HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 285/1/E182    most recent 00558.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Moreno, J. M. Articles by Vargas, F. Search for Related Content PubMed PubMed Citation Articles by Moreno, J. M. Articles by Vargas, F.

Role of endothelium-derived relaxing factors in the renal response to vasoactive agents in hypothyroid rats

Departamento de Fisiología, Facultad de Medicina, Servicio de Nefrología, Unidad Experimental, Hospital Virgen de las Nieves, 118012 Granada, Spain

Submitted 19 December 2002 ; accepted in final form 18 March 2003

This study analyzed the role of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) in the abnormal renal vascular reactivity of hypothyroid rats. Renal responses to vasoconstrictors [VC: phenylephrine (PHE) and ANG II] and vasodilators [VD: ACh, sodium nitroprusside (SNP), and papaverine (PV)] were studied in kidneys from control and hypothyroid rats under normal conditions and after NO or EDHF blockade. NO was blocked by the administration of N-nitro-L-arginine methyl ester (L-NAME) and EDHF by the administration of tetraethylammonium (TEA) or by an increased extracellular K⁺. The response to VC was also evaluated after endothelium removal. Hypothyroid kidneys showed reduced responsiveness to PHE and a normal response to ANG II. L-NAME and TEA administration produced an increased sensitivity to PHE and to ANG II in control preparations. L-NAME also increased the response to PHE in hypothyroid kidneys, but the differences between control and hypothyroid kidneys were maintained. TEA administration did not change the response to either VC in hypothyroid preparations. In endothelium-removed preparations, TEA was unable to increase pressor responsiveness to VC. Hypothyroid kidneys showed reduced responsiveness to ACh and SNP and normal response to PV. The differences between hypothyroid and control preparations in the responses to ACh and SNP were maintained after L-NAME or increased K⁺. In conclusion, this study shows that 1) the attenuated response to PHE in hypothyroidism is not related to an increased production of endothelium-derived relaxing factors NO and EDHF; 2) the response to VC in hypothyroid preparations is insensitive to EDHF blockade; and 3) hypothyroid preparations have a reduced reactivity to the NO donor, and NO-independent vasodilatation remains unaffected.

hypothyroidism; nitric oxide; endothelium-derived hyperpolarizing factor; vasoconstriction; vasodilatation

This article has been cited by other articles:

				S. Cinti, G. Mitchell, G. Barbatelli, I. Murano, E. Ceresi, E. Faloia, S. Wang, M. Fortier, A. S. Greenberg, and M. S. Obin Adipocyte death defines macrophage localization and function in adipose tissue of obese mice and humans J. Lipid Res., November 1, 2005; 46(11): 2347 - 2355. [Abstract] [Full Text] [PDF]

				F. A. Dinenno and M. J. Joyner Combined NO and PG inhibition augments {alpha}-adrenergic vasoconstriction in contracting human skeletal muscle Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2576 - H2584. [Abstract] [Full Text] [PDF]