ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Blood pressure and renal blow flow responses in heme oxygenase-2 knockout mice.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- A FunctionalAntioxidants (Basel, Switzerland) · 2026Article
- Targeting Heme Oxygenase-1 in Cardiovascular and Kidney Disease.Antioxidants (Basel, Switzerland) · 2019Review
- Functioning of an arteriovenous fistula requires heme oxygenase-2.American journal of physiology. Renal physiology · 2013Article
- Renal heme oxygenase-1 induction with hemin augments renal hemodynamics, renal autoregulation, and excretory function.International journal of hypertension · 2012Article
- Blood pressure and renal hemodynamic responses to acute angiotensin II infusion are enhanced in a female mouse model of systemic lupus erythematosus.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Attenuated renal vascular responses to acute angiotensin II infusion in smooth muscle-specific Na+/Ca2+ exchanger knockout mice.American journal of physiology. Renal physiology · 2011Article
- Heme oxygenase activity as a determinant of the renal hemodynamic response to low-dose ANG II.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- Moderate hyperbilirubinemia improves renal hemodynamics in ANG II-dependent hypertension.American journal of physiology. Regulatory, integrative and comparative physiology · 2010Article
- In vivo inhibition of renal heme oxygenase with an imidazole-dioxolane inhibitor.Pharmacological research · 2010Article
- Sex-specific effects of heme oxygenase-2 deficiency on renovascular hypertension.Journal of the American Society of Hypertension : JASHArticle
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Heme oxygenase (HO) is the enzyme responsible for the breakdown of heme-generating carbon monoxide (CO) and biliverdin in this process. HO-2 is the constitutively expressed isoform in most tissues, such as the kidney and vasculature. CO generated by HO is believed to be an important vasodilator in the renal circulation along with another gas, nitric oxide (NO). To determine the importance of HO-2 in the regulation of blood pressure and renal blood flow (RBF), we treated HO-2 knockout (KO) mice chronically with either ANG II or N(G)-nitroarginine methyl ester (l-NAME). Basal blood pressures were not different between wild-type (WT), heterozygous (HET), or KO mice and averaged 113 +/- 3 vs. 115 +/- 2 vs. 116 +/- 2 mmHg. Similar increases in blood pressure to chronic ANG II as well as l-NAME treatment were observed in all groups with blood pressures increasing an average of 30 mmHg in response to ANG II and 15 mmHg in response to l-NAME. Basal RBFs were not different between the groups averaging 6.0 +/- 0.5 (n = 6) vs. 4.8 +/- 0.6 (n = 10) vs. 5.8 +/- 0.7 (n = 6) ml*min(-1)*g(-1) kidney weight in WT, HET, and KO mice. HO-2 KO and HET mice exhibited an attenuated decrease in RBF in response to acute administration of ANG II, while no differences were observed with l-NAME. Our data indicate that blood pressure and RBF responses to increased ANG II or inhibition of nitric oxide are not significantly enhanced in HO-2 KO mice.
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