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Decrease in alpha 1-adrenoceptor reserve in mesenteric arteries isolated from spontaneously hypertensive rats.

M Kojima1, M Asano, K Aoki

  • 1Department of Pharmacology, Nagoya City University Medical School, Japan.

Journal of Hypertension
|November 1, 1989
PubMed
Summary
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Spontaneously hypertensive rats exhibit reduced alpha 1-adrenoceptor reserve in mesenteric arteries, leading to greater nifedipine inhibition of contractions. This suggests altered receptor dynamics contribute to hypertension-related vascular changes.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Hypertension Research

Background:

  • Hypertension is associated with altered vascular reactivity.
  • Alpha-1 adrenoceptors play a key role in regulating vascular tone.
  • Calcium channel blockers like nifedipine are used to treat hypertension.

Purpose of the Study:

  • To characterize alpha-1 adrenoceptor-mediated contractile responses in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY).
  • To investigate the effects of the calcium channel blocker nifedipine on these responses.
  • To explore potential differences in alpha-1 adrenoceptor reserve between SHR and WKY.

Main Methods:

  • Mesenteric arterial strips from 13-week-old male SHR and WKY rats were used.
  • Contractile responses to alpha-1 adrenoceptor agonists (phenylephrine, clonidine) were measured.

Related Experiment Videos

  • The effects of phenoxybenzamine (an alpha-1 antagonist) and nifedipine (a calcium channel blocker) were assessed.

    • Main Results:

    • Alpha-1 adrenoceptor agonists mediated contractions via alpha-1 adrenoceptors in both strains.
    • SHR exhibited higher ED50 values and weaker maximum responses to agonists compared to WKY.
    • Nifedipine produced greater inhibition of agonist-induced contractions in SHR, suggesting reduced alpha-1 adrenoceptor reserve.

    Conclusions:

    • SHR mesenteric arteries have a reduced alpha-1 adrenoceptor reserve compared to WKY rats.
    • This reduced reserve may explain the enhanced sensitivity to nifedipine-induced inhibition of alpha-1 adrenoceptor-mediated contractions in SHR.
    • Findings suggest altered alpha-1 adrenoceptor signaling contributes to the vascular dysfunction in hypertension.