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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/260874
Ver los metadatos del registro completo
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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 Técnicas2025-09-03T09:53:44Zoai: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:34982025-09-03 09:53:45.204CONICET 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 |
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Jurnalul Pentru Medicina Si Viata |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.13397 |