Search PubMed⌕ Search

Biomedical subjects

L Davidson

Publications and source records attributed to L Davidson.

At least 145 records · Page 8Linked to original sources
PubMed1984

The effect of ascorbic acid on the sulphate conjugation of ingested noradrenaline and dopamine.

Changes in the plasma concentration of free and conjugated noradrenaline (NA) and dopamine (DA) following oral administration of these catecholamines were examined in four normal males before and after treatment with ascorbic acid. The marked increase in plasma conjugated DA and NA was considerably reduced after ascorbic acid treatment, presumably due to competitive inhibition of sulphate conjugation. In one subject where there was a considerable delay in the appearance of sulphates, an early rise in free NA and DA concentration occurred. There were no changes in plasma free NA in the other subjects, although DA increased in two after ascorbic acid treatment. These findings emphasise the importance of sulphate conjugation in the gut or liver in inactivating endogenous amines in foods and indicate that interference of this protective mechanism may arise from high doses of ascorbic acid and other related compounds which compete for sulphation.

Adult↗
PubMed1984

Catecholamines in aqueous humour of glaucoma patients.

Aqueous humour catecholamine concentrations were assayed in open angle glaucoma, and cataract patients during surgery, under general anaesthesia. Plasma catecholamines were measured at the same time. Aqueous humour noradrenaline is apparently reduced by pretreatment with adrenaline, timolol and pilocarpine. (Noradrenaline concentrations were 0.599 +/- 0.239 ng/ml in glaucoma, and 0.970 +/- 0.445 ng/ml in cataract patients.) Dopamine was found in two of six cataract patients (0.123 and 0.318 ng/ml), and in all the glaucoma group (0.221 +/- 0.170 ng/ml). Plasma noradrenaline concentration was probably increased in glaucoma, when compared to the cataract patients. These results confirm our findings in the non-human primate, and suggest that adrenaline may act, at least in part, by causing denervation or inhibition of noradrenaline release in the anterior segment of the eye, and probably by release of dopamine into the aqueous humour. The unexplained and new finding of dopamine in the aqueous humour may have some bearing on the action of dopaminergic drugs for the treatment of glaucoma. Future treatment of ocular hypertension may rely more on sympathetic denervation than on conventional adrenergic therapy.

Adrenergic Agonists↗
PubMed1984

Free and sulfate-conjugated catecholamines during exercise in man.

The study examined the plasma concentration of free and sulfate-conjugated norepinephrine (NE) and epinephrine (E) at rest and after vigorous bicycle exercise. Free and total catecholamines were measured by a modified radioenzymatic assay using external standards. This assay was less costly and, in subjects with normal renal function, plasma levels were highly comparable to those obtained using internal standards. Exercise was associated with a predictable rise in plasma free NE and E concentration, which correlated with the hemodynamic changes, and a significant decrease in the levels of catecholamine sulfate conjugates. There was an inverse relationship between the degree of conjugation and the free levels of NE and E both at rest and after exercise. This suggests that the degree of conjugation is another factor determining the concentration of free amines in plasma.

Adult↗
PubMed1984

Aqueous humor catecholamines.

The catecholamines norepinephrine, (NE) epinephrine (E) and dopamine (DA) were detected for the first time in the aqueous humor of humans under general anesthesia and monkeys under ketamine. The catecholamine levels in aqueous humor of 9 humans were assayed. NE was 0.796 +/- 0.457 ng./ml., E ranged between 0 and 0.132 ng./ml. in 4 out of 9 subjects, and DA was found in 2 of the 9 eyes. (0. 123ng ./ml. and 0. 318ng ./ml..) Plasma levels were measured in 8 of the human subjects at the time of aqueous sampling -NE was 0.311 +/- 0.171, E ranged between 0 and 0.097 (4 out of 8 subjects) and DA was detected in one subject- 0.037 ng./ml.. Monkey aqueous levels were NE:2.843 +/- 0.668 and DA:0.462 +/- 0.177 ng./ml., with an intact iris. (N = 8 eyes.) NE was 0.497 +/- 0.049, and DA 0.426 +/- 0.218 ng./ml. after total iridectomy. (N = 4 eyes) E was not detected in the monkey under these conditions. Whilst NE may be produced in part by the iris, DA levels were not affected by iridectomy. This implies that DA may be produced by structures unrelated to sympathetic nerve endings of the iris in the anterior segment of the non-human primate eye, perhaps by diffusion from the ciliary body or retina. Ketamine is known to inhibit catecholamine uptake, which may explain the high levels measured in the monkey. Human aqueous catecholamine levels measured under anesthesia may be affected by a variety of the drugs used. It is postulated that dopaminergic neurones and associated receptors may be present in the anterior segment of the eye. This may explain the presence of aqueous humor dopamine and the effects of dopaminergic drugs on intraocular pressure.

Adult↗
PubMed1983

The effect of ascorbic acid on plasma sulfate conjugated catecholamines after eating bananas.

The effects of eating bananas, a rich source of biogenic amines, on the plasma concentration of free and sulfate conjugated norepinephrine (NE) and dopamine (DA), and free epinephrine (E), were examined in normal male subjects before and after treatment with ascorbic acid, 2 g daily for 7 days. There were no significant changes in the levels of free NE or E in any subjects after eating a banana, either before or after ascorbic acid. Plasma free DA became detectable in some subjects, but the overall changes were not significant. Sulfate conjugated DA and NE increased markedly after banana ingestion, as previously demonstrated in our laboratory. After ascorbic acid treatment the rise in sulfate conjugated NE was attenuated, presumably because ascorbic acid acts as a competitive inhibitor of sulfate conjugation. In contrast, the rise in conjugated DA was potentiated after ascorbic acid treatment. This may be indicative of the higher affinity of DA for phenolsulfotransferase, an inhibitory effect of ascorbic acid on dopamine-receptor coupling or of ascorbic acid protecting DA from oxidation in the gut.

Adult↗
PubMed1983

Diurnal rhythms of blood pressure, plasma renin activity, angiotensin II and catecholamines in normotensive and hypertensive pregnancies.

Diurnal patterns of blood pressure and pressor hormones after 26 weeks gestation were compared in 10 normotensive women, 13 subjects with uncomplicated hypertension, and 8 with biochemical evidence of pre-eclampsia. 4 of the pre-eclamptics showed nocturnal hypertension. Levels of plasma renin activity fell progressively from 9 a.m. to midnight in all three groups, and were significantly lower in pre-eclampsia. Plasma angiotensin II levels fell during the day in normotensives and uncomplicated hypertensives, whereas pre-eclamptics showed loss of this pattern and significantly lower levels than the other groups. Free plasma norepinephrine levels fell during the day and to a similar extent in all three groups. A diurnal pattern for free plasma norepinephrine levels, with lower levels at midnight than during the day, was seen in normotensives and uncomplicated hypertensives but not in pre-eclamptics. Plasma norepinephrine sulphate levels rose from 9.00 a.m. to midnight in normotensives and uncomplicated hypertensives. This pattern was reversed in pre-eclamptics, including 3 of the 4 subjects with nocturnal hypertension. Plasma epinephrine sulphate levels rose progressively through the day, with no significant differences between groups. Failure of plasma angiotensin II or epinephrine levels to fall at night in pre-eclampsia may contribute to nocturnal hypertension in subjects with increased vascular reactivity. Suppression of plasma renin activity and angiotensin II levels suggests that perhaps as yet unidentified pressor mechanisms are involved in pre-eclampsia.

Adolescent↗
PubMed1983

Adrenal and sympathetic nervous activity in subjects with "low' and "high' normal blood pressure.

Possible adrenal and autonomic mechanisms contributing to the onset of essential hypertension were studied in 18 men selected from the upper and lower extremes of blood pressure distribution within a larger population. In eight of the nine pairs of subjects, who were matched for age and obesity, those with higher pressure had significantly higher resting levels of both free adrenaline and noradrenaline sulphate in plasma than their lower pressure counterparts. The higher pressure group showed a positive correlation between diastolic blood pressure and both free and total noradrenaline levels (r = 0.77, P less than 0.05, and r = 0.81, P less than 0.01, respectively). In those with lower pressure, systolic blood pressure correlated closely with plasma adrenaline (r = 0.92, P less than 0.001). Increased adrenal medullary activity and altered autonomic tone appear to be features of the higher range of normal blood pressure and may precede the onset of essential hypertension.

Adrenal Medulla↗
PubMed1982

Epinephrine sulfation in the forearm: arteriovenous differences in free and conjugated catecholamines.

Simultaneously drawn arterial and forearm venous levels of free and sulfate conjugated epinephrine and norepinephrine were measured in 8 subjects in order to study the role of skeletal muscle in catecholamine sulfation. A sensitive radioenzymatic assay was used. The average free epinephrine level was 46% lower in venous than in arterial blood (p less than 0.023) while average sulfated epinephrine level was 37% higher (p less than 0.016). These findings suggest that epinephrine sulfation is occurring in the forearm, most likely in skeletal muscle. The mean venous free norepinephrine level was 21% higher than the mean arterial level (p less than 0.055) presumably reflecting release from sympathetic nerve terminals. No evidence of norepinephrine sulfation or deconjugation in skeletal muscle was found.

Adult↗
PubMed1982

Effects of meclofenamate and captopril on adrenal blood flow: contrasts in conscious rabbits at rest and after hemorrhage.

The role of prostaglandins and angiotensin II or kinins in maintaining adrenal blood flow was studied using the prostaglandin cyclo-oxygenase inhibitor meclofenamate and the kininase inhibitor captopril in resting and hemorrhaged (10 ml/kg) conscious rabbits. Meclofenamate (6 mg/kg intravenously) reduced adrenal blood flow after 3, 15 and 30 minutes by 26, 28 and 17 percent, respectively. Captopril increased adrenal flow by 20 percent, an effect subsequently reversed by meclofenamate. In contrast, hemorrhaged rabbits maintained adrenal blood flow following meclofenamate and captopril despite substantial reductions in renal blood flow with meclofenamate given before and after captopril. It is concluded that (1) adrenal blood flow at rest is modulated by vasodilator prostaglandins and to a lesser extent angiotensin II or bradykinin. (2) The adrenal effects of meclofenamate and captopril are overriden by hemorrhage, perhaps reflecting the need to increase adrenal hormones during hypovolemic stress. (3) The decrease in plasma catecholamines seen with meclofenamate at rest may be due to reduced adrenal blood flow.

Adrenal Glands↗
PubMed1982

Plasma free and sulfate conjugated catecholamine levels during acute physiological stimulation in man.

The responses of plasma free and sulfate-conjugated catecholamines to acute physiological stimulation was examined in normal male subjects. Catecholamines were measured with a sensitive radioenzymatic assay incorporating simultaneous hydrolysis of sulfate conjugates and O-methylation of free norepinephrine and epinephrine. Following 20 minutes recumbency after venepuncture 30 +/- 3% of norepinephrine and 16 +/- 5% of epinephrine was in thr free form. Free catecholamines generally increased during standing, cold immersion and isometric handgrip, but sulfates did not change. Bicycle ergometry markedly increased free catecholamines which rapidly returned to basal levels at the end of exercise. In contrast, sulfated norepinephrine decreased substantially with exercise in all subjects but returned to basal levels 3 minutes after stopping exercise. Epinephrine sulfate varied considerably between subjects but showed a similar, although smaller, fall with exercise. Thus, during physiological stimulation, which caused increases in free norepinephrine and epinephrine levels in plasma, the only consistent change in sulfated catecholamines was a marked fall in norepinephrine sulfate after bicycle exercise. This may indicate saturation of sulfotransferase activity, substrate inhibition or impaired tissue conjugation.

Adult↗
PubMed1982

Effects of meclofenamate and captopril on renal and other regional vascular beds after mild haemorrhage in conscious rabbits.

1. The role of prostaglandins and angiotensin II in blood flow regulation was studied in conscious rabbits subjected to mild haemorrhage. 2. Haemorrhage caused a 13% fall in arterial pressure and a 21% fall in cardiac output, responses which were unchanged by sodium meclofenamate, an inhibitor of prostaglandin synthesis, or captopril, an inhibitor of the angiotensin converting enzyme. 3. Haemorrhage doubled plasma adrenaline and noradrenaline levels. Plasma renin activity trebled after haemorrhage and was further elevated by captopril. 4. Renal blood flow was maintained after haemorrhage alone. Meclofenamate given immediately after haemorrhage caused a 31% fall in renal blood flow. Captopril given immediately after haemorrhage caused renal vasodilation, but when given after meclofenamate augmented renal vasoconstriction. 5. Splenic vasoconstriction was seen after haemorrhage and meclofenamate, and subsequently was augmented by captopril. 6. Results suggest that prostaglandins variably modulate regional blood flow in conscious rabbits subjected to mild haemorrhage. Enhanced sympatho-adrenal activity increases renovascular and splenic dependence on vasodilator prostaglandins, but not that of coronary, cerebral, hepatic or adrenal circulations. Renal and splenic vasoconstriction seen with meclofenamate are not due to circulating angiotensin II.

Animals↗
PubMed1981

Biochemical evidence of dysfunction of brain neurotransmitters in the Lesch-Nyhan syndrome.

Different brain regions were removed post mortem from three patients with the Lesch-Nyhan syndrome and were examined for alterations in hypoxanthine-guanine phosphoribosyl transferase (HGPRT), adenine phosphoribosyl transferase, and biochemical indexes of norepinephrine, dopamine, serotonin, gamma-aminobutyric acid (GABA), and acetylcholine neuron function, as compared with age-matched controls. The level of HGPRT activity in the material from patients with the Lesch-Nyhan syndrome was less than 1 per cent of control levels, whereas adenyl phosphoribosyl transferase was not significantly altered. All biochemical aspects of the function of dopamine-neuron terminals in the striatum (except dihydroxyphenylacetic acid levels) were decreased to 10 to 30 per cent of the control values. Serotonin and 5-hydroxyindoleacetic acid levels were increased, striatal choline acetyltransferase levels were low, and striatal glutamic acid decarboxylase and guanylate cyclase activities were unaltered. The disruption of the balance between the functions of GABA, dopamine, and acetylcholine neurons in the extrapyramidal system probably accounts for some of the symptoms observed in the Lesch-Nyhan syndrome (e.g., choreoathetosis).

Acetylcholine↗
PubMed1981

Effect of beta-adrenergic receptor blockade with propranolol on the response of plasma catecholamines and renin activity to upright tilting in normal subjects.

1 Relationship between plasma catecholamines (measured as noradrenaline and adrenaline) and plasma renin activity (PRA) were examined at rest and during passive head-up tilting for 30 min in nine normal subjects, before and after treatment with propranolol 160 mg daily for 7 days. 2 Noradrenaline (NA) and adrenaline (A) increased substantially after tilting for 15 min. There were no changes in PRA. After 30 min tilting, NA remained elevated, whereas A had returned to resting levels. A significant increase in PRA was apparent at 30 min. Pulse rate and diastolic blood pressure increased progressively during tilting. Systolic pressure did not change. 3 Treatment with propranolol reduced pulse rate and systolic blood pressure at rest and during tilting. Resting catecholamine concentrations and the response of NA to tilting were unaffected. In contrast, treatment prolonged the A response leading to significantly higher levels after 30 min tilting. Propranolol reduced PRA in six of the nine subjects and prevented the increase with tilting observed before treatment.

Adult↗