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Age- and Sodium-Sensitive Hypertension and Sex-Dependent Renal Changes in Rats With a Reduced Nephron Number

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dc.contributor.authorSalazar, Francisco
dc.contributor.authorReverte, Virginia
dc.contributor.authorSaez, Fara
dc.contributor.authorLorai, Analia
dc.contributor.authorLlinas, Maria Teresa
dc.contributor.authorSalazar, F. Javier
dc.contributor.departmentFisiología
dc.date.accessioned2025-03-18T12:47:32Z
dc.date.available2025-03-18T12:47:32Z
dc.date.issued2008-02-07
dc.description© 2008 American Heart Association, Inc.. . This document is the published version of a published work that appeared in final form in Hypertension. . To access the final edited and published work see: https://doi.org/10.1161/HYPERTENSIONAHA.107.100750
dc.description.abstractWe have demonstrated that the reduction of angiotensin II effects during the nephrogenic period reduces the nephron number and induces the development of hypertension. The hypotheses examined are that this reduction of angiotensin effects leads to the development of an age-dependent sodium sensitive hypertension and that the hypertension is angiotensin II dependent. Newborn rats were treated with an angiotensin II type 1 receptor antagonist during the first 2 weeks of age. At 3 to 4 and 11 to 12 months of age, changes in systolic blood pressure, proteinuria, and renal function in response to a prolonged high sodium intake were examined. The basal blood pressure response to the administration of the angiotensin II receptor antagonist was also evaluated at both ages. Basal blood pressure was similarly elevated (P<0.05) in male and female treated rats, and the increment was age dependent. High sodium intake only elicited a blood pressure elevation (136±1 to 154±3 mm Hg; P<0.05) and a decrease in glomerular filtration rate (28%; P<0.05) at 11 to 12 months in treated rats. Blockade of angiotensin II receptors during renal development induced an increase (P<0.05) in proteinuria that was age and sex dependent, but high sodium intake only induced an elevation in proteinuria in the younger rats (50%; P<0.05). Hypertension was maintained by angiotensin II at both ages because blood pressure decreased to normal levels after treatment with an angiotensin II type 1 receptor antagonist. This study shows that the reduction of angiotensin II effects during the nephrogenic period modifies renal function and induces the development of an angiotensin II–dependent hypertension that becomes sodium sensitive during aging.es
dc.embargo.terms1-ene-2999
dc.formatapplication/pdfes
dc.format.extent6
dc.identifier.citationHypertension, 51(4), 1184-1189
dc.identifier.doihttps://doi.org/10.1161/HYPERTENSIONAHA.107.100750
dc.identifier.issnPrint.: 0194-911X
dc.identifier.issnElectronic.: 1524-4563
dc.identifier.urihttp://hdl.handle.net/10201/151862
dc.languageenges
dc.publisherAmerican Heart Association
dc.relationSin financiación externa a la Universidades
dc.relation.publisherversionhttps://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.107.100750
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectAngiotensin
dc.subjectRenal function
dc.subjectNephrogenesis
dc.subjectProteinuria
dc.titleAge- and Sodium-Sensitive Hypertension and Sex-Dependent Renal Changes in Rats With a Reduced Nephron Numberes
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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