Hypothalamic and Plasmatic Angiotensin Metabolism in L-NAME Treated Rats

A. B. Segarra; M. Ramírez; A. B. Villarejo; I. Banegas; F. Vives; M. de Gasparo; F. Alba; J. Cobo; I. Prieto

doi:10.1055/s-0029-1243600

Hormone and Metabolic Research, Inhaltsverzeichnis

Horm Metab Res 2010; 42(3): 222-224
DOI: 10.1055/s-0029-1243600

Short Communication

Hypothalamic and Plasmatic Angiotensin Metabolism in L-NAME Treated Rats

A. B. Segarra¹ , M. Ramírez¹ , A. B. Villarejo¹ , I. Banegas¹ , F. Vives² , M. de Gasparo³ , F. Alba² , J. Cobo⁴ , I. Prieto¹

¹Unit of Physiology, Department of Health Sciences, University of Jaén, Spain
²Instituto de Neurociencia ‘Federico Oloriz’, University of Granada, Granada, Spain
³MGConsulting Co. Rossemaison, Switzerland
⁴Department of Inorganic and Organic Chemistry, University of Jaén, Spain

Abstract

In order to study the interaction between the renin-angiotensin system (RAS) and nitric oxide (NO), we analyzed the activity of aspartyl- (AspAP), glutamyl- (GluAP), alanyl- (AlaAP), and cystinylaminopeptidase (CysAP) enzymes involved in the RAS cascade, in the hypothalamus, and plasma of normotensive adult male rats after the inhibition of NO production with the NO synthase inhibitor L-NAME (L-N^G-nitroarginine methyl ester). L-NAME treatment produced a significant increase of systolic blood pressure (SBP). In plasma, while GluAP activity decreased significantly, suggesting a lower Ang III formation, the other aminopeptidases did not change after L-NAME treatment. In hypothalamus, the activities of AspAP and CysAP were not affected after L-NAME treatment. In contrast, GluAP and AlaAP increased significantly. These results suggested mainly a higher formation of Ang III, but also higher levels of Ang IV in the hypothalamus of L-NAME treated rats. Both peptides have hypertensive properties at central level. On the contrary, Ang III may counteract the hypertensive action of Ang II at the periphery. Therefore, the increased SBP in L-NAME treated rats may be due in part to the increased activity of GluAP and AlaAP in hypothalamus and to a decreased activity of GluAP in plasma.

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Correspondence

M. Ramírez-Sanchez

Unit of Physiology

University of Jaén

23071 Jaén

Spain

Telefon: +34 953 212302

Fax: +34 953 212 943

eMail: msanchez@ujaen.es