Low response of serum dopamine β-hydroxylase to stimuli in primary hypertension

DeQuattro, Vincent; Campese, Vito M.; Lurvey, Arthur; Yen, Grace; Kypridakis, George

doi:10.1016/0006-2944(76)90067-3

Cited by 14 publications

(7 citation statements)

References 23 publications

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“…There was no correlation between the percent increase in DBH levels and the percent increase in NE levels (Table 1), although in a previously reported series of 12 normotensive subjects there did appear to be such a relationship. 38 The positive significant correlation between percent increases in DBH and pulse rate might be explained if both parameters reflect the degree of circulatory adjustment to entry of interstitial fluid into the circulation after postural change. It is not surprising that DBH levels fail to reflect short-term increases in sympathetic nervous activity.…”

Section: Discussionmentioning

confidence: 99%

Lack of correlation of plasma norepinephrine and dopamine-beta-hydroxylase in hypertensive and normotensive subjects.

Lake¹,

Coleman²,

Kopin³

1977

Circulation Research

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THE ENZYME dopamine-0-hydroxylase (DBH), which is responsible for the formation of norephinephrine (NE) from dopamine, 1 is released along with the catecholamines from the adrenal medulla 2 and from stimulated sympathetic nerves in perfused organs. "5 The enzyme is present in plasma of man and other animals. 6 In animals, the levels of the enzyme are increased with stress 7 and decreased after chemical destruction of the sympathetic nerve endings but not after adrenalectomy.8 Thus, DBH in plasma appears to come from sympathetic nerve endings. In man, levels of DBH in plasma are reported to be increased by procedures that increase sympathetic neuronal activity, e.g., exercise, 9 "" immersion of the hand in cold water, 10 and insulin-induced hypoglycemia. 12 Basal levels of DBH vary widely between normal individuals, and the degree of elevation of the enzyme with stress is usually relatively small (10-25%), so increases in enzyme levels are not always observed after stress. 13 Furthermore, during the cold pressor test, levels of the other large protein molecules increase in parallel with DBH. U Thus, some investigators have found DBH to be a useful index of sympathetic function changes in DBH activity, Noth et al. 28 have stressed the need for the analysis of NE and DBH from the same plasma samples to determine whether DBH is an index of acute changes in sympathetic neuronal activity. In the present study, changes in plasma levels of DBH, total protein, a representative large protein molecule (prolactin), and NE are examined in normotensive, healthy subjects at rest, while standing, and after a standard exertion known to produce an increase in plasma levels of NE and pulse rate. 29 Since some studies have found DBH activity to be elevated in hypertensive patients or correlated with blood pressure 15 Methods Normotensive Caucasian volunteers (68 individuals of both sexes), without significant abnormalities on the basis of medical history and physical examination, and who ranged in age from 10 to 70 years, and 106 outpatients (age range, 16 to 78 years) with mild to moderate essential hypertension were asked not to take medication for 7 days nor tobacco, coffee, or tea for at least 3 hours prior to reporting for the test procedures. After a thorough explanation of the procedure, subjects gave written consent and they were asked to lie supine and relax in a quiet room. The needle of a "heparin lock" with a 3-way stopcock was inserted into an antecubital vein. A solution containing 30 units of sodium heparin (Upjohn) per milliliter sterile saline was used to flush the catheter and Downloaded from http://ahajournals.org by on June 7, 2019

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Section: Discussionmentioning

confidence: 99%

Lack of correlation of plasma norepinephrine and dopamine-beta-hydroxylase in hypertensive and normotensive subjects.

Lake¹,

Coleman²,

Kopin³

1977

Circulation Research

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“…An alternative mechanism of increased DA release may be the reduced D/3H activity (as previously found relative to TH activity in the adrenals 104 ) in several tissues (adrenal, spleen, and heart ventricle) in the prehypertensive stage of this rat model at age 6 weeks. 105 If we apply some of these findings to humans, it is conceivable that either incomplete D0H deficiency, decreased suppressibility of D/3H 31 and plasma NE 106 by a high salt intake, or as previously observed in young hypertensive patients, a reduced serum D/3H increase in response to standing and furosemide 107 may accentuate DA synthesis at the expense of NE. Moreover, in a longitudinal study (over 5 years) with originally normotensive subjects, the BP elevation found in some of them was accompanied by decreased serum D/3H activity.…”

Section: Heterogeneity Of Dopamine's Involvement In Essential Hypertementioning

confidence: 99%

Peripheral dopamine in pathophysiology of hypertension. Interaction with aging and lifestyle.

Küchel

Kuchel

1991

Hypertension

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Dopamine, an ancestral catecholamine, is physiologically natriuretic and vasodilating, thus essentially protecting against hypertension. Its actions are overshadowed by the opposite effects of its main biological partner, norepinephrine, and this is accentuated with aging. Clinical observations combined with molecular biology approaches to catecholamine-synthesizing and catecholamine-metabolizing enzymes and receptors permit the identification of some inborn defects. Subtle changes in the dopamine-norepinephrine balance may account for the enhanced peripheral noradrenergic activity seen in the setting of decreased dopaminergic activity in advanced age. These changes may contribute to the diminished ability of the aged kidney to excrete a salt load, as well as to the finding that systolic blood pressure increases with age in populations with a high, but not in those with a low, intake of salt. The attainment of advanced age in Western societies with adverse lifestyle changes (mental rather than physical stress, excess salt intake, overeating, sedentarism) appears to facilitate the development of hyperten-sion. The adaptation to all the preceding lifestyle changes necessitates an increased dopamine generation, which may initially compensate to maintain appropriate natriuresis and vasodila-tion since many patients with initial borderline essential hypertension express their sympathetic hyperfunction, in addition to increased norepinephrine release, by excessive dopamine release. However, the progression of hypertension is accompanied by a peripheral dopaminer-gic deficiency and diminished ability to excrete salt. This may represent an eventual inadequacy of a phylogenetically redundant system resulting in decreased natriuresis and vasodilation and may account for the responsiveness of established chronic hypertension to salt restriction, diuretics, and dopaminomimetic medication. (Hypertension 1991;18:709-721) O ver the last decade, it has become apparent that dopamine (DA) is an important neuro-transmitter in the peripheral nervous system. Nonneuronal (kidney, intestine, blood vessels) and neuronal (neural terminals, adrenal medulla) tissues are target organs for circulating DA and also for DA synthesized and secreted locally as a paracrine substance. DA receptors located extracellularly in plasma-exposed cellular membranes transduce their signals to the intracellular milieu through a variety of second messengers, including adenylate cyclase, phos-pholipase C, protein kinase C, and other protein kinases. Peripheral DA! receptors (typical for vascular smooth muscles and renal tubules) act via adenylate cyclase and phospholipase C stimulation, whereas DA 2 receptors presynaptically suppress the release of norepinephrine (NE) via adenylate cyclase inhibition. 1 DA has been shown to affect the actions of ion transporters as well as a variety of cellular enzymes and appears to be physiologically important in the control of renal function. The sum of the effects of physiological DA concentrations on the kidney (DA r med...

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“…basal exocytotic DA release probably preceded by accelerated DA generation from DOPA, 47 accentuated by D␤H suppression 54 and reflected by increased urinary DA excretion. 46,50 Non-modulating hypertensives who are mostly borderline were found to have increased plasma free DA.…”

Section: Dopamine In Essential Hypertensionmentioning

confidence: 99%

“…A human counterpart of these findings may be suppressed serum D␤H responses to stimuli such as posture and furosemide in borderline essential hypertension. 54 The DA abnormality in Dahl salt-sensitive rats is of different nature. Although they also have a defective D 1 -like receptor-mediated cellular signalling mechanism, 55 this defect remained not only uncompensated by increased DA but the DA synthesis appears to be attenuated.…”

Section: Experimental Evidencementioning

confidence: 99%

“…53 Even in the prehypertensive stage, adrenal D␤H activity is apparently lower in SHR and this becomes evident in the hypertensive stage also in the spleen and heart. In the lower part are human data in hypertension 54 indicating a hyporesponsiveness of serum D␤H to the combined challenge of standing plus furosemide (*P Ͻ 0.05).…”

Section: Dopamine In Essential Hypertensionmentioning

confidence: 99%

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Peripheral dopamine in hypertension and associated conditions

Küchel

1999

J Hum Hypertens

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The purpose of this study is to review the role of dopamine in hypertension and associated conditions. The analysis of literature indicates that present knowledge is mostly based on poor markers and indirect evidence of dopaminergic activity and only few molecular biological data. Alternative markers such as plasma dopamine sulfate emerge as a possible substitute for the low plasma free dopamine detectability, one of the main obstacles in understanding the relationship between circulating dopamine and its receptor actions in hypertension. Essential hypertension represents a heterogeneous entity: based on evidence in borderline and non-modulating hypertension, the tubular dopamine receptor defect may be compensated by increased dopamine synthesis (dopamine ␤-hydroxylase suppression-mediated?) and release; alternatively, compatible with data in stable, salt-sensitive and low renin-

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Low response of serum dopamine β-hydroxylase to stimuli in primary hypertension

Cited by 14 publications

References 23 publications

Lack of correlation of plasma norepinephrine and dopamine-beta-hydroxylase in hypertensive and normotensive subjects.

Lack of correlation of plasma norepinephrine and dopamine-beta-hydroxylase in hypertensive and normotensive subjects.

Peripheral dopamine in pathophysiology of hypertension. Interaction with aging and lifestyle.

Peripheral dopamine in hypertension and associated conditions

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