ArticleJournal of the American Society of Hypertension : JASH2016
Renal intramedullary infusion of tempol normalizes the blood pressure response to intrarenal blockade of heme oxygenase-1 in angiotensin II-dependent hypertension.
Article in Journal of the American Society of Hypertension : JASH, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Tempol treatment normalizes membrane expression of epithelial transport proteins in the kidney of salt-loaded hypertensive diabetic db/db mice.American journal of translational research · 2023Article
- A critical evaluation of risk to reward ratio of quercetin supplementation for COVID-19 and associated comorbid conditions.Phytotherapy research : PTR · 2022Review
- Clinical characteristics of coronavirus disease 2019 (COVID-19) patients with hypertension on renin-angiotensin system inhibitors.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2020Article
- Genetic polymorphisms associated with reactive oxygen species and blood pressure regulation.The pharmacogenomics journal · 2019Review
- Targeting Heme Oxygenase-1 in Cardiovascular and Kidney Disease.Antioxidants (Basel, Switzerland) · 2019Review
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Previous studies have demonstrated that intramedullary inhibition of heme oxygenase-1 (HO-1) increases the blood pressure and superoxide production response to angiotensin II (Ang II) infusion. The present study was designed to test the hypothesis that increased renal medullary superoxide production contributes to the increase in blood pressure in response to blockade of renal medullary HO-1 in Ang II-induced hypertension. Male C57BL/6J mice (16-24 weeks of age) were implanted with chronic intrarenal medullary interstitial (IRMI) and infused with: saline, tempol (6 mM), the HO-1 inhibitor QC-13 (25 μM), or a combination of tempol + QC-13. Tempol treatment was started 2 days before infusion of QC-13. After 2 days, Ang II was infused subcutaneously at a rate of 1 μg/kg/min for 10 days. Blood pressures on days 7-10 of Ang II infusion alone averaged 150 ± 3 mm Hg in mice receiving IRMI infusion of saline. IRMI infusion of QC-13 increased blood pressure in Ang II-treated mice to 164 ± 2 (P < .05). Renal medullary superoxide production in Ang II-treated mice was significantly increased by infusion of QC-13 alone. Ang II-treated mice receiving IRMI infusion of tempol had a blood pressure of 136 ± 3 mm Hg. Ang II-treated mice receiving IRMI infusion of tempol and QC-13 had a significantly lower blood pressure (142 ± 2 mm Hg, P < .05) than mice receiving QC-13 alone. The increase in renal medullary superoxide production was normalized by infusion of tempol alone or in combination with QC-13. These results demonstrate that renal medullary interstitial blockade of HO-1 exacerbates Ang II-induced hypertension via a mechanism that is dependent on enhanced superoxide generation and highlight the important antioxidant function of HO-1 in the renal medulla.
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