Vascular Hyperactivity in the Rat Renal Aorta Participates in the Association between Immune Complex-Mediated Glomerulonephritis and Systemic Hypertension
| Autor: | Israel Pérez-Torres, Verónica Guarner-Lans, Teresa Imelda Fortoul Vander Goes, Maria del Carmen Avila-Casado, Elizabeth Soria-Castro, Bernardo Moguel-González |
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| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
Male
medicine.medical_specialty hypertension Endothelium Arginine immune complex Health Toxicology and Mutagenesis 030232 urology & nephrology Renal function lcsh:Medicine Vasodilation Blood Pressure 030204 cardiovascular system & hematology Kidney Article 03 medical and health sciences 0302 clinical medicine Glomerulonephritis Internal medicine medicine.artery medicine Animals Endothelial dysfunction Rats Wistar Aorta business.industry lcsh:R Public Health Environmental and Occupational Health medicine.disease Rats iNOS medicine.anatomical_structure Endocrinology reactivity vascular Vasoconstriction eNOS Endothelium Vascular medicine.symptom business |
| Zdroj: | International Journal of Environmental Research and Public Health Volume 15 Issue 6 International Journal of Environmental Research and Public Health, Vol 15, Iss 6, p 1164 (2018) |
| ISSN: | 1660-4601 1661-7827 |
| Popis: | 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&rsquo 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 &le 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 &le 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. |
| Databáze: | OpenAIRE |
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