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Related Experiment Videos

Losartan and captopril follow different mechanisms to decrease pressor responses in the pithed rat

H Yokoyama1, S Minatoguchi, M Koshiji

  • 1Second Department of Internal Medicine, Gifu University School of Medicine, Japan.

Clinical and Experimental Pharmacology & Physiology
|October 7, 1997
PubMed
Summary
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Losartan and captopril reduce blood pressure responses by inhibiting noradrenaline release. Captopril additionally reduces vascular reactivity to noradrenaline via nitric oxide pathways, modulated by bradykinin B2 receptors.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology

Background:

  • Sympathetic nervous system activity influences blood pressure through noradrenaline (NA) release and vascular reactivity.
  • Angiotensin-converting enzyme (ACE) inhibitors like captopril and angiotensin II receptor blockers (ARBs) like losartan are used to manage hypertension.
  • The precise mechanisms by which these drugs affect NA release and vascular responsiveness require further elucidation.

Purpose of the Study:

  • To investigate the differential effects of losartan and captopril on noradrenaline (NA) release and vascular reactivity in a pithed rat model.
  • To determine the role of bradykinin B2 receptors and nitric oxide (NO) in the actions of these antihypertensive agents.

Main Methods:

  • Measurement of pressor responses to sympathetic nerve stimulation (SNS) and exogenous NA administration in pithed rats.

Related Experiment Videos

  • Assessment of plasma NA concentrations following SNS.
  • Administration of captopril, losartan, sodium nitroprusside (SNP), HOE 140 (bradykinin B2 antagonist), and L-NAME (NO synthase inhibitor) alone and in combination.

    • Main Results:

    • Both captopril and losartan significantly reduced pressor responses to SNS and decreased plasma NA concentrations.
    • Captopril, but not losartan, significantly reduced vascular reactivity to exogenous NA.
    • The effects of captopril on pressor responses and vascular reactivity were partially mediated by bradykinin B2 receptors and nitric oxide.

    Conclusions:

    • Losartan and captopril inhibit NA release, contributing to their antihypertensive effects.
    • Captopril exhibits an additional mechanism by reducing vascular reactivity to NA, linked to NO production via bradykinin B2 receptor activation.
    • These findings highlight distinct pharmacological profiles of ACE inhibitors and ARBs in modulating sympathetic neurovascular function.