Plasma noradrenaline concentration in essential hypertension during long‐term beta‐adrenoceptor blockade with oxprenolol.

Jones, D. H.; Daniel, J.; Hamilton, CA; Reid, JL

doi:10.1111/j.1365-2125.1980.tb04792.x

Cited by 10 publications

(2 citation statements)

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“…Most studies which have attempted to determine whether suppression of sympathetic nervous system activity is the mechanism by which f3-adrenoceptor blocking drugs lower blood pressure in patients with essential hypertension have relied on the plasma concentration of the sympathetic neurotransmitter, noradrenaline, as the sole guide to sympathetic activity (Anavekaretal., 1975;Brechtetal., 1976;Jones et al, 1980). But fallacies may arise if the plasma noradrenaline concentration is used uncritically as a measure of overall sympathetic nervous tone (Esler et al, 1979) without some form of independent corroboration .…”

Section: Discussionmentioning

confidence: 99%

“…If the clearance of noradrenaline is lowered, the plasma concentration will Clonidine lowered the noradrenaline spillover rate to below normal in hypertensive patients, to levels similar to those found in patients with idiopathic peripheral autonomic insufficiency, while propranolol had no statistically significant effect overall. (Distler et al, 1978;Jones et al, 1980). Removal of noradrenaline from plasma is achieved by neuronal uptake into sympathetic nerve endings, extraneuronal uptake by other tissues, such as vascular endothelium, and metabolic conversion by 0-methylation, oxidative deamination, and conjugation (Kopin, 1979).…”

Section: Discussionmentioning

confidence: 99%

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Effect of propranolol on noradrenaline kinetics in patients with essential hypertension.

Esler¹,

Jackman²,

Leonard³

et al. 1981

Brit J Clinical Pharma

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1 The rates of noradrenaline spillover to, and removal from, plasma were measured in ten patients with essential hypertension treated with propranolol, to ascertain if long-term administration of this drug reduces sympathetic nervous system tone. 2 The plasma clearance of noradrenaline fell with propranolol, leading to a small rise in the mean plasma noradrenaline concentration. Sympathetic nervous activity in treated patients cannot be reliably gauged from plasma noradrenaline values because these are distorted by the reduction in noradrenaline clearance. 3 There was no consistent effect on noradrenaline spillover rates, which fell in six patients, but rose in the remaining four. The magnitude of the antihypertensive response was unrelated to these changes in noradrenaline release. During propranolol treatment, noradrenaline spillover rates were in every case within the normal range, much higher than in patients treated with the known sympathetic nervous systems suppressant, clonidine. 4 The principal mode of antihypertensive action of propranolol is something other than central suppression of sympathetic tone or pre-synaptic inhibition of noradrenaline release.

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Section: Discussionmentioning

confidence: 99%