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Nitric oxide and drinking behaviour

G Calapai1, A P Caputi

  • 1Institute of Pharmacology, Faculty of Medicine, University of Messina, Italy.

Regulatory Peptides
|October 8, 1996
PubMed
Summary
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Brain nitric oxide, derived from L-arginine, inhibits drinking behavior. This pathway, particularly in the preoptic area, involves prostaglandin synthesis and regulates thirst.

Area of Science:

  • Neuroscience
  • Biochemistry
  • Physiology

Background:

  • Drinking behavior is a fundamental physiological process.
  • The brain's L-arginine/nitric oxide (NO) pathway is implicated in various regulatory functions.
  • Understanding the role of NO in thirst regulation is crucial.

Purpose of the Study:

  • To investigate the role of the brain's L-arginine/nitric oxide (NO) pathway in regulating drinking behavior.
  • To determine the specific mechanisms and brain regions involved in NO's influence on thirst.

Main Methods:

  • Drinking behavior was induced by water deprivation or intracerebroventricular (i.c.v.) injection of angiotensin II.
  • L-arginine (NO precursor) and L-NAME (NO synthase inhibitor) were administered i.c.v.
  • Agents were also injected into the preoptic area (POA).

Related Experiment Videos

  • Inhibitors of guanylate cyclase (methylene blue) and prostaglandin synthesis (acetylsalicylic acid - ASA) were used.

    • Main Results:

    • Intracerebroventricular L-arginine significantly reduced water intake induced by both water deprivation and angiotensin II.
    • L-NAME reversed the antidipsogenic effect of L-arginine.
    • L-arginine administration into the POA also produced a potent antidipsogenic effect.
    • Methylene blue and ASA antagonized the antidipsogenic effects of L-arginine in the POA.

    Conclusions:

    • Nitric oxide acts as an inhibitory signal within the preoptic area to regulate drinking behavior.
    • The antidipsogenic effect of NO is dependent on prostaglandin synthesis.
    • The L-arginine/NO pathway plays a significant role in the central control of thirst.