Plasma Dopamine Levels Research Articles

Repeated (isolation) stress increases tribulin-like activity in the rat.

1. The effect of repeated isolation stress on MAO inhibitory activity (tribulin) in rat tissues as well as on plasma catecholamine levels was investigated. 2. Animals were subjected to a daily period of isolation (9 min) and sacrificed on days 1, 2, 4, and 5. 3. In brain and cerebellum the levels of both inhibitory activities were found to be significantly higher in animals sacrificed on days 1-2 than in either controls or animals sacrificed on days 4-5. 4. In heart and kidney the highest levels of both activities were found in animals sacrificed on days 4-5. 5. Plasma levels of dopamine on day 4 were significantly higher than those in controls or in any of the experimental groups. Plasma levels of epinephrine showed step-by-step increments from day 1 up to day 5, reaching statistical significance only on day 5. Plasma levels of norepinephrine were significantly increased on days 2, 4, and 5. 6. Under the experimental conditions of this study, we have shown a rapid and short-lasting increment of tribulin in the central nervous system. Its disappearance on days 4-5 could be related to adaptation to the novel situation. Changes in the peripheral tissues appeared later, and a similar adaptation was absent during the period of observation. 7. Tribulin would be related to the stressful situation not only as an anxiety-promoting agent but also in contributing to the maintenance of high levels of circulating catecholamines.

Dose‐dependent memory impairment in Parkinson's disease

Variation in plasma dopamine level between the time of original learning and subsequent memory retrieval causes a state-dependent memory impairment in Parkinson's disease. The occurrence of this phenomenon is not related to either progression of disease or duration of therapy, but is more likely to occur with high-dosage levels of levodopa-carbidopa.

Effect of Naloxone on Blood Pressure Responses and Plasma Catecholamine Levels Following Clonidine Injection in Conscious, Unrestrained Rats

Intravenous injection of clonidine produces a biphasic blood pressure response, a transient increase followed by a prolonged decrease. Significant increases in plasma norepinephrine (NE), epinephrine (EPI), and dopamine (DA) levels occur 5 min following injection, corresponding to the hypertensive phase. Thirty minutes after clonidine injection, blood pressure, NE, EPI, and DA levels had returned to control levels. However, at 60 min, when the blood pressure had decreased to below control levels, a significant decrease in plasma NE was found. This finding confirms that clonidine decreases blood pressure, in part, by reducing sympathetic nerve activity. Naloxone, an opiate antagonist, when given prior to clonidine, abolished the hypotensive phase as well as preventing the decrease in plasma NE levels. The hypertensive phase was potentiated. Naloxone, when given alone, increased plasma NE levels at 15, 40, and 70 min following injection, indicating that naloxone increases sympathetic nerve activity peripherally, and may prevent clonidine's hypotensive phase by also increasing sympathetic activity in the central nervous system through blockade of opiate receptors. Therefore, the hypotensive effect of clonidine may involve interactions with endogenous opiate peptides.

Atrial natriuretic peptide and sodium homeostasis in chronic renal failure

In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn 17.8 +/- 2.6, mean +/- SEM, CPAH 93.5 +/- 17 ml/min per 1.73 m2, FENa 7.0 +/- 0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy age-matched controls (29.2 +/- 7.2 vs 23.2 +/- 3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260 +/- 36 vs 98 +/- 11 pg/ml, less than 0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.

Catecholamine metabolism in recurrent hereditary polyserositis. Pathogenesis of acute inflammation: the retention—leakage hypothesis

Recurrent hereditary polyserositis (RHP), also known as familial Mediterranean fever, is a genetically-determined disease characterized by paroxysmal attacks of peritonitis, pleuritis, arthritis or inflammation of other serous membranes. We have previously suggested that the pathogenesis of this disease seems to be related to abnormal catecholamine metabolism. This study compares the plasma and urine catecholamine profile in patients with RHP during different clinical states to that in controls. In RHP there were lower plasma and higher urine dopamine levels in the asymptomatic state and during attacks, while norepinephrine levels remain unchanged. However, plasma epinephrine was significantly lower in the asymptomatic state but markedly higher during attacks. The urine epinephrine values in both situations were similar but significantly lower than in controls, suggesting abnormal renal excretion of epinephrine. The urine metanephrine was markedly elevated in the asymptomatic state compared to controls, but remained unchanged during the attacks, again suggesting defective renal clearance of metanephrine. Metaraminol infusion, which induces attacks in RHP patients, was associated with an increase in plasma dopamine and epinephrine (but not norepinephrine); yet the urinary levels of dopamine, epinephrine and metanephrine remained the same, confirming the dissociation between the plasma and urinary levels of these catecholamines, probably due to abnormalities in the renal clearance mechanism. We postulate that this dissociation leads to retention of these amines in the plasma which may subsequently leak through the serous membranes (the target organs) and incite an acute inflammatory process. Cotchicine, the only known drug that protects against disease attacks, reduces the plasma levels of these amines, and thus may act by preventing retention that leads to leakage and subsequent inflammation. catecholamine/polyserositis/colchicine

Influence of dopamine and disease severity on primitive reflexes in Parkinson's disease.

Several primitive reflexes are common in patients with Parkinson's disease (PD), but can also be noted in patients who have diffuse cerebral degeneration. The glabellar response is present in virtually all patients with PD and this reflex has been of theoretical interest in PD. It has been suggested that the glabellar response is related to inhibition via dopamine pathways. We examined changes in several primitive reflexes as a function of the plasma dopamine level and the severity of PD. The probability of observing these reflexes did not vary with dopamine levels, but the corneomandibular and palmomental reflexes were significantly more likely to be present in patients with advanced disease. Our findings confirm that primitive reflexes are prominent in PD and suggest that they may be secondary to extrapyramidal disease.

Comparison of resting and stimulus-evoked catecholamine release from the femoral and renal vascular beds of the dog

Plasma levels of dopamine (DA) and noradrenaline (NA) were measured in arterial and in femoral and renal venous blood of chloralose-anaesthetised dogs at rest, and during electrical stimulation of the femoral and renal sympathetic nerve supplies. In the femoral bed, sympathetic nerve stimulation elevated venous efflux of NA, but did not reproducibly elevate DA efflux: when this was increased, it comprised less than 1% of the stimulus-evoked catecholamine efflux. By contrast, renal nerve stimulation liberated both NA and DA from the kidney, and DA comprised about 8% of the total stimulus-evoked efflux. Comparison of efflux from intact and denervated kidneys indicated substantial neurogenic release of both NA and DA at rest, with DA comprising 20% of this efflux. The results extend previous evidence for dopaminergic sympathetic innervation of the dog kidney, and suggest that both dopaminergic and noradrenergic renal nerves are tonically active in anaesthetised animals.

Effect of various therapeutic approaches on plasma potassium and major regulating factors in terminal renal failure

The development of life-threatening hyperkalemia poses a risk for patients with chronic preterminal renal failure. Various therapeutic options have been suggested for hyperkalemic emergencies in these patients; to date, however, no study has evaluated the relative efficacies of these measures in the presence of renal failure. Our goal was to examine the acute effects of a variety of therapeutic approaches, as well as those of hemodialysis, on plasma potassium levels in a hemodialysis population. Ten patients with terminal renal failure undergoing maintenance hemodialysis were enrolled in the study. Blood gas parameters and plasma sodium, potassium, glucose, osmolality, renin, aldosterone, epinephrine, norepinephrine, dopamine, and insulin were measured before, during, and after 60-minute infusions of bicarbonate, epinephrine, and insulin in glucose, and before, during, and after performance of regular hemodialysis for one hour. Hypertonic as well as isotonic intravenous bicarbonate (2 to 4 mmol/minute) induced a marked rise in plasma bicarbonate and pH, but failed to lower the plasma potassium level (5.66 versus 5.83 mmol/liter before and after). Epinephrine, 0.05 microgram/kg/minute administered intravenously, decreased plasma potassium only slightly from 5.57 to 5.25 mmol/liter, and five patients showed no decline. On the other hand, insulin in glucose, 5 mU/kg/minute intravenously, effectively lowered plasma potassium levels from 5.62 to 4.70 mmol/liter, and hemodialysis induced the most rapid decline from 5.63 to 4.29 mmol/liter. Plasma aldosterone was elevated before treatment; it correlated with plasma potassium and dropped during intravenous bicarbonate administration or hemodialysis. Pretreatment plasma renin activity, insulin, epinephrine, norepinephrine, and dopamine levels were generally normal. We conclude that in patients with terminal renal failure undergoing maintenance hemodialysis, intravenous bicarbonate is ineffective in lowering plasma potassium rapidly, and epinephrine is effective in only half the patients, whereas insulin in glucose is a fast and reliable form of therapy for hyperkalemic emergencies. Plasma aldosterone levels are appropriate in relationship to plasma potassium levels, and levels of other potassium-influencing hormones are generally normal.

Basal plasma-catecholamine-level determination using HPLC-ED and different sample cleanup techniques

Reversed phase HPLC with electrochemical detection was used for the determination of basal adrenaline, dopamine and noradrenaline levels in human plasma. These compounds demonstrated good stability during different stages of collection and long-term storage.

The effect of carbidopa on plasma and muscle levels of L-dopa, dopamine, and their metabolites following L-dopa administration to rats.

Administration of L-dopa (L-3,4-dihydroxyphenylalanine) (200 mg/kg p.o.) to rats produced elevated plasma and muscle concentrations of both L-dopa and 3-O-methyldopa (3-OMD). This effect was potentiated by simultaneous administration of carbidopa (25 mg/kg p.o.). Both L-dopa and 3-OMD accumulated in muscle after administration of L-dopa with or without carbidopa. Elevated dopamine levels were detected in both muscle and plasma after treatment with L-dopa alone. Concurrent administration of carbidopa only diminished dopamine levels in plasma, and the duration of raised dopamine levels in muscle was increased. Carbidopa administration had no effect on the elevated plasma concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) caused by L-dopa administration. In muscle, carbidopa treatment tended to prolong the duration of raised metabolite levels. Muscle appears to accumulate L-dopa at a site where decarboxylation is not totally prevented by concurrent carbidopa administration, and where dopamine is not degraded as actively as in other tissues. The muscle sink for L-dopa may influence the plasma profile of the amino acid, which has implications for the therapeutic response to L-dopa in Parkinson's disease.

Hemodynamic Effects of a Single Dose of Dopamine and <i>L</i>-Dopa in Pulmonary Hypertension Secondary to Chronic Obstructive Lung Disease

Dopamine (DA) has rarely been administered at low dosage to stable patients with pulmonary hypertension (PAH) secondary to chronic obstructive lung disease (COLD). Since L-dopa (L-DA) is metabolized into DA, it might be an oral source of DA. After informed consent 10 patients with PAH, secondary to COLD underwent right catheterization to allow measurements of pressures and cardiac output (CO) as well as arterial and mixed venous oxygen levels before and then 30 and 60 min after the beginning of intravenous DA at a rate of 4 micrograms/kg/min. A week later, the same parameters were remeasured in 5 of these patients after a single oral intake of 1.5 g L-DA. At low doses both DA and L-DA increased CO and decreased pulmonary vascular resistances, suggesting a pulmonary vasodilator effect. They also enhanced oxygen delivery and Pvo2 without decreasing Pao2. A correlation was observed between cardiac index and plasma DA level. Thus though they do have some immediate adverse side effects and their long-term effects are unknown, inotropic and vasodilator drugs may have positive effects on pulmonary circulation.

Single doses of catecholamines in the rat: Catecholaminotropic, but not hyperglycemic

1. 1. As in two “lower” vertebrates, the lamprey and the eel, single intravascular injections of physiological doses (2.5 μg/kg) of epinephrine (E) into the rat immediately increased levels of plasma dopamine (DA) and norepinephrine (NE). 2. 2. Single doses of DA (5 μg/kg) enhanced circulating NE and E, while NE (5 μg/kg) had no clear impact on the plasma levels of the other two catecholamines (CAs). 3. 3. These data are at variance with findings in the eel, where all three CAs are mutually stimulatory; and in the lamprey, where only E stimulates release of the other two CAs. 4. 4. It appears that E-stimulated CA release is widespread or ubiquitous among vertebrates, and that complex interactions between circulating CAs must be considered under experimental, physiological, and clinical conditions. 5. 5. None of the injections had a significant hyperglycemic effect.

Glucoregulatory hormone response to insulin-induced hypoglycaemia following long-term calcium antagonism with felodipine in patients with essential hypertension.

The effect of 8 weeks' treatment with the dihydropyridine calcium antagonist felodipine on glucoregulatory hormone response following insulin-induced hypoglycaemia was evaluated in 7 patients with essential hypertension, WHO grade I-II. After an iv insulin injection (0.1 IU/kg), blood glucose decrement and nadir were similar before and during felodipine treatment. Basal glucagon, noradrenaline, adrenaline, GH and cortisol levels were unchanged, and the response to insulin-induced hypoglycaemia was similar before and during felodipine treatment. Basal plasma dopamine levels were similar and did not change during insulin-induced hypoglycaemia before and during felodipine treatment. Basal serum levels of TSH, T3 and T4 were unaltered following felodipine. In conclusion, long-term treatment with felodipine did not alter the hypoglycaemic effect of exogenous insulin, or the recovery from hypoglycaemia or the glucoregulatory hormone response to insulin-induced hypoglycaemia in patients with essential hypertension.

Sustained hemodynamic improvement during long-term therapy with levodopa in heart failure: Role of plasma catecholamines

Long-term therapy with oral sympathomimetic amines in patients with heart failure has been limited by the eventual development of diminished pharmacologic efficacy. However, a previous investigation in five subjects with heart failure suggested that long-term ingestion of levodopa, which is decarboxylated endogenously to dopamine, produces a sustained improvement in cardiac function. In the present study, levodopa was administered orally (1.5 to 2.0 g) to 14 patients with heart failure while hemodynamic responses and plasma catecholamines were monitored. Initially, an increase in cardiac index and stroke volume index was accompanied by a decline in systemic vascular resistance, mean pulmonary capillary wedge pressure and mean right atrial pressure. Heart rate and mean arterial pressure were unchanged. Plasma concentrations of dopamine rose substantially after drug ingestion and correlated significantly with changes in cardiac index (r = 0.73, p less than 0.05). After 12 weeks of treatment with levodopa, the changes in cardiac index, stroke volume index, systemic vascular resistance and plasma dopamine levels persisted (n = 12 patients). Moreover, a significant decrease occurred in the heart rate at rest. Although there was an initial tendency for plasma norepinephrine concentrations to increase, a return to control levels was documented after long-term treatment. Thus, tolerance to the hemodynamic actions of levodopa did not develop during long-term administration of the drug. The hemodynamic responses observed can be ascribed to the activation of beta 1-adrenoceptors and dopamine1 receptors by dopamine generated from levodopa. The dopamine2 activity of dopamine does not appear to be responsible for the improvement in cardiac performance produced by levodopa.

Evaluation of long-term oral levodopa therapy in chronic congestive heart failure

To evaluate the long-term effects of orally administered levodopa, 11 patients with chronic congestive heart failure (NYHA III-IV) were studied during maintenance therapy (30 +/- 1 days) and after withdrawal from levodopa. The daily levodopa dose was 4 g in six patients; because of side effects the levodopa dose was reduced to 2-3 g in the remaining patients. After withdrawal of levodopa, mean pulmonary capillary wedge pressure and mean right atrial pressure increased significantly (from 19 +/- 2 to 24 +/- 3 and from 7 +/- 2 to 9 +/- 2 mmHg, respectively). Effective renal plasma flow was 329 +/- 57 during levodopa therapy and decreased significantly to 252 +/- 27 ml/min after withdrawal of levodopa. The number of ventricular premature contractions and couplets increased during levodopa therapy and decreased again significantly after withdrawal of levodopa. No significant differences between on and off levodopa were observed in resting heart rate, arterial blood pressure, cardiac index, stroke work index, systemic vascular resistance, sodium and water excretion, or creatinine clearance. Seven patients improved on levodopa therapy by one NYHA class; four of these seven patients deteriorated again by one NYHA class after withdrawal of levodopa. Regarding both clinical and hemodynamic changes after withdrawal of levodopa, three patients were classified as responders to long-term levodopa therapy. All three responders received 4 g levodopa per day. Average dopamine plasma level was 5.3 +/- 0.8 ng/ml in the responder group and 2.0 +/- 0.5 ng/ml in the nonresponder group. Long-term administration of oral levodopa is associated with beneficial clinical and hemodynamic response in only a minority of patients with chronic congestive heart failure.

Effect of oral levodopa and carbidopa on coronary spasm in variant angina pectoris

The effect of oral administration of 500 mg of levodopa with 50 mg of carbidopa, a peripheral dopadecarboxylase inhibitor, on coronary vasomotion during vasoconstrictor stimuli was examined in 15 patients with variant angina presenting with hyperventilation-induced myocardial ischemia. Patients were studied during 3 noninvasive sessions and 1 angiographic session. In all sessions the basic protocol consisted of provocation of coronary spasm by hyperventilation before and 2 hours after levodopa and carbidopa administration. During angiography, great cardiac vein blood flow, right atrial and aortic pressures were measured, and coronary angiograms were recorded at baseline and 1 to 4 minutes after each hyperventilation. Samples for dopamine plasma levels were drawn before and throughout the studies. In 3 selected patients, levodopa and carbidopa were associated with 30 mg of domperidone, an antagonist of dopamine peripheral receptors. Levodopa and carbidopa consistently prevented the occurrence of ischemia after hyperventilation in 6 of the 15 patients. This was due to inhibition of local coronary spasm in 2 patients and reduced coronary constriction in 4. Ischemia due to hyperventilation was still prevented despite addition of domperidone with levodopa and carbidopa. Plasma dopamine levels were 23 ± 15 before and 739 ± 284 pg/ml 2 hours after administration of levodopa and carbidopa. These findings are consistent with either a decreased central dopaminergic activity and associated disregulation of vasomotor tone, or a peripheral vasodilatory effect of increasing dopamine. However, the fact that levodopa and carbidopa were equally effective despite concurrent administration of domperidone favors an involvement of the central nervous system as the most likely mechanism of reduced vasoconstriction.

Fluctuations in plasma dopamine level impair memory in Parkinson's disease.

We found a causal relationship between variation in plasma dopamine level and memory impairment in Parkinson's disease. If the level of dopamine was changed between the time of original learning and a later time of attempted memory retrieval, memory performance was impaired when compared with a maintenance of similar dopamine levels on both occasions. The absolute level of dopamine did not influence memory performance. Side-effects of levodopa-carbidopa therapy include variation in dopamine level, parkinsonian symptoms, and possibly "state-dependent" impairment of memory.

Physiologic Responses to Heavy-Resistance Exercise with Very Short Rest Periods*

Heavy-resistance exercise utilizing very short rest periods is commonly used by body builders to prepare for competition. The purpose of this study was to compare the acute responses of this type of heavy-resistance exercise protocol in competitive body builders (BB) and power lifters (PL). Nine male BB and eight PL were matched for age, size and experience. A ten-station heavy-resistance exercise protocol was used. Each subject performed three sets of 10 repetition maximum (RM) with 10-s rest between sets and alternated 30-s and 60-s rest periods between exercises. No differences were observed in total work between the groups, but BB used a significantly (P less than 0.05) higher percentage of their 1 RM in the bench press and leg press exercises. Heart rate, ratings of perceived exertion (RPE), and lactate levels were obtained during the exercise protocol; significant (P less than 0.05) increases were observed above rest for these variables. RPE was significantly correlated with lactate levels (r = 0.84). Plasma epinephrine, norepinephrine, dopamine, cortisol, and lactate levels significantly increased from pre- to 5 min post-exercise. Mean plasma volumes were reduced -16.6 (+/- 3.64)% and -20.6 (+/- 8.32)% following the exercise protocol for BB and PL, respectively. Significant (P less than 0.05) decreases in eosinophil counts were observed following exercise. No significant differences were observed between BB and PL for any of the physiologic responses measured. PL exhibited a higher incidence (100%) of clinical symptoms of dizziness and nausea compared to BB (11.1%).(ABSTRACT TRUNCATED AT 250 WORDS)

Psychotic and nonpsychotic depressions: II. platelet MAO activity, plasma catecholamines, cortisol, and specific symptoms

Preliminary data are presented on levels of plasma cortisol, dopamine (DA), epinephrine (RPI), and norepinephrine (NE) before and after dexamethasone in 22 depressed patients (of whom 4 were psychotic). Platelet monoamine oxidase (MAO) activity, determined in 19 of the depressed patients, was significantly higher in the 4 psychotic patients than it was in the 15 nonpsychotic patients. Positive correlations were observed before and after dexamethasone among cortisol, DA, EPI, and platelet MAO. After dexamethasone, plasma NE correlated negatively with DA, EPI, and cortisol. The various correlations were due largely to the inclusion of the psychotic depressive subgroup. Data are also presented on the relationships between these biological measures and specific signs and symptoms.

Psychotic and nonpsychotic depressions: I. comparisons of plasma catecholamines and cortisol measures

Unconjugated plasma catecholamines and cortisol were measured before and after a 1 mg dose of dexamethasone in 22 medication-free depressed patients and 6 healthy, medication-free control subjects. Plasma dopamine (DA) levels in the psychotically depressed subgroup ( n=4) were significantly higher both before and after dexamethasone than those in the nonpsychotic depressed group and higher before dexamethasone than in the control group. Similarly, the psychotically depressed group exhibited significantly higher cortisol levels both before and after dexamethasone than the nonpsychotic depressed group or the control group. In contrast, the psychotically depressed group had significantly lower postdexamethasone plasma norepinephrine levels compared to the nonpsychotic depressed group. In both patients and controls, plasma DA was significantly higher after dexamethasome administration than before, but the magnitude of the increase was 10 times greater in controls than in patients.