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4 results on '"Michea L"'

1. Low-Chloride Diet Prevents the Development of Arterial Hypertension and Protects Kidney Function in Angiotensin II-Infused Mice.

Author

Liberona J, Araos P, Rodríguez M, León P, Stutzin A, Alzamora R, and Michea L

Subjects
Animals, Mice, Cardiomegaly prevention & control, Cardiomegaly chemically induced, Chlorides administration & dosage, Chlorides pharmacology, Glomerular Filtration Rate drug effects, Mice, Inbred C57BL, Sodium Chloride, Dietary adverse effects, Sodium Chloride, Dietary administration & dosage, Angiotensin II pharmacology, Blood Pressure drug effects, Hypertension chemically induced, Hypertension prevention & control, Kidney drug effects
Abstract

Introduction: A comprehensive pathophysiological mechanism to explain the relationship between high-salt intake and hypertension remains undefined. Evidence suggests that chloride, as the accompanying anion of sodium in dietary salt, is necessary to develop hypertension. We evaluated whether reducing dietary Cl- while keeping a standard Na+ intake modified blood pressure, cardiac hypertrophy, renal function, and vascular contractility after angiotensin II (AngII) infusion., Methods: C56BL/6J mice fed with standard Cl- diet or a low-Cl- diet (equimolar substitution of Cl- by a mixture of Na+ salts, both diets with standard Na+ content) received AngII (infusion of 1.5 mg/kg/day) or vehicle for 14 days. We measured systolic blood pressure (SBP), glomerular filtration rate (GFR), natriuretic response to acute saline load, and contractility of aortic rings from mice infused with vehicle and AngII, in standard and low-Cl- diet., Results: The mice fed the standard diet presented increased SBP and cardiac hypertrophy after AngII infusion. In contrast, low-Cl- diet prevented the increase of SBP and cardiac hypertrophy. AngII-infused mice fed a standard diet presented hampered natriuretic response to saline load, meanwhile the low-Cl- diet preserved natriuretic response in AngII-infused mice, without change in GFR. Aortic rings from mice fed with standard diet or low-Cl- diet and infused with AngII presented a similar contractile response., Conclusion: We conclude that the reduction in dietary Cl- as the accompanying anion of sodium in salt is protective from AngII pro-hypertensive actions due to a beneficial effect on kidney function and preserved natriuresis., (© 2024 The Author(s). Published by S. Karger AG, Basel.)

Published
2024
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2. Myeloid CD11c + Antigen-Presenting Cells Ablation Prevents Hypertension in Response to Angiotensin II Plus High-Salt Diet.

Author

Hevia D, Araos P, Prado C, Fuentes Luppichini E, Rojas M, Alzamora R, Cifuentes-Araneda F, Gonzalez AA, Amador CA, Pacheco R, and Michea L

Subjects
Animals, Disease Models, Animal, Epithelial Sodium Channels immunology, Inflammation, Ion Transport immunology, Mice, Mice, Transgenic, Myeloid Cells immunology, Angiotensin II metabolism, Antigen-Presenting Cells immunology, Blood Pressure immunology, CD11c Antigen immunology, Hypertension immunology, Hypertension physiopathology, Hypertension prevention & control, Sodium Chloride, Dietary metabolism
Abstract

Increasing evidence shows that antigen-presenting cells (APCs) are involved in the development of inflammation associated to hypertension. However, the potential role of APCs in the modulation of renal sodium transport has not been addressed. We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Using transgenic mice that allow the ablation of CD11c high APCs, we studied renal sodium transport, the intrarenal renin-angiotensin system components, blood pressure, and cardiac/renal tissue damage in response to angiotensin II plus a high-salt diet. Strikingly, we found that APCs are required for the development of hypertension and that the ablation/restitution of APCs produces rapid changes in the blood pressure in mice with angiotensin II plus a high-salt diet. Moreover, APCs were necessary for the induction of intrarenal renin-angiotensin system components and affected the modulation of natriuresis and tubular sodium transporters. Consistent with the prevention of hypertension, the ablation of APCs also prevented cardiac hypertrophy and the induction of several indicators of renal and cardiac damage. Thus, our findings indicate a prominent role of APCs as modulators of blood pressure by mechanisms including renal sodium handling, with kinetics that suggest the involvement of tubular cell functions in addition to the modulation of inflammation and adaptive immune response., (© 2018 American Heart Association, Inc.)

Published
2018
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4. Angiotensin-(1-9) reverses experimental hypertension and cardiovascular damage by inhibition of the angiotensin converting enzyme/Ang II axis.

Author

Ocaranza MP, Moya J, Barrientos V, Alzamora R, Hevia D, Morales C, Pinto M, Escudero N, García L, Novoa U, Ayala P, Díaz-Araya G, Godoy I, Chiong M, Lavandero S, Jalil JE, and Michea L

Subjects
Angiotensin II Type 1 Receptor Blockers chemistry, Animals, Aorta pathology, Blood Pressure drug effects, Cardiovascular Diseases prevention & control, Disease Models, Animal, Echocardiography, Endothelium, Vascular pathology, Heart Ventricles, Hemodynamics, Hypertension physiopathology, Imidazoles chemistry, Male, Oxidative Stress, Pyridines chemistry, Rats, Rats, Sprague-Dawley, Angiotensin I chemistry, Angiotensin II chemistry, Angiotensin-Converting Enzyme Inhibitors chemistry, Cardiovascular Diseases drug therapy, Hypertension drug therapy, Peptide Fragments chemistry
Abstract

Background: Little is known about the biological effects of angiotensin-(1-9), but available evidence shows that angiotensin-(1-9) has beneficial effects in preventing/ameliorating cardiovascular remodeling., Objective: In this study, we evaluated whether angiotensin-(1-9) decreases hypertension and reverses experimental cardiovascular damage in the rat., Methods and Results: Angiotensin-(1-9) (600  ng/kg per min for 2 weeks) reduced already-established hypertension in rats with early high blood pressure induced by angiotensin II infusion or renal artery clipping. Angiotensin-(1-9) also improved cardiac (assessed by echocardiography) and endothelial function in small-diameter mesenteric arteries, cardiac and aortic wall hypertrophy, fibrosis, oxidative stress, collagen and transforming growth factor type β - 1 protein expression (assessed by western blot). The beneficial effect of angiotensin-(1-9) was blunted by coadministration of the angiotensin type 2(AT2) receptor blocker PD123319 (36  ng/kg per min) but not by coadministration of the Mas receptor blocker A779 (100  ng/kg per min). Angiotensin-(1-9) treatment also decreased circulating levels of Ang II, angiotensin-converting enzyme activity and oxidative stress in aorta and left ventricle. Whereas, Ang-(1-9) increased endothelial nitric oxide synthase mRNA levels in aorta as well as plasma nitrate levels., Conclusion: Angiotensin-(1-9) reduces hypertension, ameliorates structural alterations (hypertrophy and fibrosis), oxidative stress in the heart and aorta and improves cardiac and endothelial function in hypertensive rats. These effects were mediated by the AT2 receptor but not by the angiotensin-(1-7)/Mas receptor axis.

Published
2014
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