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dc.contributor.author
Ferder, Marcelo
dc.contributor.author
Inserra, Pablo Ignacio Felipe
dc.contributor.author
Manucha, Walter Ariel Fernando
dc.contributor.author
Ferder, León
dc.date.available
2015-10-01T18:36:55Z
dc.date.issued
2013-01-30
dc.identifier.citation
Ferder, Marcelo; Inserra, Pablo Ignacio Felipe; Manucha, Walter Ariel Fernando; Ferder, León; The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system; American Physiological Society; American Journal Of Physiology-cell Physiology; 304; 30-1-2013; C1027-C1039
dc.identifier.issn
0363-6143
dc.identifier.uri
http://hdl.handle.net/11336/2257
dc.description.abstract
This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
American Physiological Society
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Vitamin D
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Hypertension
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Ras
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Pandemia
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Oxidative Stress
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Mitochondria
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Cardiovascular Disease
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Angiotensin Receptor Blocker
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Vitamin D Receptor
dc.subject.classification
Salud Pública y Medioambiental
dc.subject.classification
Ciencias de la Salud
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-03-30 10:35:44.97925-03
dc.journal.volume
304
dc.journal.pagination
C1027-C1039
dc.journal.pais
Estados Unidos
dc.description.fil
Fil: Ferder, Marcelo. Universidad de Buenos Aires. Facultad de Medicina; Argentina;
dc.description.fil
Fil: Inserra, Pablo Ignacio Felipe. Universidad Austral. Facultad de Cs.biomedicas; Argentina;
dc.description.fil
Fil: Manucha, Walter Ariel Fernando. Universidad Nacional de Cuyo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina;
dc.description.fil
Fil: Ferder, León. Ponce School of Medicine and Health Sciences; Puerto Rico;
dc.journal.title
American Journal Of Physiology-cell Physiology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1152/ajpcell.00403.2011
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://ajpcell.physiology.org/content/304/11/C1027
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