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ORIGINAL RESEARCH ARTICLE

Adrenergic Response of Splanchnic Arteries from Cirrhotic Patients: Role of Nitric Oxide, Prostanoids, and Reactive Oxygen Species

Adely Salcedo^*, Jesús Garijo, Luis Monge^*, Nuria Fernández^*, Angel Luis García-Villalón^*, Víctor Sánchez Turrión, Valentín Cuervas-Mons and Godofredo DiéGuez^*,1

^* Departamento de Fisiología and Unidad de Transplante Hepático, Hospital Universitario "Puerta de Hierro," Facultad de Medicina, Universidad Autónoma, Madrid, Spain

To whom requests for reprints should be addressed at ¹ Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo, 228029 Madrid, Spain. E-mail: gdieguez{at}uam.es

Peripheral and splanchnic vasodilatation in cirrhotic patients has been related to hyporesponsiveness to vasoconstrictors, but studies to examine the vascular adrenergic response provide contradictory results. Hepatic arteries from cirrhotic patients undergoing liver transplantation and mesenteric arteries from liver donors were obtained. Segments 3 mm long from these arteries were mounted in organ baths for testing isometric adrenergic response. The concentration-dependent contraction to noradrenaline (10^–8 to 10^–4 M) was similar in hepatic and mesenteric arteries, and prazosin ( 1-adrenergic antagonist, 10^–6 M), but not yohimbine ( 2-adrenergic antagonist, 10^–6 M), produced a rightward parallel displacement of this contraction in both types of arteries. Phenylephrine ( 1-adrenergic agonist, 10^–8 to 10^–4 M) and clonidine ( 2-adrenergic agonist, 10^–8 to 10^–4 M) also produced concentration-dependent contractions that were comparable in hepatic and mesenteric arteries. The inhibitor of cyclooxygenase meclofenamate (10^–5 M), but not the inhibitor of nitric oxide synthesis N^w-nitro-L-arginine methyl ester (L-NAME, 10^–4 M), potentiated the response to noradrenaline in hepatic arteries; neither inhibitor affected the response to noradrenaline in mesenteric arteries. Diphenyleneiodonium (DPI; 5 x 10^–6 M), but neither catalase (1000 U/ml) nor tiron (10^–4 M), decreased the maximal contraction for noradrenaline similarly in hepatic and mesenteric arteries. Therefore, it is suggested that, in splanchnic arteries from cirrhotic patients, the adrenergic response and the relative contribution of 1- and 2-adrenoceptors in this response is preserved, and prostanoids, but not nitric oxide, may blunt that response. Products dependent on NAD(P)H oxidase might contribute to the adrenergic response in splanchnic arteries from control and cirrhotic patients.

Key Words: hepatic arteries • vasoconstriction • 1-adrenoceptors • 2-adrenoceptors • prostacyclin