AI Article Synopsis
- The study examines the role of superoxide anions in blood pressure and kidney function in rats with induced malignant hypertension.
- Induction of malignant hypertension resulted in significantly higher mean arterial pressure (MAP) and renal vascular resistance (RVR) compared to non-induced rats, alongside increased urinary excretion of 8-isoprostane.
- Administration of the antioxidant tempol lowered MAP and RVR in hypertensive rats but not in normotensive rats, suggesting that superoxide anions are involved in the hypertension mechanism, partially through nitric oxide pathways.
Article Abstract
Superoxide anion contributes to the pathogenesis of various forms of hypertension, but its role in the development of malignant hypertension remains unclear. The present study was performed to determine the influence of superoxide anion on blood pressure and renal hemodynamics in transgenic rats with inducible malignant hypertension [strain name: TGR(Cyp1a1Ren2)]. Malignant hypertension was induced in male Cyp1a1-Ren2 rats (n = 6) through dietary administration of the aryl hydrocarbon, indole-3-carbinol (0.3%) for 7-9 days. Mean arterial pressure (MAP) and renal hemodynamics were measured in pentobarbital sodium-anesthetized Cyp1a1-Ren2 rats before and during intravenous infusion of the superoxide dismutase mimetic tempol (100 mumol/h). Basal MAP and renal vascular resistance (RVR) were elevated in rats induced with indole-3-carbinol compared with noninduced rats (n = 5) (184 +/- 4 vs. 127 +/- 3 mmHg, P < 0.01, and 29 +/- 2 vs. 21 +/- 1 mmHg.ml(-1).min.g, P < 0.01, respectively). Hypertensive rats had elevated excretion of urinary 8-isoprostane compared with normotensive rats (41 +/- 4 vs. 13 +/- 6 pg.min(-1).g(-1), P < 0.01). There were no differences in renal plasma flow and glomerular filtration rate between groups. Systemic administration of tempol decreased MAP (184 +/- 4 to 151 +/- 4 mmHg, P < 0.01) and RVR (29 +/- 2 to 25 +/- 2 mmHg.ml(-1).min.g, P < 0.05) in hypertensive but not in normotensive Cyp1a1-Ren2 rats. In addition, tempol administration decreased urinary excretion of 8-isoprostane (41 +/- 4 to 25 +/- 4 pg.min(-1).g(-1), P < 0.05). Renal plasma flow and glomerular filtration rate remained unaltered during tempol administration in both groups. The administration of the nitric oxide synthase inhibitor nitro-l-arginine attenuated the decrease in MAP and RVR in response to tempol. These findings indicate that superoxide anion contributes to the elevated RVR and increased arterial blood pressure, by a mechanism that is at least in part nitric oxide dependent, in Cyp1a1-Ren2 rats with malignant hypertension.
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| http://dx.doi.org/10.1152/ajprenal.00419.2004 | DOI Listing |
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