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Carbonic anhydrase II does not regulate nitrite-dependent nitric oxide formation and vasodilation
Ling Wang1,2, Courtney E Sparacino-Watkins1,2, Jun Wang3
1Pittsburgh Heart, Lung, Blood and Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, Pennsylvania.
British Journal of Pharmacology
|October 29, 2019
Summary
Carbonic anhydrase II (CAII) does not generate nitric oxide (NO) from nitrite, contrary to previous reports. Studies show CAII is not involved in nitrite-dependent NO formation, vasodilation, or platelet inhibition.
Area of Science:
- Biochemistry
- Physiology
- Vascular Biology
Background:
- Bovine carbonic anhydrase II (CAII) has been suggested to generate nitric oxide (NO) from nitrite.
- The precise role and mechanism of CAII in nitrite-dependent NO formation and vascular function remain debated.
Purpose of the Study:
- To investigate the hypothesis that CAII catalyzes NO formation from nitrite.
- To determine CAII's contribution to nitrite-dependent inhibition of platelet activation and vasodilation.
Main Methods:
- NO formation was measured using NO photolysis-chemiluminescence from reactions of purified human and bovine CAII with nitrite.
- CAII-deficient mouse models were employed to assess nitrite reduction and vasodilation in red blood cells and in vivo.
Main Results:
- Purified bovine CAII showed minimal, non-enzymatic NO generation from nitrite; this reactivity was eliminated upon further purification.
- Recombinant human CAII did not produce detectable NO from nitrite.
- CAII-deficient mice exhibited no significant differences in nitrite-dependent vasodilation or platelet inhibition.
Conclusions:
- Human, bovine, and mouse CAII are not responsible for nitrite-dependent NO formation.
- CAII does not play a significant role in nitrite reduction in red blood cells, aorta, or systemic circulation.
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