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PubMed1988

Free and conjugated plasma catecholamines, DOPA and 3-O-methyldopa in humans and in various animal species.

The aim of the present study was to determine the extent to which plasma catecholamines are conjugated in different animals compared to man and how widespread is the presence of dihydroxyphenylalanine (DOPA) and 3-methoxy-4-hydroxyphenylalanine (3-OMD) in plasma among the different animal species. Free and conjugated norepinephrine, epinephrine, and dopamine were measured in plasma in humans and in several animal species (dog, rat, Gunn rat, cat, rabbit, guinea pig, African green monkey, young pig, calf, and one American black bear) using HPLC with electrochemical detection. The same technique was used to measure free and conjugated DOPA and 3-OMD in plasma of man, dog, rat, Gunn rat, calf, and American black bear. Human plasma contains the highest concentration of total (free and conjugated) catecholamines (46.1 pmole/ml), while low concentrations (below 15 pmole/ml) were observed in unstressed rats, calves, cats, and young pigs. In man, 95.3% of total plasma catecholamines were conjugated. The extent to which plasma catecholamines were conjugated varied greatly between animal species. The conjugated fraction expressed as percentages of the total catecholamines is lowest in the young pig (4.7%) and highest in the bear (100%). Conjugated dopamine was present in the plasma of all species, varying between 3% of the total catecholamine pool in young pig to 90% in dog. Conjugated norepinephrine was also present in plasma of all species except in unstressed rats with access to food. Conjugated epinephrine was detected only in cat and rat. Free DOPA and 3-OMD were present in plasma of all tested species with especially high levels of 3-OMD being present in dog. Conjugated DOPA and 3-OMD were not consistently found in any species. Our results indicate that man, dog, bear, and African green monkey are particularly good catecholamine conjugators and that young pig, guinea pig, rabbit, and calf are poor conjugators.

Adult↗
PubMed2000

[Studies on the relationship between beta-adrenergic receptor density on cell wall lymphocytes, total serum catecholamine level and heart rate in patients with hyperthyroidism].

Hyperthyreosis mimics the hyperadrenergic state and its symptoms were though to be dependent on increased level of catecholamines. Another reason for the symptoms could be the increased density or affinity of beta-adrenergic receptors to catecholamines. The aim of the study was to examine the elements of sympathetic nervous system, thyroid hormones level and their influence on heart rate control in patients with hyperthyreosis. The study was carried out in 18 women, mean age 48.9 +/- 8.7 yrs and 6 men, mean age 54.2 +/- 8.7 yrs. The control group consisted of 30 healthy persons matched for age and sex. We examined the density of beta-adrenergic receptors using radioligand labelling method with 125I-cyanopindolol, serum total catecholamines level with radioenzymatic assay kit, the levels of free thyroid hormones using radioimmunoassays and thyreotropine level with immunoradiometric assay. Maximal, minimal and mean heart rate were studied using Holter monitoring system. The density of beta-adrenergic receptors in hyperthyreosis was 37.3 +/- 21.7 vs 37.2 +/- 18.1 fmol/mg in the control group (p = NS). Total catecholamines level was significantly decreased in hyperthyreosis group: 1.5 +/- 0.89 vs 1.9 +/- 0.73 pmol/ml (p < 0.05). There was significantly higher minimal, maximal and mean heart rate in hyperthyreosis group (p < 0.0001, p < 0.0001 and p < 0.05 respectively). There was a weak inverse correlation between minimum heart rate and triiodothyronine level (r = -0.38, p < 0.05). An inverse correlation between triiodothyronine and catecholamines level (r = -0.49, p < 0.05) was observed. Beta-adrenergic receptors density is unchanged and catecholamines level is decreased in hyperthyreosis when compared to normal subjects. There is no correlation between minimal heart rate and adrenergic receptors density or catecholamines level in hyperthyreosis.

Catecholamines↗
PubMed1975

Experimental evidence for calcium independent catecholamine secretion from the bovine adrenal medulla.

The purpose of this investigation was to establish the existence of a calcium-independent mechanism for catecholamine secretion from the adrenal medulla. Concentration-effect curves were obtained using isolated perfused (5 ml/min; 25 degrees C) bovine adrenal medullae stimulated with acetaldehyde (1-64 mM). Catecholamine secretion was the same in presence and in absence of calcium in the perfusion medium and was not diminished by the addition of magnesium (5 X 10-minus 3 M) to the calcium-free medium. Stimulation of 45-Ca-labeled adrenals with 23 mM acetaldehyde evoked secretion of catecholamines but not 45-Ca. Furthermore, examination of the distribution of 45-Ca and catecholamines in subcellular fractions (cytosol, nuclei, microsomes, mitochondria and chromaffin granules) from acetaldehyde-stimulated and nonstimulated glands showed that acetaldehyde stimulation caused no mobilization of 45-Ca from any of the intracellular pools, but significantly decreased the catecholamine content of a chromaffin granule fraction with a concomitant increase of catecholamines in the cytosolic fraction. These results establish an adrenomedullary secretory mechanism independent of both extracellular and intracellular calcium and indicate that acetaldehyde evokes catecholamine secretion by this calcium-independent mechanism, releasing the intragranular hormones into the cytoplasm prior to their extrusion from the chromaffin cell.

Acetaldehyde↗
PubMed1990

The role of catecholamines in ischemia.

In myocardial ischemia, sympathetic activity of the heart is closely connected with the progression of cell injury and the incidence of malignant arrhythmias. Adrenergic stimulation of the ischemic myocardium is due to increased local norepinephrine concentrations in the heart, whereas the plasma catecholamine levels are of minor relevance. During the first few minutes of ischemia. efferent sympathetic nerves are activated. Excessive accumulation of norepinephrine, however, is prevented since adenosine, formed in the ischemic myocardium, suppresses exocytotic norepinephrine release, and released norepinephrine is rapidly removed as long as catecholamine reuptake is functional. With progression of ischemia to more than 10 min, the myocardium is no longer protected against excess catecholamine accumulation in the interstitial space because local metabolic release mechanisms become increasingly important. This release, which is independent of central sympathetic activity and extracellular calcium, occurs in two steps: first, norepinephrine escapes from its intracellular storage vesicles and accumulates in the cytoplasma of the neuron; in a second, rate-limiting step, norepinephrine is transported across the plasma membrane into the interstitial space, using the neuronal uptake carrier in reverse of its normal transport direction. Studies using acute and chronic sympathetic denervation and antiadrenergic agents demonstrate that this local metabolic, rather than centrally induced, norepinephrine release is critically involved in the progression of ischemic cell damage and the occurrence of ventricullar fibrillation in early ischemia. As a consequence of local metabolic catecholamine release, extracellular norepinephrine reaches 1,000 times the normal plasma concentration within 20 min of ischemia. Myocardial ischemia results in a temporary supersensitivity to catecholamines of the myocytes. This is due to a twofold increase in alpha1- and a 30% increase of beta-adrenergic receptor number at the cell surface. The sensitization of adenylate cyclase during the first 20 min of total ischemia is followed by a rapid inactivation of the enzyme that also includes the coupling protein Gs. The deleterious combination of extremely high norepinephrine concentrations with an at least temporarily enhanced responsiveness of the tissue to catecholamines is thought to accelerate the propagation of the wavefront of irreversible cell damage in the ischemic myocardium. Moreover, the inhomogenous distribution of catecholamine excess within the heart is considered to promote malignant arrhythmias by unmasking and enhancing electrophysiological disturbances in early ischemia.

Animals↗
PubMed1976

Correlation between changes in endogenous catecholamine release from the heart and various physiological responses in anesthetized dogs.

Correlations between the concentration of endogenous catecholamines in coronary sinus blood and various physiological responses to adrenergic stimulation were studied in anesthetized dogs. Plasma catecholamine levels both in coronary sinus and aortic blood were measured by means of a modification of the radiometric-enzymatic assay for tissue catecholamines, and found to be 0.769 +/- 0.110(S.E.) and 0.972 +/-0.127(S.E.) ng/ml, respectively, under basal conditions. Circulating catecholamine levels increased after the intracoronary injection of 6-hydroxydopamine, which has an indirect sympathomimetic action. Both the increment in catecholamine release from the heart and the intensity of physiological response were dose-related. A frequency-dependent increase in coronary sinus blood catecholamine levels occurred during right cardioaccelerator nerve stimulation. Maximum values were observed with a stimulation frequency of 10 Hz, at which maximum physiological responses were obtained. A highly significant correlation was found between endogenous catecholamine levels in coronary sinus blood and the dp/dt of left ventricular pressure (r = 0.750, p less than 0.001), as well as mean coronary blood flow (r =0.706, p less than 0.001). The present preparation may prove to be a reliable means of studying the role of the sympathetic system in regulating cardiac function.

Animals↗
PubMed1991

Characteristics of catecholamine release from adrenal chromaffin cells cultured in medium containing ethanol--II. Carbachol and veratrine-induced release.

Dissociated bovine adrenal chromaffin cells were grown in culture either in control medium or in medium containing ethanol (200 mM) and the release of catecholamines induced by veratrine and carbachol was then studied. Cells grown in ethanol showed greater spontaneous release of catecholamines, but both carbachol and veratrine evoked release of a smaller maximum fraction of stored catecholamines than that from control cells. Spontaneous catecholamine release as well as that induced by veratrine were sensitive to inhibition by tetrodotoxin. Catecholamine release induced by veratrine could be prevented almost completely by the Ca2+ channel blocker cadmium, but not to any great extent by the organic dihydropyridine Ca2+ antagonist nitrendipine. Carbachol-induced catecholamine release was similarly resistant to inhibition by nitrendipine, but was inhibited by cadmium. The results suggest that cell cultures grown in ethanol-containing medium show many alterations in the characteristics of catecholamine release. Alterations in receptor- and voltage-operated ion channels in the membrane of ethanol-treated cells may underlie these changes.

Adrenal Glands↗
PubMed1991

Effects of pirenzepine, AF-DX 116 and gallamine on the release of catecholamines from the dog adrenal gland in response to splanchnic nerve stimulation: interaction of M1 and M2 receptors with nicotinic receptors.

The present study was undertaken to examine how muscarinic antagonists modify the release of catecholamines evoked by splanchnic nerve stimulation (SNS) from the dog adrenal gland in vivo, in an attempt to elucidate whether muscarinic receptors play a functional role in catecholamine release. Output of epinephrine and norepinephrine was determined from adrenal venous blood by using high-performance liquid chromatography with electrochemical detection. SNS (1 and 3 Hz) produced increases in catecholamine output in a frequency-dependent manner. Intravenous administration of pirenzepine (10-100 micrograms/kg), a selective M1 receptor antagonist, or AF-DX 116 (30-300 micrograms/kg) and gallamine (0.3-3 mg/kg), selective M2 receptor antagonists, did not modify the SNS-induced increases in catecholamine output. C6 (hexamethonium) inhibited the SNS-induced increases in catecholamine output partially in a dose of 1 mg/kg and remarkably in a dose of 10 mg/kg. The combination of C6 (1 mg/kg) with pirenzepine (10 micrograms/kg), AF-DX 116 (30 micrograms/kg) or gallamine (0.3 mg/kg) inhibited the SNS-induced increases in catecholamine output more potently than C6 did by itself. The inhibition by C6 alone was about 50%, but that by each combination reached to about 80%. These results suggest that M2 receptors as well as M1 receptors play a facilitatory role in catecholamine release from the adrenal gland in response to SNS when the nicotinic receptor-mediated mechanism is partially inhibited.

Adrenal Glands↗
PubMed1990

In situ studies of catecholamine-induced lipolysis in human adipose tissue using microdialysis.

The effects of catecholamines on lipolysis in situ were investigated in humans. Subcutaneous adipose tissue was microdialyzed with solvents containing adrenergic agents. Norepinephrine caused a rapid increase in the glycerol level in adipose tissue (lipolysis index) that was further increased by the alpha adrenoreceptor blocker phentolamine. At 10(-11) mol/l of norepinephrine caused a 100% stimulation of lipolysis (P less than .025). In the presence of phentolamine the lipolytic effects of catecholamines at 10(-12) mol/l was isoproterenol greater than epinephrine greater than norepinephrine. All these three lipolytic catecholamines caused a transient increase in the adipose tissue dialysate glycerol level, which peaked after 20 to 30 min of catecholamine exposure and then declined. The apparent tachyphylaxia could not be overcome by a gradual increase of the catecholamine concentration from 10(-12) to 10(-8) mol/l. However, the selective alpha-2 adrenoreceptor agonist clonidine caused a continuous and dose-dependent decrease in the dialysate glycerol level; the minimum effective concentration was 10(-9) mol/l. In conclusion, catecholamines have a lipolytic effect in situ at much lower concentrations than those in the circulation. This effect is transient and is related to beta adrenoreceptors. In additio, catecholamines have alpha adrenoreceptor-mediated effects on lipolysis in situ.

Adipose Tissue↗
PubMed1979

[Catecholamines for treatment of severe heart failure (author's transl)].

In patients with severe heart failure there is increased sympathetic-adrenergic activity functioning as a compensatory mechanism. Despite of increased plasma catecholamine levels myocardial sensivity to catecholamines administered for therapeutic reasons is not diminished. The positive inotropic effect of catecholamines is more pronounced as compared to digitalis glycosides. The therapeutic efficacy of catecholamines, particularly their capability to increase cardiac output, is strongly dependent on their action on alpha- and beta2-receptors. In order to enhance cardiac performance, catecholamines are mainly used under three clinical settings: 1. severe heart failure and cardiogenic shock secondary to acute myocardial infarction, 2. 'Low cardiac output syndrome" following cardiac surgery, and 3. chronic congestive heart failure refractory to therapy with glycosides and diuretics. The use of catecholamines in the presence of acute myocardial infarction may be hazardous due to the accompanying increase of myocardial oxygen consumption. Among the available catecholamines, clinical interest recently focused on dopamine and dobutamine. Particularly with the primarily cardioselective beta-stimulating agent dobutamine a marked positive inotropic effect can be achieved in a range of dosage not significantly affecting heart rate and peripheral resistance. Positive inotropic agents may be even more effective when used in combination with vasodilators, which decrease impedance to left ventricular ejection.

Catecholamines↗
PubMed1990

Free and conjugated catecholamines in patients with cirrhosis.

A defect of conjugation may play a role in the elevated plasma free norepinephrine observed in patients with cirrhosis. Plasma free, sulfoconjugated, and glucuronoconjugated catecholamine concentrations were assessed in 15 patients with cirrhosis and in 15 age-matched control subjects. Plasma free norepinephrine and epinephrine levels were significantly higher in patients with cirrhosis (481 +/- 75 and 96 +/- 16 pg/ml, respectively) than in those of the control group (307 +/- 33 and 42 +/- 10 pg/ml, p less than 0.05 and p less than 0.01, respectively). Plasma free dopamine levels were similar in both groups. Sulfoconjugated catecholamines were the predominant form in plasma from both cirrhotic patients and control subjects. The ratio of conjugated to total catecholamines was similar in the two groups. Therefore, it is unlikely that a defect in conjugation of catecholamines is contributing to the excessive plasma free norepinephrine and epinephrine concentrations found in patients with cirrhosis. Moreover, in patients with cirrhosis, no significant relation was found between plasma conjugated catecholamines and the severity of liver disease. This study shows that cirrhosis does not induce alteration in conjugation of catecholamines and that hepatocellular function is not essential for conjugation of circulating catecholamines.

Adult↗
PubMedDate not supplied

Beta-adrenergic receptors and catecholamines in acute myocardial infarction.

Lymphocyte beta-adrenergic receptor density and plasma catecholamine concentrations were determined in 28 patients with acute myocardial infarction and compared with those in patients with angina pectoris and healthy persons. In patients with acute myocardial infarction beta-adrenergic receptor density was significantly lower (p less than 0.001) and plasma catecholamine levels significantly higher (p less than 0.001) as compared with corresponding values in patients with angina pectoris or healthy persons. beta-adrenergic receptor density in patients with angina pectoris were not significantly different from those in controls. A significant negative correlation between beta-adrenergic receptor density and plasma norepinephrine levels was observed in patients with acute myocardial infarction (r = -0.593; p less than 0.001; r = -0.615; p less than 0.001 respectively). It is suggested that decreased beta-adrenergic receptor density is a consequence of elevated plasma catecholamine levels in patients with acute myocardial infarction. It has been well documented that acute myocardial infarction is associated with enhanced activity of the sympathetic nervous system. Several studies have already been done showing that urinary excretion of catecholamines and plasma catecholamine concentrations are raised in the acute phase of myocardial infarction. Particularly high levels of plasma catecholamines appeared to be related to the severity of clinical course of myocardial infarction and were found in patients with cardiogenic shock, heart failure and arrhythmias. It is of interest that the peak elevation of plasma catecholamines correlated with the extent of myocardial damage as reflected by peak plasma CK activity and also correlated with acute and long-term mortality.(ABSTRACT TRUNCATED AT 250 WORDS)

Catecholamines↗
PubMed1989

Renal catecholamine metabolism.

Renal catecholamine metabolism encompasses: (1) catecholamine metabolism within the kidney intrinsic to renal sympathetic nervous function and renal tubular production of dopamine; (2) the overflow of catecholamines, released within the kidney, into the renal vein; (3) the excretion into urine of catecholamines and catecholamine metabolites, and (4) the extraction of catecholamines from plasma by the kidney. Study of these elements of catecholamine metabolism by the kidney provides a theoretical underpinning for the use of biochemical methodology in the experimental and clinical investigation of the properties of the renal sympathetic nerves.

Catecholamines↗
PubMed1989

[Role of fetal catecholamines before and during birth].

It is true that developing fetus in uterus may be mostly influenced by maternal conditions. However, there is little evidence to prove the existence of nervous connection between fetus and mother. The biochemical and physiological phenomena of fetus in utero may be controlled mainly by fetal autonomy with nutritional supply from mother. The sympathoadrenal system of fetus has received much attention with the technical progress of catecholamine assays. Fetal plasma catecholamine concentrations during birth are remarkably higher than those in adult life. The function of those high catecholamine concentrations has been shown to control fetal circulation during hypoxia, to maintain glucose supply to the heart and brain, and to prepare the lung for ventilation. So it may be said that fetal plasma catecholamine surge at birth is essential to neonatal adaptation. Amniotic fluid catecholamines and their metabolites were higher in intrauterine growth retarded fetus, which consumed own catecholamine reserve in adrenal medulla before parturition. It is possible to estimate the fetal condition by measuring the concentration of catecholamines and their metabolites in amniotic fluid. The amniotic norepinephrine, epinephrine and particularly dopamine concentration has been found to increase toward term. The rise in dopamine has been assumed to stimulate intrauterine synthesis of prostaglandins. We demonstrated that L-dopa was metabolized to dopamine in fetal kidney and that dopamine in amniotic fluid was originated from fetal urine.

Amniotic Fluid↗
PubMed1988

Inhibition by opioid agonists and enhancement by antagonists of the release of catecholamines from the dog adrenal gland in response to splanchnic nerve stimulation: evidence for the functional role of opioid receptors.

The aim of the present study is to examine how opioid agonists and antagonists modify the splanchnic nerve stimulation (SNS)-induced release of catecholamines from the dog adrenal gland in vivo, in an attempt to elucidate whether opioid receptors play a functional role in controlling catecholamine release. Output of epinephrine (EPI) and norepinephrine (NE) was determined from adrenal venous blood by using high-performance liquid chromatography with electrochemical detection. SNS (0.3, 1 and 3 Hz) produced increases in both EPI and NE output in a frequency-dependent manner. Leu-enkephalin (10-100 micrograms/kg i.v.) and morphine (10-100 micrograms/kg i.v.) attenuated the increase in EPI and NE output induced by 1 or 3 Hz of SNS without affecting the basal catecholamine output. A 25 to 40% reduction of the SNS-induced increase in catecholamine output was observed after the treatment with 100 micrograms/kg of leu-enkephalin or morphine. The increase in EPI and NE output induced by 1 and 3 Hz of SNS was enhanced markedly by naloxone (10-1000 micrograms/kg i.v.) and by naltrexone (10-1000 micrograms/kg i.v.). The SNS-induced increase in catecholamine output doubled after treatment with 100 and 1000 micrograms/kg of naloxone or naltrexone. Basal catecholamine output and the increase in output induced by 1 Hz of SNS were unaffected by naloxone or naltrexone. These results suggest that endogenously released opioid peptides inhibit the release of catecholamines by activating opioid receptors in the adrenal gland of the dog.

Adrenal Glands↗
PubMed1986

Effects of mu-opioid receptor stimulation in the hypothalamic paraventricular nucleus on basal and stress-induced catecholamine secretion and cardiovascular responses.

Previous work from this laboratory has demonstrated that opioid peptides, acting at mu-receptors in the brain, stimulate central sympathetic outflow thereby increasing plasma catecholamine concentrations in unstressed rats. Brain sites involved in opioid-mediated catecholamine secretion have not been characterized fully. Additionally, brain opioid effects on sympathoadrenal catecholamine secretion during stress have not been defined. Because the paraventricular hypothalamic nucleus (PVN) plays a central role in autonomic and cardiovascular regulation, we administered the mu-selective enkephalin analog, D-Ala2-NMe-Phe4-Gly(ol)5enkephalin (DAGO), directly into PVN in conscious, unstressed rats and determined the changes in plasma catecholamine concentrations, blood pressure and heart rate. Then, during the peak response, rats were subjected to restraint stress and the same parameters were again measured. Under basal conditions, picomolar doses of DAGO injected into PVN increased plasma concentrations of catecholamines, especially epinephrine, and raised blood pressure. These effects were dose-related (0.01-0.3 nmol) and antagonized by naloxone given either systemically or directly into PVN. Tachycardia was also observed except at the highest dose of DAGO (0.3 nmol). Thus, mu-receptor stimulation in PVN increases central sympathetic outflow in nonstressful situations, producing increased adreno-medullary catecholamine secretion, blood pressure and heart rate. During restraint stress, PVN microinjections of DAGO blunted stress-induced tachycardia, apparently by a vagal mechanism as this effect was blocked by atropine methyl nitrate. PVN DAGO had no significant effect on the plasma catecholamine responses to restraint stress. In contrast, naloxone injected into PVN augmented stress-induced epinephrine secretion. Thus, PVN mu-receptors may regulate heart rate during stress, and an endogenous opioid released during restraint stress may modulate adrenomedullary responses to stress.

Animals↗
PubMed1988

Life-threatening complications of cardiac operations and occurrence of myocardial catecholamine bombs.

Myocardial catecholamine bombs (huge local intra-axonal accumulations of catecholamine, mainly norepinephrine, within cardiac tissue) were observed in (right auricular) myocardial biopsy specimens in 16 of 65 adult patients selected randomly from a series of elective cardiac operations. The occurrence of catecholamine bombs was in highly significant correlation (p less than 0.001) with the occurrence of life-threatening complications of cardiac operations (life-threatening arrhythmias [ventricular tachycardias, ventricular fibrillation, asystole], clinically evident perioperative myocardial infarction/postoperative low-output syndrome, death). There was a very close correlation between the occurrence of catecholamine bombs and life-threatening arrhythmias. Life-threatening arrhythmias occurred in 13 patients. Eight of them belonged to the group of 16 patients with catecholamine bombs and five belonged to the group of 49 patients with no bombs; the difference (8/16 versus 5/49) is very clear (p less than 0.001). It was our experience that dangerous arrhythmias related to catecholamine bombs may occur as late as during the second postoperative week. We believe our observations are of considerable clinical importance, because catecholamine bombs are easily identified by fluorescence microscopic examination of right auricular myocardial specimens retrieved intraoperatively, and patients at high risk can then be selected (during the operation) for more extensive and prolonged surveillance and possibly prophylactic treatment.

Adult↗
PubMed1988

Neuropeptide Y inhibits the nicotine-mediated release of catecholamines from bovine adrenal chromaffin cells.

The possible role of neuropeptide Y (NPY) in catecholamine secretion was studied by using bovine adrenal chromaffin cells. NPY produced a concentration-dependent inhibition of nicotine-stimulated norepinephrine and epinephrine release from bovine chromaffin cells with IC50 (concentration of NPY which inhibits 50% of maximum release of catecholamines) values of 1.8 x 10(-9) M and 1.7 x 10(-9) M, respectively. Catecholamine release induced by 56 mM KCl was not inhibited by NPY at these concentrations but was inhibited by high concentration (2 x 10(-6) M) of NPY. This inhibition was not affected by the concentration of nicotine used for catecholamine release or the presence of alpha, beta adrenergic and muscarinic antagonists. A structurally related peptide, human pancreatic polypeptide, showed a similar inhibitory effect on catecholamine release, but peptide YY or avian pancreatic polypeptide had little or no effect. N-propionyl[3H]NPY binds to a single class of saturable binding sites on bovine adrenal medulla membranes with a KD = 0.32 +/- 0.07 nM and Bmax = 63 +/- 16 fmol/mg of protein. The rank order of potency of NPY and other structurally similar peptides to displace N-propionyl[3H]NPY from binding is human pancreatic polypeptide greater than or equal to NPY much greater than peptide YY greater than avian pancreatic polypeptide, and is correlated with their potency to inhibit catecholamine release. These results suggest a modulatory role for NPY through a specific NPY receptor in the secretion of catecholamine from the adrenal.

Adrenal Glands↗
PubMed1986

Quantitative analysis of the contribution of pulmonary and hind limb circulation to the clearance of exogenous catecholamines.

The contribution of pulmonary and hind limb circulation to the clearance of exogenous catecholamines was analyzed quantitatively. During infusion of clinical doses of norepinephrine, epinephrine and dopamine in dogs, the plasma level of catecholamine and the plasma flow were measured simultaneously. Percentage of contribution was calculated from the following equation; transorgan difference of plasma catecholamine (nanograms per milliliter) X plasma flow (milliliters per minute) X 100/dose (nanograms per minute). This value means the percentage of the amount of catecholamine cleared by an organ to the amount of catecholamine administered into the body. Small but significant transpulmonary gradients of plasma levels of norepinephrine, epinephrine and dopamine and large translimb gradients of plasma levels of these catecholamines were observed. The plasma flow of pulmonary circulation was increased by infusion of epinephrine and dopamine, whereas it remained unchanged by infusion of norepinephrine. The plasma flow of hind limb circulation showed no significant change by infusion of catecholamines. The calculated contribution values indicate that pulmonary circulation clears 35.7% of norepinephrine (at 0.2 ng X kg-1 X min-1), 27.1% of epinephrine (0.2 ng X kg-1 X min-1) and 21.5% of dopamine (10 micrograms X kg-1 X min-1) administered exogenously, and that the corresponding figures for hind limb circulation are 8.2, 7.8 and 4.5%.

Animals↗