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Biomedical subjects

N T Buu

Publications and source records attributed to N T Buu.

At least 91 records · Page 5Linked to original sources
PubMed1981

The extra-adrenal synthesis of epinephrine in rats. Possible involvement of dopamine sulfate.

Bilaterally adrenalectomized rats were administered [3H]L-dopa, [3H]DA, and [3H]DASO4. Both [3H]L-dopa and [3H]DASO4 were found to generate [3H]E in the urine and kidney tissues of adrenalectomized rats, whereas [3H]DA did not produce any detectable [3H]E. [3H]CAs in tissues and urine were analyzed by reverse-phase high-performance liquid chromatography. The identities of the [3H]CAs in the urine were further verified by a double-labeling radioenzymatic technique. The results demonstrated that in the rat E can by synthesized outside the adrenals and that DASO4 can serve as an intermediate in such a synthesis. [3H]DASO4 was also converted to [3H]DA and [3H]NE, indicating that it can be metabolized in vivo and could be the source of free DA in urine.

Adrenal Glands↗
PubMed1980

Conjugation of catecholamines, a variable to be accounted for in human hypertension.

A subgroup of essential hypertensive (EH) patients with high sympathetic tone had low plasma conjugated norepinephrine (NE) and epinephrine (E), but elevated free NE and E and a hyperresponsiveness to various stimuli to the autonomic nervous system. Pheochromocytoma patients could also be divided according to conjugated NE + E levels, this time into normal and elevated conjugated groups. The latter seem to be somewhat protected by the conjugation, showing less free NE and E 'flooding' during hypertensive crises and lower VMA excretion. The degree of catecholamine conjugation can thus modify the sympathetic tone in hypertension.

Adrenal Gland Neoplasms↗
PubMed1979

Dopamine-4-O-sulfate: a possible precursor of free norepinephrine.

Incubation of dopamine-4-O-sulfate with purified bovine dopamine-beta-hydroxylase led to the formation of free norepinephrine. The production of free norepinephrine was completely inhibited in the presence of 5.6 mM of fusaric acid, an inhibitor of dopamine-beta-hydroxylase. No sulfatase activity was detected in the incubation medium. The reaction of dopamine-4-O-sulfate with dopamine-beta-hydroxylase followed Michaelis-Menten kinetics, showing an apparent Km of 2.6 mM.

Adrenal Glands↗
PubMed1978

Free and conjugated catecholamines in human hypertension.

1. Noradrenaline and adrenaline in the adrenal vein of essential hypertensive patients are almost exclusively (99%) unconjugated or free. However only 17% of dopamine is free, the rest is conjugated. The further the site of sampling from the adrenal vein the closer come the free catecholamines to their normal peripheral venous proportion (noradrenaline + adrenaline 20%, dopamine less than 1% of total catecholamines). Deviations from these patterns help to detect the site and type of secretion of phaeochromocytoma. 2. Essential hypertensive patients have, compared with control subjects, higher conjugated plasma dopamine, less urinary free and conjugated dopamine with blunted urinary free dopamine and sodium responsiveness to frusemide. Conjugated noradrenaline + adrenaline, mean arterial pressure and age are positively interrelated. 3. Patients with primary aldosteronism have elevated plasma and urinary total dopamine. After removal of the adenoma urinary dopamine excretion decreases to normal. 4. Elevated conjugated dopamine appears to reflect a compensatory activation of the dopaminergic vasodilator pathway in hypertension, the total urinary dopamine excretion an intrinsic deficiency or compensatory increase of a dopamine-modulated natriuretic mechanism.

Adrenal Gland Neoplasms↗
PubMed1978

Dopamine-sodium relationship: is dopamine a part of the endogenous natriuretic system?

A possible role of DA as an endogenous natriuretic hormone was reviewed under three aspects: (1) its excretion in response to saline vs. albumin-induced volume expansion, (2) the origin of urinary free DA and (3) urinary free DA excretion in an unexplained salt-retaining condition, idiopathic edema. We have shown (1) that the urinary free DA excretion increase in response to saline is specifically related to salt and does not occur when the same degree of volume expansion is induced by albumin, (2) that this increase in free DA originates in the kidney and (3) that idiopathic edema patients excrete less free DA than control subjects. It is proposed that free DA originating in the kidney is a rather sal than volume-dependent endogenous natriuretic factor. Its deficiency may contribute to excessive sodium retention in idiopathic edema. However, DA is probably not the single natriuretic hormone but a part of a natriuretic system, components of which are other renal vasodilating and natriuretic substances such as prostaglandins and kallikrein-bradykinin.

Animals↗
PubMed1977

Competitive inhibition of catechol O-methyltransferase by RO-4-4602.

RO-4-4602, a peripheral L-DOPA decarboxylase (EC 4.1.1.28) inhibitor was shown to also inhibit the activity of catechol O-methyltransferase (COMT) (EC 2.1.1.6). Kinetic study indicated that the inhibition is of a competitive nature. The apparent Ki values of 7 X 10(6), 5.3 X 10(-6, and 9 X 10-6) M calculated from Lineweaver-Burke plots when dopamine, norepinephrine, and epinephrine, respectively, were used as substrate, showed that this drug is the most potent inhibitor of COMT yet known.

Animals↗
PubMed1977

Effects of saline and albumin on plasma and urinary catecholamines in dogs.

Volume expansion by infusion of saline and 25% albumin has been compared in dogs to differentiate volume- and salt-induced catecholamine changes previously observed in humans. Plasma and urinary norepinephrine (NE) and epinephrine (E) decreased following both saline (urinary) NE+E, from 17.3 +/- 3.4 to 6.8 +/- 1.5 ng/min; P less than 0.005) and albumin (from 29.9 +/- 3.4 to 12.5 +/- 2; P less than 0.001) infusion. Urinary dopamine increased in saline-expanded dogs (from 3.4 +/- 0.6 to 4.4 +/- 0.8 ng/min, P less than 0.05), but did not significantly change in control and albumin-expanded dogs; whereas plasma free dopamine remained uninfluenced by saline or albumin. The mean renal clearance of dopamine more than doubled (from 110 +/- 37 to 272 +/- 96 ml/min; P less than 0.05) in response to saline expansion, but did not significantly change in response to albumin expansion or in control animals. A significant correlation between the increase of urinary dopamine and the tubular rejection fraction of sodium was found in saline-expanded dogs (P less than 0.05), or when all experiments (saline, albumin expansion, and control dogs) were considered together (P less than 0.001). The data indicate that : 1) the increase in urinary dopamine excretion (concomitant with sodium excretion) is related to the saline infusion rather than to the suppression of the sympathetic nervous system induced by plasma volume expansion; 2) this increased urinary dopamine originates probably in the kidney. Dopamine may thus be somehow related to regulation of urinary sodium excretion, either as an endogenous natriuretic factor or a response reflecting natriuresis.

Albumins↗
PubMed1977

Catecholamines, cyclic AMP and renin in two contrasting forms of essential hypertension.

Essential hypertension (EH) can be subdivided according to the sympathetic and renin activity into two contrasting forms: (1) borderline beta-hyperadrenergic renin hyperresponsive and (2) stable beta-hypoadrenergic renin hyporesponsive EH. These two forms probably represent two expreme poles in the spectrum of EH in which sympathetic and renin hyper- or hyporeactivity cannot be accounted for by catecholamine determinations solely. beta-Adrenergic responsiveness monitored by plasma cyclic AMP determinations revealed plasma cyclic AMP, renin and circulatory hyperresponsiveness to isoproterenol in borderline hyperadrenergic EH while the opposite, cyclic AMP and renin hyporesponsiveness to insulin-induced hypoglycemia have been described in low renin stable EH. The kidney is in the center of the adrenergic abnormality in the two forms of EH with the borderline one excreting into the urine catecholamines not accounted for by their glomerular filtration. Catecholamines solely, however, do not account for the differences in both forms of EH which can probably be attributed to their different beta-adrenergic responsiveness.

Adrenergic beta-Antagonists↗
PubMed1977

Catecholamine excretion in "idiopathic" edema: decreased dopamine excretion, a pathogenic factor?

In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146 +/- 13 SE ng/ml/m2 vs. 212 +/- 32, P less than 0.05 in the supine position and 140 +/- 9 vs. 199 +/- 20, P less than 0.005 combined values of supine and recumbent positions) and was also lower when pooled values for urinary dopamine excretions both before and after furosemide were compared in idiopathic edema patients and in control subjects (270 +/- 30 ng/ml vs. 480 +/- 70, P less than 0.05). These patients have lower basal sodium excretions, decreased tubular rejection fractions of sodium in the upright position and lower urinary sodium excretions following furosemide administration. The urinary sodium and dopamine excretions before and following furosemide are positively correlated in control (P less than 0.05), idiopathic edema patients (P less than 0.02) and in both groups combined (P less than 0.005). Idiopathic edema patients have normal urinary noradrenaline and adrenaline excretions but, as previously observed, elevated: 1) plasma renin activity while either recumbent or upright, and 2) plasma aldosterone concentrations while upright. These results suggest that a decrease in urinary dopamine, a catecholamine recently recognized to have natriuretic action, possibly reflects a suppression of the renal dopaminergic system and may contribute to the excessive sodium retention in idiopathic edema either directly or indirectly through the renin-aldosterone system.

Adult↗
PubMed1977

A new method for the hydrolysis of conjugated catecholamines.

A new method of hydrolysis of conjugated CA's in plasma and urine has been developed. It is based on the lyophilization of dilute perchloric acid solutions of plasma and urine. The hydrolysis of the CA conjugates was more complete by this method than by the standard method by enzymatic hydrolysis. The identity of the products was verified by TLC. DA, undetectable in 95% of normal subjects, was found to exist almost exclusively in the conjugated form, averaging 0.74 +/- 0.17 (S.E.) ng/ml. Free and conjugated NE and E in human plasma were 0.23 +/- 0.03 and 0.32 +/- 0.27 ng/ml, respectively. The new and simple method of hydrolysis of conjugated CA's may help in the search for the physiological meaning of the conjugation.

Adult↗