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Brain renin-angiotensin system modifies the blood pressure response to intracerebroventricular cadmium in rats

Varoni, Maria Vittoria and Palomba, Domenico and Macciotta, Nicolò Pietro Paolo and Antuofermo, Elisabetta and Deiana, Graziella and Baralla, Elena and Anania, Vittorio Domenico and Demontis, Maria Piera (2010) Brain renin-angiotensin system modifies the blood pressure response to intracerebroventricular cadmium in rats. Drug and Chemical Toxicology, Vol. 33 (3), p. 302-309. eISSN 1525-6014. Article.

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DOI: 10.3109/01480540903418496

Abstract

In order to elucidate the involvement of the brain renin-angiotensin system (RAS) in cadmium intracerebroventricular (ICV) hypertension, we evaluated the effects of a pretreatment with different drugs: clonidine, an α2 adrenergic agonist, enalapril and captopril, both ACE inhibitors, and saralasin, a competitive nonselective AT1 and AT2 receptor antagonist. We used a rat strain with low levels of kallikrein (LKR) that was more sensitive to ICV cadmium hypertension, compared with normal kallikrein rats (NKRs), the control strain. The interplay between the kallikrein-kinin system and the RAS in the LKR strain caused various hemodynamic alterations, which we believe were the result of elevated RAS activity in these animals. Moreover, we suggest that the defective kallikrein-kinin system in LKR may also cause an alteration in the activation of brain RAS in these animals. The LKR displayed elevated concentrations of plasma AII, hypertrophy of the myocardium, and initial alterations in the renal glomerulotubular system. With the exception of clonidine, all of the other drugs showed greater antihypertensive effects of differing statistical significance in LKR, compared with NKR. Both ACE inhibitors were able to significantly reduce pressor response to cadmium ICV in LKR throughout the experiment, whereas in NKR, they were only able to reduce the hypertensive peak of cadmium. A significant protective effect was also observed in LKR pretreated with saralasin, while no effect was observed in NKR. These findings confirm the presence of brain RAS activation in LKR and its contribution to the central control of pressor response to cadmium ICV.

Item Type:Article
ID Code:7577
Status:Published
Refereed:Yes
Uncontrolled Keywords:RAS, cadmium, intracerebroventricular (ICV), kinins, kallikrein, ACE-inhibitors, AT receptor antagonist
Subjects:Area 07 - Scienze agrarie e veterinarie > AGR/17 Zootecnica generale e miglioramento genetico
Area 07 - Scienze agrarie e veterinarie > VET/07 Farmacologia e tossicologia veterinaria
Area 07 - Scienze agrarie e veterinarie > VET/03 Patologia generale e anatomia patologica veterinaria
Divisions:001 Università di Sassari > 01 Dipartimenti > Scienze zootecniche
002 Altri enti e centri di ricerca del Nord Sardegna > Istituto zooprofilattico sperimentale della Sardegna, Sassari
001 Università di Sassari > 01 Dipartimenti > Patologia e clinica veterinaria
001 Università di Sassari > 01 Dipartimenti > Biologia animale
Publisher:Informa Healthcare
eISSN:1525-6014
Deposited On:17 May 2012 11:57

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