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Related Experiment Videos

Brain histamine regulates pressor responses to peripheral hyperosmolality.

V F Akins1, S L Bealer

  • 1Department of Physiology, University of Tennessee, Memphis 38163.

The American Journal of Physiology
|September 1, 1990
PubMed
Summary

Brain histamine (HA) plays a key role in regulating blood pressure during dehydration. Blocking histamine H1 receptors in the brain significantly reduces the pressor response to hyperosmolality.

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Area of Science:

  • Neuroscience
  • Physiology
  • Pharmacology

Background:

  • Peripheral hyperosmolality, a state of increased solute concentration in the blood, can trigger physiological responses to maintain fluid balance.
  • Brain histamine (HA) is a neurotransmitter implicated in various autonomic functions, including cardiovascular regulation.

Purpose of the Study:

  • To investigate the role of central histamine in the pressor response to peripheral hyperosmolality in conscious rats.
  • To determine which histamine receptor subtypes (H1 or H2) are involved in this response.

Main Methods:

  • Intravenous infusion of hypertonic saline (HTS) to induce peripheral hyperosmolality in Sprague-Dawley rats.
  • Central administration of histamine receptor antagonists (H1 antagonist promethazine, H2 antagonist cimetidine) via intracerebroventricular injection.

Related Experiment Videos

  • Measurement of mean arterial pressure (MAP) to assess the pressor response.
  • Microdissection and measurement of brain histamine levels in specific hypothalamic nuclei (SON, PVN).
  • Microdialysis to measure extracellular histamine concentrations in the PVN and SON.
  • Main Results:

    • Intravenous HTS infusion significantly increased MAP in control rats and rats pretreated with the H2 antagonist cimetidine.
    • The pressor response to HTS was abolished in a dose-dependent manner after central administration of the H1 antagonist promethazine.
    • Intravenous HTS infusion led to decreased total brain HA levels in the SON, PVN, and posterior hypothalamus.
    • Extracellular HA concentrations increased in the SON but not the PVN during HTS infusion.

    Conclusions:

    • Endogenous brain histamine, particularly acting via H1 receptors, is critically involved in mediating the pressor response to peripheral hyperosmolality.
    • Histaminergic pathways in the brain, especially within the SON, play a significant role in cardiovascular adjustments to changes in body fluid osmolality.