PubMed Health⌕ Search

Biomedical subjects

N T Buu

Publications and source records attributed to N T Buu.

107 records · Page 6Linked to original sources
PubMed1976

Circadian variations of the urinary excretion of catecholamines and electrolytes.

Concomitant measurements of circadian variations in the urinary excretion of dopamine (DA), homovanillic acid (HVA), norepinephrine (NE), epinephrine (E) as well as of creatinine, sodium and potassium under controlled dietary conditions during relative physical and emotional rest in 13 volunteers have shown that maximum excretion of all these substances occurred in the afternoon period between 14:30h and 18:00h, and minimum excretion in the morning between 4:00h and 5:00h. The changes were in some cases progressive from one collection period to the other, and synchronized for NE and E. DA and HVA excretions fluctuated from subject to subject. Excretory rhythms of sodium and potassium were found to be similar to those of the catecholamines. This can be explained by diurnal changes in renal blood flow and different renal excretory mechanisms of catecholamines. None of the catecholamines correlated with the urinary volume but urinary NE and E positively correlated with urinary creatinine, urinary NE and E with urinary DA and urinary sodium with urinary E. There are some common patterns in the diurnal rhythms of catecholamines and electrolytes but their interrelationship is different for individual catecholamines.

Adult↗
PubMed1974

Biological actions in vivo and in vitro of two gamma-aminobutyric acid (GABA) analogues: beta-chloro GABA and beta-phenyl GABA.

1 The synthesis of two analogues of gamma-aminobutyric acid (GABA), beta-chloro GABA and beta-phenyl GABA is described.2 The activity of brain GABA aminotransferase was inhibited by beta-chloro GABA (5.7 x 10(-5)M) and beta-phenyl GABA (4.6 x 10(-3)M) in a competitive manner with GABA.3 beta-Chloro GABA exhibited 50% of the inhibitory activity of GABA in blocking the discharge of the crayfish stretch receptor neurone; beta-phenyl GABA had no detectable effect.4 Injection of beta-phenyl GABA (200 mg/kg) into normal or epileptic cats (cobalt) caused the appearance of synchronized slow-wave EEG activity.5 Administration of beta-chloro GABA (200 mg/kg) to epileptic cats (cobalt) produced a temporary diminution or abolition of epileptic discharges while causing no alteration in normal EEG activity.6 beta-Chloro GABA and beta-phenyl GABA had no effect on the concentrations of catecholamines or of amino acids in mouse brain.7 The results suggest that both beta-chloro GABA and beta-phenyl GABA may pass the blood-brain barrier.

Amino Acids↗
PubMedDate not supplied

Hypertension in hyperthyroidism: is there an epinephrine connection?

Since hypertension seen in euthyroid subjects with depressed conjugated epinephrine and moderately elevated free epinephrine in plasma is strikingly similar to the beta-hyperadrenergic, high-output hypertension seen in some hyperthyroid patients, the possibility is discussed that thyroid action on sulfoconjugation could affect the biodisposability of endogenous free E and so indirectly the manifestation of sympathetic hyperactivity. There is only circumstantial evidence for such a possibility at present. Differences in the conjugation system may be operative in dealing with endogenous as well as exogenous catecholamines. If the latter are used in evaluating the adrenergic receptor reactivity, this may result in incorrect dose-response curves if the concentrations of catecholamines remaining free following infusion are not monitored. The conjugation of catecholamines, E in particular, is a variable which has to be taken account of in the investigation of catecholamine-like manifestation of T3 and T4 excess and in the evaluation of adrenergic influences on thyroid function.

Blood Pressure↗
PubMedDate not supplied

Atrial natriuretic factor in the spinal cord of normotensive and hypertensive rats.

Atrial natriuretic factor (ANF) was investigated in the rat spinal cord and hypothalamus using two radioimmunoassays. ANF was also quantified in both tissues of Spontaneously Hypertensive Rats and Dahl rats. Spinal cord and hypothalamus were found to be immunoreactive to proANF and its near-NH2- or near-COOH-terminal fragments. A major part of the extracted ANF was a COOH-terminal peptide smaller than or the same as ANF (Ser99-Tyr 126). SHR had higher hypothalamic and spinal cord ANF concentrations than Wistar Kyoto rats, while the Dahl salt-sensitive animals exhibited an increase in spinal cord ANF when compared with the Dahl salt-resistant group. The data suggest that spinal cord may produce ANF locally with processing similar to that in hypothalamus. Changes in ANF concentrations occurring during the course of hypertension remain to be further investigated.

Animals↗
PubMedDate not supplied

Effect of prolonged high salt intake on atrial natriuretic factor's kinetics in rats.

Plasma atrial natriuretic factor (ANF) paradoxically decreases after 5 weeks (but not after 3 weeks) of 8% NaCl intake in normotensive rats. As this phenomenon remains unaccounted for by changes in ANF production, we studied the disappearance of [125I]ANF(99-126) from the circulation as an alternative explanation of plasma ANF decline. Following 5 weeks (but not 3 weeks) of an 8% NaCl diet, plasma concentrations of [125I]ANF were significantly decreased and metabolic clearance rate and volume of distribution were increased compared to control rats fed a 0.8% NaCl diet. By studying [125I]ANF tissue uptake we noted significantly greater peptide uptake after 5 weeks (but not after 3 weeks) of high salt consumption in several tissues. We hypothesize that prolonged (at least 5 weeks) 8% NaCl ingestion increases the density and/or affinity of ANF binding sites. These changes may be responsible for the previously observed decline in plasma ANF concentrations after a prolonged high salt intake.

Animals↗
PubMedDate not supplied

An increase in urinary catecholamines of renal origin in patients with "borderline" hypertension.

Plasma and urinary catecholamines (norepinephrine and epinephrine) and urinary dopamine excretion were studied in 45 essential hypertensive patients subdivided into borderline (labile) and stable hypertension. Borderline hypertensive patients had a higher mean fractional renal clearance of catecholamines (the clearance of catecholamines relative to creatinine clearance) than both control subjects and stable hypertensive patients. A significantly positive correlation between the renal clearance of catecholamines and urinary dopamine excretion was also found in those with borderline hypertension, but not in control subjects or those with stable hypertension. These data indicate that patients with borderline hypertension have a relatively exaggerated renal catecholamine release. They probably reflect an increased sympathetic discharge to the kidney in "borderline" hypertension, occuring to a lesser degree in stable hypertension and control subjects. Thus, urinary catecholamine measurements do not specifically reflect the level of circulating catecholamines, particularly in borderline hypertension.

Adult↗
PubMedDate not supplied

Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?

Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.

Adolescent↗
PubMedDate not supplied

Sulfoconjugation of catecholamines, nutrition, and hypertension.

Sulfoconjugation is an important metabolic pathway determining the fate and potential cardiovascular action of ingested phenolic substances. Among the three catecholamines, dopamine (DA) is to the highest degree sulfoconjugated and has the highest affinity toward the phenolsulfotransferase (PST). The concentration of some sulfated catecholamines, particularly of DA sulfate, increases following ingestion of catecholamines or their precursors. This can be confounded with blood-derived increases in DA sulfate associated with BP peaks in some hypertensive patients. We mimicked, therefore, the latter condition by infusion of free DA into normotensive subjects. At low DA infusion rates, plasma DA sulfate exceeded free DA concentrations, and there were no changes in blood pressure and pulse rate. At higher DA infusion rates, blood pressure and pulse rate increased only while plasma free DA concentrations exceeded those of DA sulfate, indicating that free DA remains biologically active only prior to being conjugated. A similar increase in DA sulfate from alimentary sources (e.g., eating a banana) remains without cardiovascular response and is not associated with an overflow of free DA, since all the ingested DA is conjugated in the gut. We describe a patient with pheochromocytoma who experienced repeated hypertensive crises after ingestion of food containing some biogenic amines, (once also documented by NE increase), possibly due to a phenol sulfoconjugation defect (e.g., substrate inhibition of the PST or its genetic deficiency). Platelet PST-determinations may serve as a screening tool to detect subjects with sulfoconjugation defects since they probably reflect the PSt activity in the gut where ingested phenols are sulfoconjugated.

Adrenal Gland Neoplasms↗
PubMedDate not supplied

Dopamine surges in hyperadrenergic essential hypertension.

From a total of 61 referred hypertensive patients, 21 were clinically suspected of pheochromocytoma but in none was this diagnosis confirmed. Instead we found nine of the 21 patients had surges of conjugated dopamine during hyperadrenergic periods unaccounted for by rise in norepinephrine (NE) or epinephrine (E). Overall, essential hypertensive (EH) patients had in plasma (ng/ml) higher conjugated dopamine (DA) (2.3 +/- 0.2 vs 1.0 +/- 0.1, p less than 0.01), increasing with age (p less than 0.01), lower conjugated NE + E (0.6 +/- 0.1 vs 1.2 +/- 0.2, p less than 0.01), and higher free E (p less than 0.007), lower urinary free DA and total DA but higher free NE + E excretions (each p less than 0.05) than 24 control subjects. Following the DA surges, a short-lived urinary overflow of total DA occurred. The patients with DA surges were older, had a higher incidence of low conjugated NE + E (less than 0.23 ng/ml), a higher proportion of arterial free DA, and higher venous baseline conjugated plasma DA than the rest of the patients. Patients with low conjugated NE + E had in turn higher plasma DA concentrations at several regional sampling sites than patients with normal conjugated NE + E. High conjugated DA in EH probably results from pulsatile DA surges leading to a rise of baseline plasma conjugated DA. In the short run DA pulses can result in temporary alpha- and beta-adrenergic actions of huge arterial free DA concentrations prior to DA conjugation; in the long run the excessive high affinity DA conjugation may take preference to the lower affinity NE and lowest affinity E conjugation and free E increases. Both result in an acute or chronic increase of sympathetic tone.

Adolescent↗
PubMedDate not supplied

Regional sources of free and sulfoconjugated catecholamines in hypertension.

To elucidate the sources of free catecholamines (CA) and their sulfates in hyperadrenergic essential hypertensives (EH), their arteriovenous differences were determined radioenzymatically and by sulfatase hydrolysis (with correction for cross-contamination) across several organs and regions in 16 hyperadrenergic essential hypertensive patients. Comparison with arterial concentrations showed that: the adrenal venous outflow contains 240 times more free epinephrine (E), 55 times more free norepinephrine (NE), and 7 times more free dopamine (DA) concentrations, but E, NE, and DA sulfates are not different; free E concentrations are lower in the peripheral venous blood; NE sulfate concentrations are higher in the superior vena cava (p less than 0.05 for all differences noted). The data suggest the following conclusions for hyperadrenergic EH patients: with the exception of NE sulfate added into the superior vena cava region, no other organ or region can be associated with a net DA or NE sulfate release. The proportional adrenal vein concentrations of DA:NE:E are approximately 1:10:50, which are very close to those seen in other studies performed under different degrees of stress. Free E is extracted in peripheral tissues. The DA surges in hyperadrenergic EH patients probably result from the pulsatile, predominantly adrenal, release of free DA.

Arteries↗
PubMedDate not supplied

Bromocriptine decreases blood pressure of spontaneously hypertensive rats without affecting the adrenomedullary synthesis of catecholamines.

Because of controversial data on the role of adrenomedullary catecholamines (CA) in the hypertension of spontaneously hypertensive rats (SHR) and in the hypotensive action of bromocriptine, we studied the effect of chronic bromocriptine treatment on blood pressure (BP), adrenal CA synthesis, tissue CA, and urinary excretions of CA and their metabolites in SHR. We found that the hypertension of 12-week-old SHR (systolic BP, 181 +/- 13 mm Hg) was reduced to 123 +/- 8 mm Hg when they received bromocriptine between 4 and 12 weeks of age (2 X 600 micrograms/kg/day, intraperitoneally). Although the urinary epinephrine (E) and the synthesis of adrenal norepinephrine (NE), E, and dopamine (DA), as well as the tissue content of CA in adrenals, heart, and kidney, remained unchanged after bromocriptine treatment, the urinary NE and DA excretions were lower in bromocriptine-treated SHR than in sham-treated SHR (NE, 2.7 +/- 0.3 versus 4.2 +/- 0.3 nmol/24 h in control SHR; DA, 18.7 +/- 1.6 versus 28.2 +/- 2.2 nmol/24 h in control SHR). In SHR, bromocriptine treatment did not affect the previously observed selectively increased adrenal turnover and synthesis of DA or the urinary excretions of normetanephrine (NM), dihydroxyphenylacetic acid (DOPAC), 3-methoxytyramine (3-MT), or homovanillic acid (HVA). The results suggest that the bromocriptine-induced decrease of BP in SHR is not mediated by changes in adrenomedullary CA and that bromocriptine decreases the BP of SHR without affecting the previously observed increased adrenal DA release of SHR. Thus, other central or peripheral dopaminergic agonist actions of bromocriptine bypassing the adrenal medulla must be considered in the hypotensive action of the drug.

Adrenal Medulla↗
PubMedDate not supplied

Dopamine negatively modulates its own blood pressure increasing action.

To evaluate the mechanisms of the hypertensive action of dopamine and its dependence on its metabolic patterns we infused a borderline hypertensive dose of free dopamine into healthy subjects. The moderate rise in systolic and diastolic blood pressure with an expected considerable increase of plasma free dopamine concentrations was associated within 30 minutes with an increase in plasma free norepinephrine and huge increases in plasma 3-4-dihydroxyphenylacetic acid, homovanillic acid and dopamine sulfate, the latter mostly between 60 and 180 minutes of infusion when diastolic blood pressure decreased. The overall pre-, per- and postinfusion changes in systolic blood pressure were negatively correlated with corresponding changes of free dopamine and dopamine sulfate. Reproducible patterns of blood pressure responses to the dopamine infusion made possible a subdivision into those who were blood pressure responders (who generated dopamine sulfate with delay) and non responders (who generated dopamine sulfate immediately). The data suggests that the 4 micrograms/kg/min dopamine infusion rate raises blood pressure indirectly via norepinephrine. Free dopamine and dopamine sulfate (the velocity of generation of which may be an inherited trait) are probably negative modulators of this action.

Adult↗