Vascular Hyperactivity in the Rat Renal Aorta Participates in the Association between Immune Complex-Mediated Glomerulonephritis and Systemic Hypertension

Israel Pérez-Torres, Bernardo Moguel-González, Elizabeth Soria-Castro, Verónica Guarner-Lans, María Del Carmen Avila-Casado and Teresa Imelda Fortoul Vander Goes
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Israel Pérez-Torres: Departamento de Patología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México 14080, México
Bernardo Moguel-González: Departamento de Patología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México 14080, México
Elizabeth Soria-Castro: Departamento de Patología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México 14080, México
Verónica Guarner-Lans: Departamento de Fisiología Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México 14080, México
María Del Carmen Avila-Casado: Departamento de Patología, Instituto Nacional de Cardiología “Ignacio Chávez”, Ciudad de México 14080, México
Teresa Imelda Fortoul Vander Goes: Departamento de Biología Celular y Tisular, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México 04510, México

IJERPH, 2018, vol. 15, issue 6, 1-15

Abstract: Introduction : systemic hypertension (SH) involving endothelial dysfunction contributes to immune complex-mediated glomerulonephritis (ICGN). Objective, we demonstrate a relationship between ICGN and SH by analyzing vascular reactivity in renal aortic rings. Methods : 48 male Wistar rats were divided into four groups: (a) control (C); (b) injected with bovine serum albumin (BSA); (c) receiving 200 mg/L NAME (an analog of arginine that inhibits NO production) in drinking water; and (d) receiving BSA and 200 mg/L NAME. Rats were pre-immunized subcutaneously with BSA and Freund’s adjuvant. After 10 days, groups (b) and (c) received 1 mg/mL of BSA in saline intravenous (IV) daily for 35 days. The urine of 24 h was measured at days 0, 15, 30 and 45. Results : vascular reactivity to norepinephrine (NE), acetylcholine (Ach) and NAME were tested. Creatinine clearance, vasodilatation, eNOS and elastic fibers were diminished ( p ≤ 0.001). Blood pressure, vasoconstriction, iNOS were increased, and glomerular alterations were observed in groups (b), (c) and (d) when compared to group (a) ( p ≤ 0.001). Conclusions: SH contributes to the development of progressive renal disease in ICGN. Alterations of the vascular reactivity are mediated by the endothelium in the renal aorta. Thus, the endothelium plays a determinant role in the production of vasoactive substances such as NO during this process.

Keywords: glomerulonephritis; hypertension; reactivity vascular; eNOS; iNOS; immune complex (search for similar items in EconPapers)
JEL-codes: I I1 I3 Q Q5 (search for similar items in EconPapers)
Date: 2018
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