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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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Regulation of Angiogenesis and Blood Supply

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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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.
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Antianginal Drugs: Nitrates and β-Blockers01:16

Antianginal Drugs: Nitrates and β-Blockers

In cardiovascular health, antianginal drugs combat angina pectoris — a condition marked by chest pain owing to diminished blood flow to the heart.
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Related Experiment Video

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Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells
08:32

Application of Genetically Encoded Fluorescent Nitric Oxide (NO•) Probes, the geNOps, for Real-time Imaging of NO• Signals in Single Cells

Published on: March 16, 2017

Nitric oxide synthases: regulation and function.

Ulrich Förstermann1, William C Sessa

  • 1Department of Pharmacology, Johannes Gutenberg University Medical Center, 55101 Mainz, Germany. ulrich.forstermann@uni-mainz.de

European Heart Journal
|September 6, 2011
PubMed
Summary
This summary is machine-generated.

Nitric oxide synthase (NOS) produces nitric oxide (NO), a key signaling molecule. Different NOS isoforms play vital roles in neuronal function, immune responses, and cardiovascular health, with implications for various diseases and drug actions.

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Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds

Published on: February 16, 2022

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Physiology

Background:

  • Nitric oxide (NO) is a critical signaling molecule produced by three isoforms of NO synthase (NOS).
  • NOS isoforms (nNOS, NOS II, eNOS) utilize l-arginine, oxygen, and essential cofactors like NADPH and BH(4).
  • Each NOS isoform has distinct physiological roles, ranging from neurotransmission to immune defense and vascular homeostasis.

Purpose of the Study:

  • To elucidate the diverse functions and biochemical properties of the three major nitric oxide synthase (NOS) isoforms.
  • To highlight the involvement of NOS isoforms in physiological processes and pathological conditions.
  • To discuss the pharmacological implications of NOS activity, particularly in relation to cardiovascular health and erectile dysfunction.

Main Methods:

  • Review of existing literature on NOS isoforms, their substrates, cofactors, and functions.
  • Analysis of the roles of nNOS in the central nervous system and peripheral tissues.
  • Examination of NOS II's role in inflammatory and infectious diseases.
  • Investigation of eNOS in endothelial cells and its contribution to vascular health.

Main Results:

  • Neuronal NOS (nNOS) is crucial for synaptic plasticity, blood pressure regulation, and smooth muscle relaxation, notably in penile erection, and is required for phosphodiesterase 5 inhibitor efficacy.
  • Inducible NOS (NOS II) produces large amounts of NO, exerting cytostatic effects and contributing to inflammatory diseases and septic shock.
  • Endothelial NOS (eNOS) maintains blood vessel dilation, regulates blood pressure, and offers vasoprotective and anti-atherosclerotic benefits, but is susceptible to oxidative stress and uncoupling.

Conclusions:

  • The three NOS isoforms (nNOS, NOS II, eNOS) are essential for diverse physiological functions, including neurotransmission, immune response, and cardiovascular regulation.
  • Dysfunction of NOS, particularly eNOS uncoupling due to oxidative stress, contributes to endothelial dysfunction and cardiovascular diseases.
  • Pharmacological interventions targeting NOS or its pathways, such as phosphodiesterase 5 inhibitors and treatments for oxidative stress, are critical for managing various health conditions.