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Adenosine Regulates Renal Nitric Oxide Production in Hypothyroid Rats

MARTHA FRANCO^*, EDILIA TAPIA^*, FLAVIO MARTÍNEZ, MA. EUGENIA DAVILA, JUANA INÉS GRIMALDO, KLELIA MEDINA^* and JAIME HERRERA-ACOSTA^*

^* Department of Nephrology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Department of Pharmacology Facultad de Medicina, San Luis Potosí, Mexico.
Department of Nuclear Medicine, Facultad de Medicina, San Luis Potosí, Mexico.

Correspondence to Dr. Martha Franco, Nephrology Department, Instituto Nacional de Cardiología, Juan Badiano No. 1, Mexico City, Tlalpan 14080, Mexico. Phone: 525-573-6902; Fax: 525-573-7716; E-mail: jherrera{at}rtn.net.mx .

Abstract

Abstract. In the hypothyroid kidney, exogenous adenosine (ADO) produces vasodilation and restores renal function to near-normal values. This study evaluates whether this response is mediated by nitric oxide synthesis stimulated by adenosine. GFR and urinary excretion of NO₂^-/NO₃^- (UNO₂^-/NO₃^-) were measured in normal (NL) and hypothyroid (HTX) rats under basal conditions and during infusion of: intra-aortic ADO, intravenously, 1,3-dipropyl-8p-sulfophenylxanthine (DPSPX), 8-cyclopentyl-1,3-dipropyl xanthine (DPCPX), N-nitro-L-arginine methylester (L-NAME) + ADO, L-NAME + PSPX, L-NAME + DPCPX, and intrarenal (IR) ADO or DPCPX + IR ADO. Intra-aortic ADO induced a fall in GFR and increased UNO₂^-/NO₃^- slightly in NL rats; in HTX rats, both GFR and UNO₂^-/NO₃^- increased significantly. DPSPX and DPCPX increased UNO₂^-/NO₃^- excretion in NL animals with minor changes in GFR; the blockers increased both GFR and UNO₂^-/NO₃^- in HTX rats. L-NAME completely blocked the increase in NO₂^-/NO₃^- induced by ADO, DPSPX, and DPCPX. The intrarenal infusion of ADO at 1, 10, and 35 nmol/kg per min progressively decreased GFR with a slight increase in UNO₂^-/NO₃^- in NL rats; in the HTX, GFR increased with the highest dose and UNO₂^-/NO₃^- progressively increased. DPCPX prevented the fall in GFR induced by intrarenal ADO in NL rats, with no further changes in UNO₂^-/NO₃^-; in HTX rats, intrarenal ADO under A1 blockade further increased GFR and UNO₂^-/NO₃^-. Arterial and venous ADO concentrations were lower in the HTX rats. In the HTX kidney, NO production was stimulated by ADO, most likely through activation of A2 or A3 receptors, whereas A1 receptors had an inhibitory effect. Thus, ADO receptors are involved in the regulation of kidney function in pathophysiologic conditions.

This article has been cited by other articles:

				M. Franco, R. Bautista, O. Perez-Mendez, L. Gonzalez, U. Pacheco, L. G. Sanchez-Lozada, J. Santamaria, E. Tapia, R. Monreal, and F. Martinez Renal interstitial adenosine is increased in angiotensin II-induced hypertensive rats Am J Physiol Renal Physiol, January 1, 2008; 294(1): F84 - F92. [Abstract] [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673