title: Captopril avoids hypertension, the increase in plasma angiotensin II but increases angiotensin 1-7 and angiotensin II-induced perfusion pressure in isolated kidney in SHR.
abstract: We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats. Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma. Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P<0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups. Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α₁-adrenoceptor agonist. Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages. Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT₁R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.
authors.affiliation: Unidad de Biomedicina, Facultad de Estudios Superiores Iztacala, Universidad Nacional Autónoma de México, Tlalnepantla, Mexico.
authors.forename: P
authors.initials: P
authors.lastname: Castro-Moreno
authors.forename: J P
authors.initials: JP
authors.lastname: Pardo
authors.forename: R
authors.initials: R
authors.lastname: Hernández-Muñoz
authors.forename: J J
authors.initials: JJ
authors.lastname: López-Guerrero
authors.forename: L
authors.initials: L
authors.lastname: Del Valle-Mondragón
authors.forename: G
authors.initials: G
authors.lastname: Pastelín-Hernández
authors.forename: M
authors.initials: M
authors.lastname: Ibarra-Barajas
authors.forename: R
authors.initials: R
authors.lastname: Villalobos-Molina
mesh_terms: D000375:Aging; D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood* / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000009:adverse effects / Q000627:therapeutic use*; D000818:Animals; D000959:Antihypertensive Agents / Q000009:adverse effects / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000009:adverse effects / Q000627:therapeutic use*; D006973:Hypertension / Q000209:etiology / Q000517:prevention & control*; D007668:Kidney / Q000098:blood supply / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D007672:Kidney Cortex / Q000187:drug effects / Q000378:metabolism; D007679:Kidney Medulla / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010446:Peptide Fragments / Q000097:blood; D058246:Prehypertension / Q000097:blood / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D013047:Specific Pathogen-Free Organisms; D014655:Vascular Resistance / Q000187:drug effects*
chemical_list: C544067:Agtr1a protein, rat; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D010446:Peptide Fragments; D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D000803:Angiotensin I; D002216:Captopril; C118790:angiotensin I (1-7)