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Relaxation and decrease in [Ca2+]i by hydrochlorothiazide in guinea-pig isolated mesenteric arteries

P Pickkers1, A D Hughes

  • 1Department of Clinical Pharmacology, St. Mary's Hospital Medical School, Imperial College of Science Technology and Medicine, London.

British Journal of Pharmacology
|February 1, 1995
PubMed
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Hydrochlorothiazide, a diuretic, relaxes arteries by opening calcium-activated potassium channels. This action reduces intracellular calcium and impairs calcium influx, leading to vasodilation.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Thiazide diuretics like hydrochlorothiazide are widely used to treat hypertension.
  • The precise cellular mechanisms underlying their vasodilatory effects are not fully understood.
  • Intracellular calcium concentration ([Ca2+]i) plays a critical role in vascular smooth muscle contraction.

Purpose of the Study:

  • To investigate the effect of hydrochlorothiazide on intracellular calcium concentration ([Ca2+]i) and vascular tone in guinea-pig mesenteric arteries.
  • To elucidate the cellular mechanisms responsible for hydrochlorothiazide-induced vasodilation.

Main Methods:

  • Vascular myography was used to measure arterial tone in guinea-pig mesenteric arteries.
  • Fura-2, a calcium-sensitive fluorescent dye, was employed to monitor intracellular calcium concentration ([Ca2+]i).

Related Experiment Videos

  • Pharmacological agents including noradrenaline, charybdotoxin, and caffeine were used to modulate vascular tone and calcium levels.

    • Main Results:

    • Hydrochlorothiazide induced relaxation of noradrenaline-precontracted arteries, accompanied by a decrease in [Ca2+]i.
    • Pretreatment with hydrochlorothiazide inhibited noradrenaline-induced contraction and the associated rise in [Ca2+]i.
    • Hydrochlorothiazide-induced vasodilation and reduction in [Ca2+]i were abolished by charybdotoxin, indicating the involvement of Ca(2+)-activated K+ channels.
    • Hydrochlorothiazide did not affect calcium release from intracellular stores but slightly reduced the sensitivity of the contractile machinery to calcium.
    • The drug's action was attributed to the opening of Ca(2+)-activated K+ channels, leading to hyperpolarization and reduced calcium influx through voltage-operated calcium channels.

    Conclusions:

    • Hydrochlorothiazide promotes vasodilation by activating Ca(2+)-activated K+ channels.
    • This activation leads to membrane hyperpolarization, decreased intracellular calcium, and subsequent relaxation of vascular smooth muscle.
    • These findings provide a cellular mechanism for the antihypertensive effects of hydrochlorothiazide.