Episodic Dopamine Discharge in Paroxysmal Hypertension

Küchel, Otto

doi:10.1001/archinte.1986.00360190079011

Cited by 22 publications

(5 citation statements)

References 20 publications

(7 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The increased dopamine‐sulfate was hypothesized to act as reservoir for free dopamine, which when produced in surges caused episodic hypertension and symptoms. A subsequent case report of a patient with attacks of flushing associated with an increase in circulating free dopamine lent further support to the hypothesis proposed by Kuchel 32–35 …”

Section: Basis and Mechanisms Of The Disordersupporting

confidence: 69%

“…Approximately 50 years later, Otto Kuchel reported a similar series of mainly women, with episodic hypertension and attacks of flushing and other symptoms, in whom he described abnormalities in the disposition of circulating sulfate‐conjugated and free dopamine 32–34 . In these studies and a subsequent report, 35 the syndrome was associated with increased levels of circulating dopamine sulfate, but normal levels of norepinephrine and epinephrine.…”

Section: Basis and Mechanisms Of The Disordermentioning

confidence: 95%

See 1 more Smart Citation

Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma

Eisenhofer

Sharabi

Pacák

2008

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

Among overall numbers of patients tested for pheochromocytoma, less than 2% harbor the tumor. Among the rest, there is often no satisfactory explanation for the signs and symptoms leading to suspicion of pheochromocytoma. This group includes patients with severe symptomatic paroxysmal hypertension, often referred to as pseudopheochromocytoma, a condition that can be debilitating for patients and perplexing for clinicians. Similar to patients with the real tumor, patients with pseudopheochromocytoma can be misdiagnosed with panic disorder. However, pseudopheochromocytoma is characterized by an absence of panic or emotional distress preceding the onset of hypertension and symptoms of catecholamine excess. Because the clinical manifestations of pseudopheochromocytoma are similar, if not identical, to those due to excess circulating catecholamines in patients with the tumor, the most attractive explanation for the disorder is that it involves altered function of the autonomic nervous system. In line with this hypothesis, recent findings suggest that enhanced adrenal release of epinephrine and exaggerated cardiovascular responsiveness to catecholamines both contribute to the paroxysmal hypertension and symptoms of catecholamine excess in pseudopheochromocytoma. From this pattern, one would predict that therapeutic interventions that inhibit adrenal secretion of epinephrine or block adrenoceptor-mediated responses to catecholamines might provide a logical approach to therapy.

show abstract

Section: Basis and Mechanisms Of The Disordersupporting

confidence: 69%

Section: Basis and Mechanisms Of The Disordermentioning

confidence: 95%

Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma

Eisenhofer

Sharabi

Pacák

2008

Annals of the New York Academy of Sciences

View full text Add to dashboard Cite

show abstract

“…2 Some evidence suggests a renal dopaminergic defect in low renin 3 and stable EH. 4 However, such a defect cannot be found in borderline EH patients, who present an opposite profile, that is, higher, occasionally episodic plasma dopamine release 5 and higher urinary excretion of dopamine and some of its metabolites. 2 Because most of these patients have an increased sympathetic activity, an accelerated dopamine generation may partly reflect their increased sympathetic tone.…”

Section: Dopaminergic Abnormalities In Borderline Essential Hypertensmentioning

confidence: 99%

Dopaminergic abnormalities in borderline essential hypertensive patients.

1991

View full text Add to dashboard Cite

To explore whether an altered metabolic pathway of dihydroxyphenylalanine (DOPA) may be related to some previously observed dopamine abnormalities in borderline hypertension, we measured basal and DOPA-induced (500 mg orally) changes in blood pressure and pulse rate as well as in three hourly plasma and urine samples. We found that borderline hypertensive patients compared with controls 1) showed a higher baseline urinary excretion of methoxytyramine, a marker of exocytotic dopamine release, with a greater DOPA-induced decrease of systolic blood pressure without reflex tachycardia; 2) had in response to DOPA a blunted plasma DOPA and free dopamine increase but an accentuated plasma dopamine sulfate and urinary DOPAC excretion; and 3) eliminated comparable quantities of dopamine in urine despite a lower rise in the glomerular DOPA load. Furthermore, although DOPA elicited natriuresis in both groups, its effect was greater in borderline hypertensive patients, who lacked the urinary sodium correlation with urinary dopamine excretion seen in control subjects. These data are compatible with increased basal exocytotic dopamine release and accelerated neuronal and renal (extraneuronal) dopamine generation from administered DOPA in borderline hypertension. The DOPA-induced hypernatriuresis exceeding augmented dopamine in borderline hypertensive patients, contrasting with the urinary sodium and dopamine correlation in control subjects, suggests that DOPA induced an additional natriuresis in borderline hypertensive patients by a decrease in renal sympathetic tone because of its central inhibition of sympathetic outflow, which also may account for the absence of reflex tachycardia. {Hyperten-sion 1991;17:997-1002)

show abstract

“…60 A closer analysis has shown that the mean DA sulfate increase is due to a subgroup of borderline hypertensive patients, particularly those with anxiety-related episodic hypertension. 30,35 In addition, most of the patients with high DA sulfate had a decreased NA and A sulfoconjugation. 61 Since phenolsulfotransferase activity and sulfate availability are limit-ing factors in sulfoconjugation, it is conceivable that the high affinity DA sulfoconjugation occurs at the expense of the lower affinity NA and A conjugation and affect the biological impact of both antagonistic systems; low sulfoconjugation may increase the availability of free NA and A and their prohypertensive action whereas high sulfoconjugation decreases the free DA availability and its antihypertensive action.…”

Section: Dopamine In Essential Hypertensionmentioning

confidence: 99%

“…27 Selective plasma DA increases were found in post-traumatic stress disorders 28 and hypoxia. 29 The hypoxia-related DA release independent on sympathoadrenomedullary activity may be relevant to a selective DA increase observed in episodically flushing hypertensive patients; 30 in these patients anxiety-associated hyperventilation often accompanies episodic hypertension. 31 Hyperventilation results in respiratory alkalosis-induced decreased oxygen release to tissues which may act as a DA releasing trigger.…”

Section: Dopamine Responses To Stressmentioning

confidence: 99%

Peripheral dopamine in hypertension and associated conditions

Küchel

1999

J Hum Hypertens

View full text Add to dashboard Cite

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-

show abstract

Episodic Dopamine Discharge in Paroxysmal Hypertension

Cited by 22 publications

References 20 publications

Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma

Unexplained Symptomatic Paroxysmal Hypertension in Pseudopheochromocytoma

Dopaminergic abnormalities in borderline essential hypertensive patients.

Peripheral dopamine in hypertension and associated conditions

Contact Info

Product

Resources

About