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Biomedical subjects

O Kuchel

Publications and source records attributed to O Kuchel.

At least 91 records · Page 5Linked to original sources
PubMed1986

Episodic dopamine discharge in paroxysmal hypertension. Page's syndrome revisited.

Dopamine concentration, a marker of the sympathetic discharge additional to norepinephrine and epinephrine levels, was determined in 31 patients. These patients, mostly women, had essential hypertension and hypertensive episodes that mimicked pheochromocytoma, except that the patients were rather plethoric (instead of pale) and often had associated nausea, epigastric discomfort, and polyuria. During and after hypertensive paroxysms, plasma free norepinephrine and epinephrine levels did not increase, but we found a mean eightfold and 16-fold increase of free and sulfated plasma dopamine levels, respectively, and similar although less marked dopamine level increases in the urine collected following the paroxysm. The hypertensive paroxysms, spontaneous or precipitated by stimulation of the autonomic nervous system, were similar to those described by Page as simulating diencephalic stimulation. Dopamine level may be a marker of the sympathetic discharge, undetected by measurements of free norepinephrine level, and may explain some clinical features of Page's syndrome.

Adrenal Gland Neoplasms↗
PubMed1986

Role of sulfate conjugation of catecholamines in blood pressure regulation.

Catecholamine sulfates were found to be inactive at vascular receptor sites. Only at one nonvascular receptor site important for blood pressure (BP) regulation was dopamine-3-O-sulfate found to be an inhibitory modulator of the adrenocortical secretion of aldosterone in vitro. However, sulfation of catecholamines (CA) does play an important role in BP regulation, as shown by the following observations: Sulfoconjugated CA with a long half-life are sometimes better markers of CA release than free CA, which have short half-lives. This is particularly true of dopamine (DA) sulfate because free DA, being rapidly sulfoconjugated, is usually undetectable. This led to the recognition of a previously unsuspected role of DA in paroxysmal hypertension and orthostatic hypotension. Measurements of CA sulfates reveal potentially important storage functions for sulfoconjugation that can rapidly inactivate excessive circulating free CA and so mitigate their cardiovascular impact while building up a pool of conjugated CA. The possibility that free CA can be generated from this pool through deconjugation whenever a need for them arises should be further investigated. Reproducible individual differences in the velocity of the sulfoconjugation of infused free CA can be detected, which suggests a genetic control of certain components of the sulfoconjugating process. These differences in sulfoconjugation probably modulate the cardiovascular action of CA and of some drugs with similar structure that also undergo sulfoconjugation.

Adrenal Cortex↗
PubMed1985

Atrial natriuretic factor inhibits the early pathway of steroid biosynthesis in bovine adrenal cortex.

We have previously determined that atrial natriuretic factor (ANF) is a potent inhibitor of steroid secretion in cultured bovine zona glomerulosa and fasciculata cells. The present report describes a comparison of the effect produced by ANF on aldosterone, deoxycorticosterone and progesterone secretions by zona glomerulosa cells and on cortisol, corticosterone and progesterone secretions by zona fasciculata cells. The equipotent inhibitory action of ANF on the stimulated secretion of these steroids in both cell types indicates a common site of action prior to progesterone synthesis at which ANF inhibits the steroidogenic pathway.

Adrenal Cortex↗
PubMed1985

Gluco- and mineralocorticoids may regulate the natriuretic effect and the synthesis and release of atrial natriuretic factor by the rat atria in vivo.

Adrenalectomy abolished the acute natriuretic effect of ANF which was partially restored to about 50% by combined therapy with gluco- and mineralocorticoids. It is suggested that the lack of effect of ANF may be due to a decreased renal vascular reactivity to the peptide in adrenalectomized animals. Simultaneous administration of Dexamethasone and Deoxycorticosterone acetate to adrenalectomized rats produced a marked increase in immunoreactive ANF in atrial tissue and plasma. The administration of NaCl to these animals produced a relatively lower concentration of atrial ANF and a further increase in plasma ANF. Our results suggest that glucocorticoids may regulate synthesis and release of ANF by the atria and mineralocorticoids may have a permissive role. Furthermore, the presence of steroids is necessary for the NaCl-stimulated ANF release.

Adrenalectomy↗
PubMed1985

In vivo release of adrenal catecholamines in rats by fusaric acid.

We studied the effect of fusaric acid, an inhibitor of dopamine beta-hydroxylase (D beta H), on plasma and peripheral tissue catecholamine (CA) content and on urinary excretion of CA in the rat. We found that fusaric acid treatment resulted in a rapid decline of adrenal epinephrine (E) and norepinephrine (NE) and an increase of adrenal dopamine (DA); the kidney and heart NE and DA contents were affected in a pattern similar to that of the adrenals. In contrast, the E concentrations in the kidneys and heart were markedly elevated after a single intraperitoneal dose of fusaric acid (100 mg/kg); the maximum response was observed at 60 min, when kidney E increased from 9.3 +/- 4.4 to 101 +/- 24 pmol/g tissue and heart E in both atrium and ventricle rose from 92 +/- 8 to 607 +/- 85 pmol/g tissue and from 70 +/- 4 to 632 +/- 50 pmol/g tissue, respectively. In addition, a large increase of CA (predominantly of E) was found in the plasma of treated rats, where E, NE and DA were 27, 6.6 and 2.7 times higher than control values, respectively. The excretions of urinary E and NE were also significantly elevated during treatment. Fusaric acid-treated bilaterally adrenalectomized rats did not exhibit any increase in plasma, heart and kidney E concentrations. The results suggest that fusaric acid stimulates adrenal CA release in vivo, resulting in large increases of the main adrenal CA, E in peripheral tissues, plasma and urine. The decline in the adrenal E content is thus not only due to its decreased synthesis but also increased release.

Adrenal Glands↗
PubMed1985

CSF sulfoconjugated catecholamines in man: their relationship with plasma catecholamines.

Simultaneous plasma and cerebrospinal free and sulfoconjugated norepinephrine, epinephrine, dopamine and homovanillic acid determinations in 38 patients with various neurological disorders have shown consistently lower concentrations of dopamine sulfate, norepinephrine sulfate, and epinephrine sulfate in the cerebrospinal fluid than in plasma. An approximately three fold increase of plasma dopamine sulfate concentrations following banana ingestion did not result in increased dopamine sulfate concentrations in cerebrospinal fluid. There were positive correlations between plasma and cerebrospinal fluid concentrations of free norepinephrine and epinephrine as well as norepinephrine sulfate, dopamine sulfate and free homovanillic acid. Cerebrospinal fluid and plasma are apparently separated by the blood-brain barrier impermeable to catecholamine sulfates from the blood. Some other data and the observed positive correlation between cerebrospinal fluid and plasma dopamine and norepinephrine sulfates suggests however that catecholamine sulfates may pass from cerebrospinal fluid to the blood and reflect events in the brain.

Adolescent↗
PubMed1985

Effect of metoclopramide on plasma catecholamine release in essential hypertension.

The catecholamine (CA)-releasing action of metoclopramide (MCP) observed in patients with pheochromocytoma was tested in 20 subjects with essential hypertension and compared with the same effect of glucagon in 10 of them. We found that even in the absence of pheochromocytoma, MCP is a CA-releasing substance, moderately increasing systolic blood pressure and pulse rate. The release of CA is reflected by an increase in concentrations of free norepinephrine and total (free plus sulfated) epinephrine 3 minutes and of total dopamine and norepinephrine 10 minutes after the MCP bolus dose, whereas glucagon had an effect on the release of free epinephrine. Regional catheterization before and after MCP dosing in one subject showed a considerable increase in adrenal epinephrine and norepinephrine concentrations 45 seconds after the MCP bolus dose. MCP has a free CA-releasing potency much like that of glucagon. Because the released free CA is readily sulfoconjugated, the effect on CA release can be more easily detected when conjugated CA is determined. MCP should thus be used with caution in pheochromocytoma as well as in other forms of hypertension.

Adult↗
PubMed1985

The platelet phenolsulfotransferase is not indispensable for the sulfoconjugation of plasma catecholamines.

To investigate the role of platelets, a proposed primary site of catecholamine sulfoconjugation, we determined plasma free and sulfoconjugated catecholamines and platelet phenolsulfotransferase activity in severe platelet defficiency states. We found that even in the presence of very low platelet counts, the plasma concentrations of sulfoconjugated catecholamines were within normal limits. Although the platelet phenolsulfotransferase activity expressed per number of platelets was normal there was a considerable decrease of the total platelet phenolsulfotransferase activity. This suggests that the platelet phenolsulfotransferase is not indispensable for the sulfoconjugation of catecholamines and this process can occur elsewhere. A preliminary finding of lower platelet phenolsulfotransferase activity in platelet deficiency states with reduced platelet generation (because of reduced megakaryocytes) than in those states with a decreased platelet survival, suggests that the phenolsulfotransferase is synthesised in the megakaryocytes and the platelets are only carriers of this enzyme.

Arylsulfotransferase↗
PubMed1985

Orthostatic hypotension: a posture-induced hyperdopaminergic state.

To explore the role of dopaminergic mechanisms in orthostatic hypotension we compared the postural responses of 20 such patients to those of a control group by radioenzymatic determination of free and sulfated catecholamines and related indices. Patients with orthostatic hypotension, unlike control subjects, experienced an increase in total plasma dopamine (DA) (free + sulfate) in response to upright posture (p less than 0.01). Of the 20 patients with orthostatic hypotension, 16 were normo- or hyperadrenergic with normal basal and posture-responsive or hyperresponsive plasma free and total norepinephrine (NE). The other 4 were hypoadrenergic with low basal and posture-unresponsive NE. Hypoadrenergic patients had, in the upright position, no increase in pulse rate and more severe hypotension, less diuresis and natriuresis, lower urinary free and total DA, lower total NE excretion, and higher plasma and urinary total DA:total NE ratio than normo- or hyperadrenergic patients or control subjects. Normo- or hyperadrenergic patients had higher PRA and plasma aldosterone in the upright position than hypoadrenergic patients or control subjects (all p less than 0.05). We suggest that an excessive increase in free DA occurs in response to upright posture, perhaps representing a compensatory reaction of the remaining autonomic nervous system to an excessive fall in blood pressure. The free dopamine may be biologically active but it is so rapidly sulfoconjugated that it can be detected only as DA sulfate. These findings, combined with reports of orthostatic hypotension precipitated by administration of dopaminomimetic drugs and relieved by administration of dopaminergic antagonists, are consistent with the interpretation that excessive DA release may perpetuate, by its vasodilating and natriuretic action, the orthostatic hypotension.

Adult↗
PubMed1985

Effects of L-DOPA on the concentrations of free and sulfoconjugated catecholamines in plasma, cerebrospinal fluid, urine, and central and peripheral nervous system tissues of the rat.

The effects of subcutaneous injection of L-beta-3,4-dihydroxyphenylalamine (L-DOPA) on the concentrations of the catecholamines and catecholamine sulfates in the central and peripheral nervous systems of the rat were studied. The results showed that free 3,4-dihydroxyphenylethylamine (DA, dopamine) increased rapidly and markedly in the hypothalamus and striatum after L-DOPA but DA sulfate did not change. Increased concentrations of DA sulfate were detected in the CSF and in the plasma, where it reached a concentration of 130.8 +/- 12.8 ng/ml at 2 h, seven times the level of free DA (19.1 +/- 2.9 ng/ml). In the kidney the ratio of DA sulfate to free DA was reversed in favor of free DA. Urine samples of L-DOPA-treated rats showed a higher increase of free DA than DA sulfate, but free norepinephrine (NE) and NE sulfate remained unchanged. Concentrations of free DA and free NE in the adrenal glands of L-DOPA-treated rats showed no change. Adrenal DA sulfate and NE sulfate were not detectable in the control and L-DOPA-treated rats, suggesting that the adrenal glands lack the capacity to take up or store catecholamines and their sulfate counterparts from the plasma.

Adrenal Glands↗
PubMed1985

Peripheral dopamine synthesis and metabolism in spontaneously hypertensive rats.

We have studied several parameters of peripheral dopamine synthesis and metabolism in spontaneously hypertensive rats during the development of hypertension. Compared to Wistar-Kyoto rats, there was an increased dopamine content in 8-week-old spontaneously hypertensive rats in the adrenals (1.6 +/- 0.1 vs. 1.2 +/- 0.1 nmol/pair in Wistar-Kyoto rats) and kidneys (97 +/- 12 vs. 63 +/- 7 pmol/g tissue in Wistar-Kyoto rats), but the dopamine content in peripheral organs from normotensive 4-week-old spontaneously hypertensive rats did not differ from Wistar-Kyoto rats. In the heart, the dopamine increase was observed in 14-week-old spontaneously hypertensive rats (systolic blood pressure: spontaneously hypertensive rats, 189 +/- 9; Wistar-Kyoto rats, 106 +/- 2 mm Hg;) in both atrium (spontaneously hypertensive rats, 133 +/- 14; Wistar-Kyoto rats, 86 +/- 20 pmol/g tissue) and ventricle (spontaneously hypertensive rats, 41 +/- 6; Wistar-Kyoto rats, 23 +/- 5 pmol/g tissue). Urinary free dopamine and dihydroxyphenylacetic acid, but not norepinephrine or normetanephrine, in spontaneously hypertensive rats significantly increased between the ages of 7 and 11 weeks, reflecting the dopamine changes in tissue and suggesting a selective increase of the rate of dopamine synthesis and release.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1985

Circadian variations of free and sulfoconjugated catecholamines in normal subjects.

Normotensive recumbent subjects exhibit an early (11 p.m.) nocturnal increase in plasma dopamine, norepinephrine and epinephrine sulfates. In individual patients, this peak value is followed by a smaller nocturnal peak of catecholamine sulfates, while free catecholamine levels change in a direction opposite to catecholamine sulfates. This reciprocity of changes cannot however be demonstrated in the whole group. The origin of the nocturnal peaks of catecholamine sulfates is unknown. It may be due to a nocturnal decrease of the renal clearance of catecholamine sulfates, an increased generation of sulfates for reasons other than an increase in the free catecholamine substrate, or possibly a release of catecholamine sulfates from the brain.

Adult↗
PubMed1985

Effect of enalapril on renin, angiotensin converting enzyme activity, aldosterone and prostaglandins in patients with hypertension.

Enalapril (MK-421) was administered orally as a single dose of 2.5, 5.0, 10 and 20 mg to 13 patients with either essential or renovascular hypertension. At these doses, enalapril produced a moderate reduction in both supine and standing blood pressure as well as a significant reduction in angiotensin I-converting enzyme activity, an increase in peripheral plasma renin activity and a decrease in plasma aldosterone concentration 4 to 8 hours after administration of the drug. Plasma levels of prostaglandins E1 and E2 were unchanged. The calculated ratio of urinary Na/K was increased in the patients with renal artery stenosis after enalapril. Creatinine clearance was increased in the patients with essential hypertension and reduced in the patients with renal artery stenosis. No adverse effects occurred in these patients treated with single doses of enalapril.

Adult↗
PubMed1985

[Multiple intracranial aneurysms associated with primary hyperaldosteronism].

Multiple intracranial aneurysms have been reported in association with polycystic disease of the kidney, brain tumor, pituitary adenoma and coarctation of the aorta. We report the association of multiple aneurysms with primary hyperaldosteronism due to bilateral adrenal hyperplasia in an 18 year old left-handed man who presented with subarachnoid hemorrhage and arterial hypertension. We report the excellent outcome of this patient in spite of a difficult and surgical management. Ligation of all three intracranial aneurysms was performed after an extra-intracranial arterial bypass was done as a protective measure.

Adolescent↗
PubMed1984

The bicuculline-like properties of dopamine sulfate in rat brain.

To determine whether the convulsive action of intraventricularly injected dopamine sulfate, a dopamine metabolite present in rat brain and human cerebrospinal fluid, could be due to its interaction with GABAergic pathway, we compared the convulsive effect of dopamine sulfate with that of bicuculline in the conscious rat and determined the interaction of dopamine sulfate with [3H] GABA binding and uptake in rat brain tissues. The results showed that the convulsive effects of dopamine sulfate and of bicuculline could be abolished by GABA agonists diazepam and muscimol, but not by DA antagonists haloperidol and metoclopramide. In addition they were additive. Both dopamine 3-O-sulfate and dopamine-4-O-sulfate, like bicuculline, could displace sodium-independent [3H] GABA binding to rat brain synaptic membranes (IC50 = 400 microM) but had no action on GABA uptake. DA sulfate had no effect on [3H] strychnine binding to rat brain homogenates. This evidence together with the structural resemblance between dopamine sulfate and GABA suggested that the convulsive activity of dopamine sulfate may result from its interaction with central GABA receptors.

Animals↗