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Related Experiment Videos

Stress causes decrease in vascular relaxation linked with altered phosphorylation of heat shock proteins.

L C Fuchs1, A D Giulumian, L Knoepp

  • 1Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912, USA. lfuchs@mail.mcg.edu

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|August 12, 2000
PubMed
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Behavioral stress impairs vascular relaxation by increasing phosphorylated heat shock protein 27 (P-HSP27) and decreasing phosphorylated heat shock protein 20 (P-HSP20). P-HSP27 inhibits P-HSP20 phosphorylation, linking stress to reduced vascular function.

Area of Science:

  • Physiology
  • Molecular Biology
  • Stress Response

Background:

  • Cyclic nucleotide-dependent vascular relaxation is linked to heat shock protein (HSP) phosphorylation.
  • Increased phosphorylated HSP27 (P-HSP27) correlates with impaired relaxation, while increased phosphorylated HSP20 (P-HSP20) is associated with relaxation.
  • Cellular stress alters HSP expression in vitro.

Purpose of the Study:

  • To investigate if behavioral stress in vivo affects vascular expression and phosphorylation of HSP20 and HSP27.
  • To determine the impact of behavioral stress on cyclic nucleotide-dependent vascular relaxation.
  • To explore the mechanistic link between P-HSP27 and P-HSP20 in stress-induced vascular dysfunction.

Main Methods:

  • Borderline hypertensive rats were subjected to restraint and air-jet stress or served as controls.

Related Experiment Videos

  • Vascular relaxation of the aorta was assessed using forskolin and sodium nitroprusside.
  • Aortic expression and phosphorylation of HSP27 and HSP20 were analyzed.
  • In vitro experiments tested the effect of P-HSP27 on HSP20 phosphorylation.

    • Main Results:

    • Behavioral stress impaired aortic relaxation in response to both forskolin and sodium nitroprusside.
    • Stress increased aortic expression and phosphorylation of HSP27 in vascular smooth muscle.
    • Stress decreased the amount of phosphorylated HSP20 (P-HSP20).
    • P-HSP27 inhibited HSP20 phosphorylation in a concentration-dependent manner in vitro.

    Conclusions:

    • Behavioral stress in vivo alters vascular HSP27 and HSP20 phosphorylation.
    • Increased P-HSP27 inhibits P-HSP20, contributing to impaired vascular relaxation.
    • These findings reveal a molecular mechanism linking behavioral stress to reduced vascular function, mirroring effects of cellular stress.