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Forebrain pathways mediating stress-induced renin secretion

L D Van de Kar1

  • 1Loyola University of Chicago, Stritch School of Medicine, Department of Pharmacology, Maywood, Illinois 60153, USA.

Clinical and Experimental Pharmacology & Physiology
|February 1, 1996
PubMed
Summary

Stress activates plasma renin levels, but this response is blunted in aged rats. Specific brain nuclei, including the paraventricular nucleus and amygdala, are crucial for mediating stress-induced renin release via catecholaminergic and serotonergic pathways.

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Area of Science:

  • Neuroendocrinology
  • Stress Physiology
  • Renin-Angiotensin System

Background:

  • Plasma renin levels increase in response to various stressors.
  • The neural pathways mediating stress-induced renin release are not fully understood.
  • Aging may affect the stress response, including renin release.

Purpose of the Study:

  • To investigate the neural mechanisms underlying stress-induced increases in plasma renin concentration.
  • To identify specific brain regions and pathways involved in mediating the renin response to conditioned fear stress.
  • To explore the role of catecholaminergic and serotonergic systems in this response.

Main Methods:

  • Utilized various stressors including foot-shock, immobilization, and conditioned fear in rats.

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  • Employed electrolytic and neurotoxic lesions to target specific brain nuclei (PVH, amygdala, dorsal raphe nucleus).
  • Administered pharmacological agents targeting specific neurotransmitter receptors (e.g., 5HT1A agonists).
  • Assessed plasma renin concentrations and adrenocortical responses.

    • Main Results:

    • Conditioned fear stress failed to elevate plasma renin in aged rats.
    • Lesions in the paraventricular hypothalamic nucleus (PVH) and central amygdaloid nucleus blocked conditioned fear stress-induced renin release.
    • Destruction of catecholaminergic terminals in the PVH and electrolytic lesions in the dorsal raphe nucleus inhibited this response.
    • Serotonin1A receptor agonists reduced stress-induced renin release, while benzodiazepines were ineffective.
    • Sympathectomy and adrenal medullectomy did not abolish the renin response to stress.

    Conclusions:

    • Aversive information processing involves the amygdala, brainstem catecholaminergic cells, and dorsal raphe serotonergic cells, ultimately stimulating the PVH to modulate renin release.
    • The sympathetic system is not the sole mediator of stress-induced renin release.
    • Serotonergic pathways, particularly via 5HT1A receptors, play a significant role in inhibiting stress-induced renin release.