Plasma norepinephrine and dihydroxyphenylglycol in essential hypertension.

Abstract

The aim of the present study was to examine whether essential hypertension is associated with altered plasma concentrations of dihydroxyphenylglycol, the principal presynaptic metabolite of norepinephrine. Forearm venous plasma dihydroxyphenylglycol and norepinephrine were determined at rest and during graded orthostasis in 47 normotensive control subjects and 58 outpatients with essential hypertension. There was no group difference in age. At supine rest as well as during sitting and standing, hypertensive subjects had plasma norepinephrine concentrations similar to those in normotensive control subjects, but plasma dihydroxyphenylglycol concentrations were higher than those in normotensive control subjects. Both groups snowed a linear relation between plasma dihydroxyphenylglycol (ordinate) and plasma norepinephrine (abscissa). The resulting regression line was steeper (p<0.02) and its ordinate intercept higher (/?<0.01) in hypertensive than in control subjects. Eleven normotensive and 14 hypertensive subjects were also tested 3 hours after desipramine (1.5 mg/kg orally) was administered to inhibit neuronal norepinephrine reuptake. The drug did not alter plasma norepinephrine, but did reduce plasma dihydroxyphenylglycol and did abolish plasma dihydroxyphenylglycol responses to upright posture in both groups of subjects. The mean plasma dihydroxyphenylglycol concentration observed in the presence of desipramine again was higher in the hypertensive than in the control group (p<0.01) and closely agreed, in both groups, with the dihydroxyphenylglycol concentration given by the ordinate intercept of the dihydroxyphenylglycol versus norepinephrine regression line in the absence of desipramine. Thus, the desipramine-resistant and desipramine-sensitive component of plasma dihydroxyphenylglycol (i.e., dihydroxyphenylglycol formed from vesicular norepinephrine leaking out of the transmitter stores and from synaptic norepinephrine subsequent to neuronal recapture, respectively) appear to contribute to the elevated plasma dihydroxyphenylglycol concentration in essential hypertension. (Hypertension 1991;17:546-552) T he available evidence indicates a role of the sympathetic nervous system in the development and maintenance of primary hypertension both in humans and spontaneously hypertensive rats (SHR).1 -7 Despite this widely held view, the plasma norepinephrine concentration, which has been used as a measure of sympathetic tone, is not consistently elevated above normal in patients with essential hypertension. 89 However, even plasma norepinephrine levels within the normal range are inappropriately high when the high blood pressure in these individuals is taken into consideration. This Supported by the Ernst and Hedda Wollheim-Stiftung, Wurzburg, FRG.Address for correspondence: Josef Ludwig, Medizinische Poliklinilc der Universitat, KlinikstraBe 6-8, W-8700 Wurzburg, FRG.Received July 31, 1990; accepted in revised form November 30, 1990. may indicate a reduced baroreceptor reflex sensitivity 1011 or an enhanced dens...

Plasma Metadrenalines: Do they Provide Useful Information about Sympatho-Adrenal Function and Catecholamine Metabolism?

“…The regression line for the relationship between plasma noradrenaline and DHPG intersected the yaxis well above the origin, consistent with formation of most DHPG from metabolism of noradrenaline leaking from vesicles and not released by nerves [3,4,30]. In contrast, the relationship between nor metadrenaline and noradrenaline intersected the yaxis closer to the origin, consistent with formation of most (60%) normetadrenaline from neuronally released noradrenaline.…”

Dietary methyl-consuming compounds and metabolic syndrome

“…66 A lack of methyl groups may decrease the degradation of catecholamines and thus contribute to elevated circulating catecholamines. Hence, the increased level of unmethylated intermediates of catecholamines, such as dihydroxyphenylglycol and dihydroxymandelic acid [71][72][73] observed in patients with hypertension and CVD may be related to methyl depletion/deficiency.…”