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Updated: Jul 11, 2026

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[Development of genetically engineered mice lacking all three nitric oxide synthase isoforms].

Masato Tsutsui1, Hiroaki Shimokawa, Tsuyoshi Morishita

  • 1Department of Pharmacology, School of Medicine, University of Occupational and Environmental Health, Iseigaoka, Kitakyushu, Japan. mt2498@med.uoeh-u.ac.jp

Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan
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Summary

Mice lacking all nitric oxide synthase (NOS) genes developed cardiovascular diseases, including arteriosclerosis. This highlights the critical role of the endogenous NOS system in maintaining cardiovascular homeostasis.

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Area of Science:

  • Physiology
  • Molecular Biology
  • Genetics

Context:

  • The roles of nitric oxide (NO) in vivo are complex and debated.
  • Pharmacological studies face challenges with NOS inhibitor specificity.
  • Gene knockout studies show compensatory mechanisms by other NOS isoforms.

Purpose:

  • To elucidate the ultimate roles of endogenous NO by eliminating all three NOS isoforms.
  • To develop and characterize mice lacking all three NOS genes (n/i/eNOS(-/-)).

Summary:

  • Triply n/i/eNOS(-/-) mice exhibited complete absence of NOS expression and activity.
  • These mice showed reduced survival and fertility rates.
  • Phenotypes included polyuria, polydipsia, nephrogenic diabetes insipidus, and spontaneous arteriosclerosis.

Impact:

  • Provides the first evidence that genetic disruption of all NOSs causes cardiovascular diseases in vivo.
  • Demonstrates the critical role of the endogenous NOS system in maintaining cardiovascular homeostasis.
  • Offers a valuable model for studying NO's physiological functions and related diseases.