in the regulation of coronary blood flow during metabolic stress. However, there is sparse information on the mechanism of adenosine-induced dilation at the microcirculatory levels. In the present study, we examined the role of endothelial nitric oxide (NO), G proteins, cyclic nucleotides, and potassium channels in coronary arteriolar dilation to adenosine. Pig subepicardial coronary arterioles (50 to 100 [mu]m in diameter) were isolated, cannulated, and pressurized to 60 cm H2O without flow for in vitro study. The arterioles developed basal tone and dilated dose dependently to adenosine. Disruption of endothelium, blocking of endothelial ATP-sensitive potassium (KATP) channels by glibenclamide, and inhibition of NO synthase by NG-nitro-L-arginine methyl ester and of soluble guanylyl cyclase by 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one produced identical attenuation of vasodilation to adenosine. Combined administration of these inhibitors did not further attenuate the vasodilatory response. Production of NO from coronary arterioles was significantly increased by adenosine. Pertussis toxin, but not cholera toxin, significantly inhibited vasodilation to adenosine, and this inhibitory effect was only evident in vessels with an intact endothelium. Tetraethylammonium, glibenclamide, and a high concentration of extraluminal KCl abolished vasodilation of denuded vessels to adenosine; however, inhibition of calcium-activated potassium channels by iberiotoxin had no effect on this dilation. Rp-8-Br-cAMPS, a cAMP antagonist, inhibited vasodilation to cAMP analog 8-Br-cAMP but failed to block adenosine-induced dilation. Furthermore, vasodilations to 8-Br-cAMP and sodium nitroprusside were not inhibited by glibenclamide, indicating that cAMP- and cGMP-induced dilations are not mediated by the activation of KATP channels. These results suggest that adenosine activates both endothelial and smooth muscle pathways to exert its vasodilatory function. On one hand, adenosine opens endothelial KATP channels through activation of pertussis toxin-sensitive G proteins. This signaling leads to the production and release of NO, which subsequently activates smooth muscle soluble guanylyl cyclase for vasodilation. On the other hand, adenosine activates smooth muscle KATP channels and leads to vasodilation through hyperpolarization. It appears that the latter vasodilatory process is independent of G proteins and of cAMP/cGMP pathways.
(C) 1999 American Heart Association, Inc.
|
Author Keywords: | adenosine; microcirculation; nitric oxide; K+ channel.
|
References: | 1. Nakhostine N, Lamontagne D. Adenosine contributes to hypoxia-induced vasodilation through ATP-sensitive K+ channel activation. Am J Physiol. 1993;265:H1289-H1293.
2. Ely SW, Berne RM. Protective effects of adenosine in myocardial ischemia. Circulation. 1992;85:893-904.
3. Berne RM. The role of adenosine in the regulation of coronary blood flow. Circ Res. 1980;47:807-813.
4. Olsson RA, Pearson JD. Cardiovascular purinoceptors. Physiol Rev. 1990;70:761-845.
5. Schiele JO, Schwabe U. Characterization of the adenosine receptor in microvascular coronary endothelial cells. Eur J Pharmacol. 1994;269:51-58.
6. Parent R, Pare R, Lavallee M. Contribution of nitric oxide to dilation of resistance coronary vessels in conscious dogs. Am J Physiol. 1992;262:H10-H16.
7. Vials A, Burnstock G. A2-purinoceptor-mediated relaxation in the guinea-pig coronary vasculature: a role for nitric oxide. Br J Pharmacol. 1993;109:424-429.
8. Abebe W, Hussain T, Olanrewaju H, Mustafa SJ. Role of nitric oxide in adenosine receptor-mediated relaxation of porcine coronary artery. Am J Physiol. 1995;269:H1672-H1678.
9. Sabouni MH, Hussain T, Cushing DJ, Mustafa SJ. G proteins subserve relaxations mediated by adenosine receptors in human coronary artery. J Cardiovasc Pharmacol. 1991;18:696-702.
10. Mustafa SJ, Askar AO. Evidence suggesting an Ra-type adenosine receptor in bovine coronary arteries. J Pharmacol Exp Ther. 1985;232:49-56.
11. Murray KJ. Cyclic AMP and mechanisms of vasodilation. Pharmacol Ther. 1990;47:329-345.
12. Silver PJ, Kazmerez W, DiSalvo J. Adenosine-mediated relaxation and activation of cyclic AMP-dependent protein kinase in coronary arterial smooth muscle. J Pharmacol Exp Ther. 1984;228:342-347.
13. Jackson WF, Konig A, Dambacher T, Busse R. Prostacyclin-induced vasodilation in rabbit heart is mediated by ATP-sensitive potassium channels. Am J Physiol. 1993;264:H238-H243.
14. King AD, Milavec-Krizman M, Muller-Schweinitzer E. Characterization of the adenosine receptor in porcine coronary arteries. Br J Pharmacol. 1990;100:483-486.
15. White TD, Angus JA. Relaxant effects of ATP and adenosine on canine large and small coronary arteries in vitro. Eur J Pharmacol. 1987;143:119-126.
16. Jones CJH, Kuo L, Davis MJ, Chilian WM, DeFily DV. Role of nitric oxide in the coronary microvascular responses to adenosine and increased metabolic demand. Circulation. 1995;91:1807-1813.
17. Matsunaga T, Okumura K, Tsunoda R, Tayama S, Tabuchi T, Yasue H. Role of adenosine in regulation of coronary flow in dogs with inhibited synthesis of endothelium-derived nitric oxide. Am J Physiol. 1996;270:H427-H434.
18. Makujina SR, Olanrewaju HA, Mustafa SJ. Evidence against KATP channel involvement in adenosine receptor-mediated dilation of epicardial vessels. Am J Physiol. 1994;267:H716-H724.
19. Herlihy JT, Bockman EL, Berne RM, Rubio R. Adenosine relaxation of isolated vascular smooth muscle. Am J Physiol. 1976;230:1239-1243.
20. Cushing DJ, Brown GL, Sabouni MH, Mustafa SJ. Adenosine receptor-mediated coronary artery relaxation and cyclic nucleotide production. Am J Physiol. 1991;261:H343-H348.
21. Chilian WM, Eastham CL, Marcus ML. Microvascular distribution of coronary vascular resistance in beating left ventricle. Am J Physiol. 1986;251:H779-H788.
22. Kuo L, Chancellor JD. Adenosine potentiates flow-induced dilation of coronary arterioles by activating KATP channels in endothelium. Am J Physiol. 1995;269:H541-H549.
23. Dunne MJ, Bullett MJ, Li G, Wollheim CB, Petersen OH. Galanin activates nucleotide-dependent K+ channels in insulin-secreting cells via a pertussis toxin-sensitive G-protein. EMBO J. 1989;8:413-420.
24. Kirsch GE, Codina J, Birnbaumer L, Brown AM. Coupling of ATP-sensitive K+ channels to A1 receptors by proteins in rat ventricular myocytes. Am J Physiol. 1990;259:H820.
25. Kuo L, Davis MJ, Chilian WM. Myogenic activity in isolated subepicardial and subendocardial coronary arterioles. Am J Physiol. 1988;255:H1558-H1562.
26. Kuo L, Chilian WM, Davis MJ. Interaction of pressure- and flow-induced responses in porcine coronary resistance vessels. Am J Physiol. 1991;261:H1706-H1715.
27. Ishizaka H, Kuo L. Acidosis-induced coronary arteriolar dilation is mediated by ATP-sensitive potassium channels in vascular smooth muscle. Circ Res. 1996;78:50-57.
28. Nelson MT, Quayle JM. Physiological roles and properties of potassium channels in arterial smooth muscle. Am J Physiol. 1995;268:C799-C822.
29. Nelson MT. Ca2+-activated potassium channels and ATP-sensitive potassium channels as modulators of vascular tone. Trends Cardiovasc Med. 1993;3:54-60.
30. Shimokawa H, Flavahan NA, Vanhoutte PM. Loss of endothelial pertussis toxin-sensitive G protein function in atherosclerotic porcine coronary arteries. Circulation. 1991;83:652-660.
31. Ishizaka H, Gudi SR, Frangos JA, Kuo L. Coronary arteriolar dilation to acidosis: role of ATP-sensitive potassium channels and pertussis toxin-sensitive G proteins. Circulation. 1999;99:558-563.
32. Botelho LHP, Rothermel JD, Coombs RV, Jastorff B. cAMP analog antagonists of cAMP action. Methods Enzymol. 1988;159:159-172.
33. Cellek S, Kasakov L, Moncada S. Inhibition of nitrergic relaxations by a selective inhibitor of the soluble guanylate cyclase. Br J Pharmacol. 1996;118:137-140.
34. Crooks MJ, Brown KF. The binding of sulfonylureas to serum albumin. J Clin Pharmacol. 1976;25:1175-1178.
35. Olsen KM, Kearns GL, Kemp SF. Glyburide protein binding and the effect of albumin glycation in children, young adults, and older adults with diabetes. J Clin Pharmacol. 1995;35:739-745.
36. Hein TW, Kuo L. LDLs impair vasomotor function of the coronary microcirculation: role of superoxide anions. Circ Res. 1998;83:404-414.
37. Armstead WM. Role of ATP-sensitive K+ channels in cGMP-mediated pial artery vasodilation. Am J Physiol. 1996;270:H423-H426.
38. Rubanyi G, Vanhoutte PM. Endothelium-removal decreases relaxations of canine coronary arteries caused by [beta]-adrenergic agonists and adenosine. J Cardiovasc Pharmacol. 1985;7:139-144.
39. Newman WH, Becker BF, Heier M, Nees S, Gerlach E. Endothelium-mediated coronary dilation by adenosine does not depend on endothelial adenylate cyclase activation: studies in isolated guinea pig hearts. Pflugers Arch. 1988;413:1-7.
40. Davis CA III, Sherman AJ, Yaroshenko Y, Harris KR, Hedjbeli S, Parker MA, Klocke FJ. Coronary vascular responsiveness to adenosine is impaired additively by blockade of nitric oxide synthesis and a sulfonylurea. J Am Coll Cardiol. 1998;31:816-822.
41. Canty JM Jr, Schwartz JS. Nitric oxide mediates flow-dependent epicardial coronary vasodilation to changes in pulse frequency but not mean flow in conscious dogs. Circulation. 1994;89:375-384.
42. Gurevicius J, Salem MR, Metwally AA, Silver JM, Crystal GJ. Contribution of nitric oxide to coronary vasodilation during hypercapnic acidosis. Am J Physiol. 1995;268:H39-H47.
43. Arnold WP, Mittal CK, Katsuki S, Murad F. Nitric oxide activates guanylate cyclase and increases guanosine 3':5'-cyclic monophosphate levels in various tissue preparations. Proc Natl Acad Sci U S A. 1977;74:3203-3207.
44. Murphy ME, Brayden JE. Nitric oxide hyperpolarizes rabbit mesenteric arteries via ATP-sensitive potassium channels. J Physiol. 1995;486:47-58.
45. Bolotina VM, Najibi S, Palacino JJ, Pagano PJ, Cohen RA. Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle. Nature. 1994;368:850-852.
46. Luckhoff A, Busse R. Calcium influx into endothelial cells and formation of endothelium-derived relaxing factor is controlled by the membrane potential. Pflugers Arch. 1990;416:305-311.
47. Seiss-Geuder M, Mehrke G, Daut J. Sustained hyperpolarization of cultured guinea pig coronary endothelial cells induced by adenosine. J Cardiovasc Pharmacol. 1992;20:S97-S100.
48. vanCalker D, Hamprecht B. Adenosine regulates via two different types of receptors, the accumulation of cyclic AMP in cultured brain cells. J Neurochem. 1979;33:999-1005.
49. Sabouni MH, Cushing DJ, Mustafa SJ. Adenosine receptor-mediated relaxation in coronary artery: evidence for a guanylyl nucleotide-binding regulatory protein involvement. J Pharmacol Exp Ther. 1989;251:943-948.
50. Miyoshi H, Nakaya Y. Activation of ATP-sensitive K+ channels by cyclic AMP-dependent protein kinase in cultured smooth muscle cells of porcine coronary artery. Biochem Biophys Res Commun. 1993;193:240-247.
|
Language: | English.
|
Document Type: | Integrative Physiology.
|
Journal Subset: | Clinical Medicine.
|
ISSN: | 0009-7330
|
NLM Journal Code: | daj, 0047103
|
Annotation(s) | |
|
|