Key result
Renal adrenergic vasoconstriction in hypertension is mediated primarily through alpha-2 receptors.
Why the study?
Efferent renal nerve activity and its role in adrenergic vasoconstriction in hypertensive humans were evaluated to understand sympathetic activity and receptor mediation.
Indicates increased renal sympathetic activity in hypertension; leaves open therapeutic implications for renal denervation.
In a series of investigations we have evaluated efferent renal nerve activity in hypertensive man. Net renal release of noradrenaline, calculated as the arterio-venous gradient for noradrenaline across the kidney times flow, was taken as an index of local adrenergic activity. Renal blood flow, under various circumstances, was determined by xenon-washout. At rest noradrenaline release was variable but enhanced release, indicative of increased sympathetic activity, invariably was found during isometric exercise. The latter was associated with renal vasoconstriction. Further studies, employing intrarenal infusions of either the alpha-1 antagonist doxazosin or the alpha-2 antagonist yohimbine in doses that do not produce systemic effects, demonstrate that adrenergic vasoconstriction both at rest and during isometric exercise is accomplished mainly through alpha-2 receptors. It may be that an alpha- adrenoceptor mediated vascular response also determines the efficacy of chronic beta-blockade.
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Leeuw et al. (1987) studied Hypertension. Intrarenal doxazosin or yohimbine was evaluated on Adrenergic vasoconstriction.
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