Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy

Autores
Juncos, Luis Isaias; Adeoye, Akinwunmi Oluwaseun; Martin, Fernando Luis; Juncos, Julio Pedro; Baigorria, Sandra Teresita; Garcia, Nestor Horacio
Año de publicación
2024
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Experimental glomerulonephritis results in hypertension that is sensitive to salt. Nevertheless, salt retention alone cannot explain the increase in blood pressure. Angiotensin antagonistic therapy reduces hypertension caused by puromycin amino nucleosides (PAN). We investigated the hypothesis that PAN modifies renal vascular reactivity through processes dependent on angiotensin. Long-Evans rats were given an intraperitoneal injection of either puromycin (150 mg/kg) or saline (controls). Group 1 was fed a normal sodium diet (NSD, n = 9). Group 2 was given 30 mg/L of quinapril (Q) in addition to NSD (NSD + Q; n = 6). Group 3 received a high sodium diet (HSD, n = 7), and Group 4 received HSD + Q (n = 7). Systolic blood pressure (SBP), plasma creatinine, proteinuria, and sodium balance were monitored for 12 days. On day 15, renal vascular reactivity was assessed by administering increasing doses of angiotensin II, acetylcholine (ACh), and sodium nitroprusside (SNP) directly into the renal artery. SBP progressively increased in all PAN groups. This increase in SBP was greater in the HSD groups and was not significantly altered by Q treatment. SBP increased by 22 ± 4% (NSD), 51 ± 5% (NSD + Q), 81 ± 10% (HSD), and 65 ± 8% (HSD + Q). The renal blood flow of PAN rats did not return to baseline despite their normal renal vasoconstrictor responses to angiotensin II. Additionally, they showed reduced renal vasodilator responses to SNP and Ach. The vasodilator responses to both vasodilators were surprisingly unaffected by the inhibition of the angiotensin-converting enzyme (ACE). Renal vasodilator responses to both endothelium-dependent and independent variables were reduced in early PAN-induced hypertension. We found that the angiotensin-mediated mechanism is not responsible for this altered renal vasoreactivity.
Fil: Juncos, Luis Isaias. Fundacion J Robert Cade; Argentina
Fil: Adeoye, Akinwunmi Oluwaseun. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Federal University Oye-Ekiti; Nigeria
Fil: Martin, Fernando Luis. Fundacion J Robert Cade; Argentina
Fil: Juncos, Julio Pedro. Fundacion J Robert Cade; Argentina
Fil: Baigorria, Sandra Teresita. Fundacion J. Robert Cade; Argentina
Fil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Fundacion J. Robert Cade; Argentina
Materia
Sodio
Angiotensin II
Kidney
Creatinine
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/260874
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/260874
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathyJuncos, Luis IsaiasAdeoye, Akinwunmi OluwaseunMartin, Fernando LuisJuncos, Julio PedroBaigorria, Sandra TeresitaGarcia, Nestor HoracioSodioAngiotensin IIKidneyCreatininehttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Experimental glomerulonephritis results in hypertension that is sensitive to salt. Nevertheless, salt retention alone cannot explain the increase in blood pressure. Angiotensin antagonistic therapy reduces hypertension caused by puromycin amino nucleosides (PAN). We investigated the hypothesis that PAN modifies renal vascular reactivity through processes dependent on angiotensin. Long-Evans rats were given an intraperitoneal injection of either puromycin (150 mg/kg) or saline (controls). Group 1 was fed a normal sodium diet (NSD, n = 9). Group 2 was given 30 mg/L of quinapril (Q) in addition to NSD (NSD + Q; n = 6). Group 3 received a high sodium diet (HSD, n = 7), and Group 4 received HSD + Q (n = 7). Systolic blood pressure (SBP), plasma creatinine, proteinuria, and sodium balance were monitored for 12 days. On day 15, renal vascular reactivity was assessed by administering increasing doses of angiotensin II, acetylcholine (ACh), and sodium nitroprusside (SNP) directly into the renal artery. SBP progressively increased in all PAN groups. This increase in SBP was greater in the HSD groups and was not significantly altered by Q treatment. SBP increased by 22 ± 4% (NSD), 51 ± 5% (NSD + Q), 81 ± 10% (HSD), and 65 ± 8% (HSD + Q). The renal blood flow of PAN rats did not return to baseline despite their normal renal vasoconstrictor responses to angiotensin II. Additionally, they showed reduced renal vasodilator responses to SNP and Ach. The vasodilator responses to both vasodilators were surprisingly unaffected by the inhibition of the angiotensin-converting enzyme (ACE). Renal vasodilator responses to both endothelium-dependent and independent variables were reduced in early PAN-induced hypertension. We found that the angiotensin-mediated mechanism is not responsible for this altered renal vasoreactivity.Fil: Juncos, Luis Isaias. Fundacion J Robert Cade; ArgentinaFil: Adeoye, Akinwunmi Oluwaseun. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Federal University Oye-Ekiti; NigeriaFil: Martin, Fernando Luis. Fundacion J Robert Cade; ArgentinaFil: Juncos, Julio Pedro. Fundacion J Robert Cade; ArgentinaFil: Baigorria, Sandra Teresita. Fundacion J. Robert Cade; ArgentinaFil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Fundacion J. Robert Cade; ArgentinaJurnalul Pentru Medicina Si Viata2024-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/260874Juncos, Luis Isaias; Adeoye, Akinwunmi Oluwaseun; Martin, Fernando Luis; Juncos, Julio Pedro; Baigorria, Sandra Teresita; et al.; Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy; Jurnalul Pentru Medicina Si Viata; Journal of Medicine and Life; 17; 3; 3-2024; 309-3131844-122X1844-3117CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.25122/jml-2023-0367info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:53:29Zoai:ri.conicet.gov.ar:11336/260874instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:53:29.841CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
title Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
spellingShingle Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
Juncos, Luis Isaias
Sodio
Angiotensin II
Kidney
Creatinine
title_short Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
title_full Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
title_fullStr Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
title_full_unstemmed Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
title_sort Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy
dc.creator.none.fl_str_mv Juncos, Luis Isaias
Adeoye, Akinwunmi Oluwaseun
Martin, Fernando Luis
Juncos, Julio Pedro
Baigorria, Sandra Teresita
Garcia, Nestor Horacio
author Juncos, Luis Isaias
author_facet Juncos, Luis Isaias
Adeoye, Akinwunmi Oluwaseun
Martin, Fernando Luis
Juncos, Julio Pedro
Baigorria, Sandra Teresita
Garcia, Nestor Horacio
author_role author
author2 Adeoye, Akinwunmi Oluwaseun
Martin, Fernando Luis
Juncos, Julio Pedro
Baigorria, Sandra Teresita
Garcia, Nestor Horacio
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Sodio
Angiotensin II
Kidney
Creatinine
topic Sodio
Angiotensin II
Kidney
Creatinine
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Experimental glomerulonephritis results in hypertension that is sensitive to salt. Nevertheless, salt retention alone cannot explain the increase in blood pressure. Angiotensin antagonistic therapy reduces hypertension caused by puromycin amino nucleosides (PAN). We investigated the hypothesis that PAN modifies renal vascular reactivity through processes dependent on angiotensin. Long-Evans rats were given an intraperitoneal injection of either puromycin (150 mg/kg) or saline (controls). Group 1 was fed a normal sodium diet (NSD, n = 9). Group 2 was given 30 mg/L of quinapril (Q) in addition to NSD (NSD + Q; n = 6). Group 3 received a high sodium diet (HSD, n = 7), and Group 4 received HSD + Q (n = 7). Systolic blood pressure (SBP), plasma creatinine, proteinuria, and sodium balance were monitored for 12 days. On day 15, renal vascular reactivity was assessed by administering increasing doses of angiotensin II, acetylcholine (ACh), and sodium nitroprusside (SNP) directly into the renal artery. SBP progressively increased in all PAN groups. This increase in SBP was greater in the HSD groups and was not significantly altered by Q treatment. SBP increased by 22 ± 4% (NSD), 51 ± 5% (NSD + Q), 81 ± 10% (HSD), and 65 ± 8% (HSD + Q). The renal blood flow of PAN rats did not return to baseline despite their normal renal vasoconstrictor responses to angiotensin II. Additionally, they showed reduced renal vasodilator responses to SNP and Ach. The vasodilator responses to both vasodilators were surprisingly unaffected by the inhibition of the angiotensin-converting enzyme (ACE). Renal vasodilator responses to both endothelium-dependent and independent variables were reduced in early PAN-induced hypertension. We found that the angiotensin-mediated mechanism is not responsible for this altered renal vasoreactivity.
Fil: Juncos, Luis Isaias. Fundacion J Robert Cade; Argentina
Fil: Adeoye, Akinwunmi Oluwaseun. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Federal University Oye-Ekiti; Nigeria
Fil: Martin, Fernando Luis. Fundacion J Robert Cade; Argentina
Fil: Juncos, Julio Pedro. Fundacion J Robert Cade; Argentina
Fil: Baigorria, Sandra Teresita. Fundacion J. Robert Cade; Argentina
Fil: Garcia, Nestor Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigaciones en Ciencias de la Salud. Universidad Nacional de Córdoba. Instituto de Investigaciones en Ciencias de la Salud; Argentina. Fundacion J. Robert Cade; Argentina
description Experimental glomerulonephritis results in hypertension that is sensitive to salt. Nevertheless, salt retention alone cannot explain the increase in blood pressure. Angiotensin antagonistic therapy reduces hypertension caused by puromycin amino nucleosides (PAN). We investigated the hypothesis that PAN modifies renal vascular reactivity through processes dependent on angiotensin. Long-Evans rats were given an intraperitoneal injection of either puromycin (150 mg/kg) or saline (controls). Group 1 was fed a normal sodium diet (NSD, n = 9). Group 2 was given 30 mg/L of quinapril (Q) in addition to NSD (NSD + Q; n = 6). Group 3 received a high sodium diet (HSD, n = 7), and Group 4 received HSD + Q (n = 7). Systolic blood pressure (SBP), plasma creatinine, proteinuria, and sodium balance were monitored for 12 days. On day 15, renal vascular reactivity was assessed by administering increasing doses of angiotensin II, acetylcholine (ACh), and sodium nitroprusside (SNP) directly into the renal artery. SBP progressively increased in all PAN groups. This increase in SBP was greater in the HSD groups and was not significantly altered by Q treatment. SBP increased by 22 ± 4% (NSD), 51 ± 5% (NSD + Q), 81 ± 10% (HSD), and 65 ± 8% (HSD + Q). The renal blood flow of PAN rats did not return to baseline despite their normal renal vasoconstrictor responses to angiotensin II. Additionally, they showed reduced renal vasodilator responses to SNP and Ach. The vasodilator responses to both vasodilators were surprisingly unaffected by the inhibition of the angiotensin-converting enzyme (ACE). Renal vasodilator responses to both endothelium-dependent and independent variables were reduced in early PAN-induced hypertension. We found that the angiotensin-mediated mechanism is not responsible for this altered renal vasoreactivity.
publishDate 2024
dc.date.none.fl_str_mv 2024-03
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/260874
Juncos, Luis Isaias; Adeoye, Akinwunmi Oluwaseun; Martin, Fernando Luis; Juncos, Julio Pedro; Baigorria, Sandra Teresita; et al.; Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy; Jurnalul Pentru Medicina Si Viata; Journal of Medicine and Life; 17; 3; 3-2024; 309-313
1844-122X
1844-3117
CONICET Digital
CONICET
url http://hdl.handle.net/11336/260874
identifier_str_mv Juncos, Luis Isaias; Adeoye, Akinwunmi Oluwaseun; Martin, Fernando Luis; Juncos, Julio Pedro; Baigorria, Sandra Teresita; et al.; Angiotensin II-independent abnormal renal vascular reactivity during puromycin nephropathy; Jurnalul Pentru Medicina Si Viata; Journal of Medicine and Life; 17; 3; 3-2024; 309-313
1844-122X
1844-3117
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.25122/jml-2023-0367
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
application/pdf
application/pdf
application/pdf
dc.publisher.none.fl_str_mv Jurnalul Pentru Medicina Si Viata
publisher.none.fl_str_mv Jurnalul Pentru Medicina Si Viata
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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