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The adrenaline-alpha 2-adrenoceptor-mediated vasoconstrictor axis.
Clinical Science (London, England : 1979)
|January 1, 1985
Summary
Essential hypertension involves higher plasma adrenaline, increasing adrenergic activity. This adrenaline enhances vasoconstriction via multiple adrenoceptors, contributing to elevated blood pressure.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
- Pharmacology
Background:
- Essential hypertension is linked to elevated plasma adrenaline concentrations, suggesting increased adrenergic activity.
- Adrenaline acts as a co-transmitter, enhancing noradrenaline release and contributing to vasoconstriction.
Purpose of the Study:
- To investigate the role of adrenaline and adrenoceptors in essential hypertension.
- To explore adrenaline's contribution to vasoconstriction and vascular smooth muscle contraction.
Main Methods:
- Infusion of adrenaline in forearm vasculature with blocked alpha 1- and beta-adrenoceptors.
- Assessment of platelet sensitivity to adrenaline in counteracting PGI2 effects on intracellular calcium.
- Comparison between untreated hypertensive, treated hypertensive, and normotensive subjects.
Main Results:
- Adrenaline can induce vasoconstriction via post- and extra-junctional alpha 2-adrenoceptors.
- Platelets in untreated hypertensive patients show increased sensitivity to adrenaline.
- These effects are normalized by antihypertensive treatment.
Conclusions:
- Adrenaline contributes to enhanced vascular smooth muscle contraction through pre- and post-junctional adrenoceptors.
- Increased adrenaline sensitivity in hypertension may be linked to elevated intracellular calcium concentrations.
- Antihypertensive treatment can normalize these heightened hormonal effects.