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Related Concept Videos

Nitric Oxide Signaling Pathway01:28

Nitric Oxide Signaling Pathway

Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
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The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
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Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...
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Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.

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En Face Detection of Nitric Oxide and Superoxide in Endothelial Layer of Intact Arteries
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Involvement of inducible nitric oxide synthase in blood flow decrease in vein induced by hen-egg white lysozyme.

Hisae Oku1, Yuko Ogawa, Emiko Iwaoka

  • 1School of Pharmaceutical Sciences, Mukogawa Women's University, Nishinomiya, Hyogo, Japan.

Biological & Pharmaceutical Bulletin
|July 3, 2007
PubMed
Summary

This study reveals two pathways regulating allergic reactions in mice: one independent of inducible nitric oxide synthase (iNOS) involving thromboxane A2 and endothelin-1, and another dependent on iNOS, involving cyclooxygenase enzymes and prostacyclin. Inducible nitric oxide synthase exacerbates allergic responses.

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Area of Science:

  • Immunology
  • Pharmacology
  • Physiology

Background:

  • An in vivo assay system was developed to identify allergy-preventive substances by measuring blood flow decrease in mouse tail vein microcirculation after hen-egg white lysozyme (HEL) sensitization.
  • Blood flow decrease in this model is influenced by nitric oxide (NO), thromboxane A2 (TXA2), prostacyclin (PGI2), endothelin-1 (ET-1), and cyclooxygenase (COX) enzymes (COX-1, COX-2), as well as inducible nitric oxide synthase (iNOS) and constitutive nitric oxide synthase (cNOS).

Purpose of the Study:

  • To investigate the specific role of inducible nitric oxide synthase (iNOS) in the HEL-induced microcirculation blood flow decrease using an iNOS knockout (KO) mouse model.
  • To elucidate the distinct pathways involved in regulating blood flow changes during allergic sensitization.

Main Methods:

  • Utilized an in vivo assay system involving hen-egg white lysozyme (HEL) sensitization in mice.
  • Employed iNOS knockout (KO) mice and compared their responses to wild-type (WT) mice.
  • Administered selective inhibitors for COX-1, COX-2, TXA2 synthase, ET-1 receptor blockers, nonselective NOS inhibitors, and a PGI2 agonist to assess their effects on blood flow decrease.

Main Results:

  • The blood flow decrease in HEL-sensitized iNOS KO mice was less pronounced than in WT mice.
  • In iNOS KO mice, the blood flow decrease was unaffected by selective COX-1, COX-2 inhibitors, or a PGI2 agonist, but was inhibited by a nonselective NOS inhibitor, TXA2 synthase inhibitor, and ET-1 receptor blocker.
  • These findings suggest the existence of both iNOS-independent (via TXA2 and ET-1) and iNOS-dependent (via COX-1, COX-2, and PGI2) pathways regulating blood flow decrease.

Conclusions:

  • The blood flow decrease in the HEL sensitization model operates through at least two distinct pathways.
  • Inducible nitric oxide synthase (iNOS) appears to act as an exacerbating factor in allergic responses, while constitutive nitric oxide synthase (cNOS) also plays a role.
  • The developed HEL-sensitization assay system is a valuable tool for discovering novel allergy-preventive agents targeting new mechanisms.