Sympathoadrenal contribution to plasma dopa (3,4-dihydroxyphenylalanine) in rats

1992 ◽  
Vol 83 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Ehud Grossman ◽  
Aaron Hoffman ◽  
Ines Armando ◽  
Zaid Abassi ◽  
Irwin J. Kopin ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Urinary Excretion ◽  
Chemical Sympathectomy ◽  
Tissue Concentrations ◽  
Catecholamine Biosynthesis ◽  
Endogenous Dopamine ◽  
Urinary Dopamine ◽  
Arterial Plasma ◽  
6 Hydroxydopamine ◽  
Intact Rats

1. To determine the sources of dopa (3,4-dihydroxyphenylalanine) in plasma, we measured regional arteriovenous differences, tissue concentrations and urinary excretion of dopa during systemic intravenous infusions of I-[3H]dopa into anaesthetized intact rats and rats pretreated with the sympathetic neurotoxin, 6-hydroxydopamine. 2. In intact rats, large arteriovenous increments in plasma dopa concentrations were noted in the femoral (47%) and adrenal (141%) beds, with a small arterial-portal venous increment (11%), whereas in the kidney there was a substantial (47%) arteriovenous decrement in plasma dopa levels. Skeletal muscle appeared to be a major source of dopa in arterial plasma. 3. Treatment with 6-hydroxydopamine abolished the afferent-efferent increment of plasma dopa concentrations in the femoral bed. The arteriovenous decrement of plasma dopa concentrations in the kidney was preserved, and the arteriovenous increment in the adrenal bed was decreased by about half. Arterial plasma dopa levels fell by 41%. 4. Regional extraction percentages of I-[3H]dopa were used to estimate the clearances and rates of appearance (spillovers) of dopa in plasma. Dopa spillover was detected in the femoral, renal, splanchnic and adrenal beds, with skeletal muscle accounting for about 44% and the kidneys accounting for about 18% of dopa in arterial plasma. Whereas chemical sympathectomy decreased the femoral and renal spillover of dopa by 90% or more, arterial dopa levels and estimated dopa spillover into arterial plasma were decreased by only about 45%. 5. The kidneys accounted for 22% of dopa clearance from arterial plasma. From the renal extraction of I-[3H]dopa and the urinary excretion of [3H]dopamine, it was estimated that 77% of dopa removed in the kidneys was excreted as dopamine in intact animals and 69% was excreted as dopamine in sympathectomized animals. Conversely, about 80% of urinary endogenous dopamine was derived from plasma dopa, regardless of 6-hydroxydopamine treatment. 6. The results indicate that endogenous dopa in arterial plasma is derived substantially but not exclusively from sympathetic nerve endings that are destroyed by 6-hydroxydopamine, especially in skeletal muscle and the kidneys. Regional dopa spillover therefore probably reflects regional catecholamine biosynthesis. In rats, urinary dopamine is derived mainly from renal decarboxylation of circulating dopa.

Derivation of Urinary Dopamine from Plasma Dihydroxyphenylalanine in Humans

1993 ◽  
Vol 84 (5) ◽  
pp. 549-557 ◽  
Author(s):  
Efrat Wolfovitz ◽  
Ehud Grossman ◽  
Carol J. Folio ◽  
Harry R. Keiser ◽  
Irwin J. Kopin ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Laboratory Animals ◽  
Dietary Salt ◽  
Salt Loading ◽  
Renal Uptake ◽  
Dihydroxyphenylacetic Acid ◽  
Endogenous Dopamine ◽  
Urinary Dopamine ◽  
Arterial Plasma ◽  
A Minor

1. Dihydroxyphenylalanine is the precursor of all endogenous catecholamines. In laboratory animals, renal uptake and decarboxylation of circulating dihydroxyphenylalanine accounts for most of dopamine in urine. Dopamine is natriuretic, and in rats, dietary salt loading increases renal dihydroxyphenylalanine uptake by increasing the rate of entry (spillover) of dihydroxyphenylalanine into arterial plasma. In experimental animals and in humans, dietary salt loading increases urinary excretion of dihydroxyphenylalanine and dopamine. The present study examined in humans the extent to which circulating dihydroxyphenylalanine is the source of urinary dopamine and of the dopamine metabolite dihydroxyphenylacetic acid, and whether, as in animals, dietary salt loading affects dihydroxyphenylalanine spillover. 2. L-Dihydroxyphenylalanine (0.33 μg min−1 kg−1) was infused intravenously for 300 min after 7 days of a low-salt (mean 41 mmol/day) or a high-salt (mean 341 mmol/day) diet in 12 healthy subjects. Concentrations of dihydroxyphenylalanine, dopamine and dihydroxyphenylacetic acid were measured in urine and in antecubital venous plasma. Infusion of L-dihydroxyphenylalanine produced a steady-state mean dihydroxyphenylalanine level about 10 times the endogenous level. About 30% of infused dihydroxyphenylalanine estimated to be delivered to the kidneys via the arterial plasma was excreted as dopamine, and about 30% was excreted as dihydroxyphenylacetic acid. 3. Dietary salt loading increased urinary excretion rates of dihydroxyphenylalanine [from 0.08 ± (SEM) 0.01 to 0.14 ± 0.03 nmol/min, t = 2.80, P <0.02] and dopamine (from 1.03 ± 0.19 to 1.30 ± 0.28 nmol/min, t = 2.35, P <0.05), whereas dihydroxyphenylalanine spillover appeared to be unchanged. 4. Renal uptake and decarboxylation of circulating dihydroxyphenylalanine accounted for virtually all the urinary excretion of endogenous dopamine, but for only a minor portion of the excreted endogenous dihydroxyphenylacetic acid. 5. We conclude that in humans: (1) circulating dihydroxyphenylalanine is the main source of urinary dopamine but only a minor source of urinary dihydroxyphenylacetic acid; and (2) increased spillover of endogenous dihydroxyphenylalanine does not account for the increased excretion of these compounds during salt loading.

Cardiovascular responses during feeding in newborn lambs

1989 ◽  
Vol 257 (3) ◽  
pp. R568-R573
Author(s):  
B. L. Langille ◽  
S. L. Adamson ◽  
S. A. Jones
Keyword(s):  
Blood Pressure ◽  
Skeletal Muscle ◽  
Gastrointestinal Tract ◽  
Pressor Response ◽  
Sympathetic Innervation ◽  
Cardiovascular Responses ◽  
Bottle Feeding ◽  
Chemical Sympathectomy ◽  
Thyroid Glands ◽  
6 Hydroxydopamine

We examined the cardiovascular responses to bottle feeding in newborn lambs. Feeding induced a persistent rise in blood pressure, from 76.3 +/- 1.9 mmHg to 114 +/- 3.8 mmHg, that lasted for the duration of the feeding episode. This was accompanied by a transient tachycardia that lasted for approximately 10 s at the beginning of each feeding episode. Vasoconstriction of the hindlimb circulation, the gastrointestinal tract, kidneys, and adrenal and thyroid glands contributed to the pressor response, whereas changes in skeletal muscle resistance were not statistically significant. Of tissues assessed, only those actively involved in feeding (tongue and esophagus) vasodilated. Feeding tachycardia was greatly inhibited or abolished by the beta-blocker propranolol but the alpha-blocker phentolamine caused only moderate inhibition of the pressor response. Furthermore, chemical sympathectomy with 6-hydroxydopamine delayed the onset of the pressor response but did not abolish the ultimate rise in pressure. These findings indicate that feeding causes a significant pressor response in newborn lambs that is only partially mediated by sympathetic innervation.

CYTOCHROME c CONCENTRATIONS DURING RAT AND GUINEA PIG DEVELOPMENT

PEDIATRICS ◽  
1964 ◽  
Vol 33 (1) ◽  
pp. 106-110
Author(s):  
Peter R. Dallman ◽  
Herbert C. Schwartz
Keyword(s):  
Skeletal Muscle ◽  
Cytochrome C ◽  
Guinea Pig ◽  
Mammalian Species ◽  
Fetal Tissue ◽  
Developmental Pattern ◽  
Newborn Rat ◽  
Tissue Concentrations ◽  
Functional Changes

Cytochrome c concentrations were determined in tissues of the rat and the guinea pig, two mammalian species of contrasting developmental pattern. The relatively mature newborn guinea pig had approached adult concentrations of cytochrome c by one day of age. The less mature newborn rat did not attain comparable values until later in its development. The increase from the low fetal tissue concentrations to adult values occurred in the following sequence: heart concentrations increased earliest, followed by brain, skeletal muscle, and liver. Renal concentrations were the last to rise. Changes in cytochrome c concentration could be related to functional changes within these tissues as well as the over-all pattern of maturation represented by each of these species.

Effects of thyroid hormones on urinary and renal kallikreins

1992 ◽  
Vol 263 (3) ◽  
pp. E430-E434
Author(s):  
S. Avigdor ◽  
F. Alhenc-Gelas ◽  
J. Bouhnik
Keyword(s):  
Thyroid Hormones ◽  
Urinary Excretion ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Single Measurement ◽  
Kidney Weight ◽  
Plasma Aldosterone Concentration ◽  
Renal Kallikrein ◽  
Enzyme Changes ◽  
Intact Rats

The effects of thyroid hormones on the urinary excretion of kallikrein and on renal kallikrein were studied in rats. Total and active urinary kallikrein was decreased after thyroidectomy, but renal kallikrein content remained unchanged. Diuresis increased, and kidney weight and plasma aldosterone concentration decreased. Treatment with 3,5,3'-triiodo-L-thyronine restored the urinary kallikrein in thyroidectomized rats to normal and increased it in intact rats. It also produced increases in kidney weight and plasma aldosterone and a decrease in diuresis. The effect of thyroid hormones on the urinary kallikrein response to mineralocorticoids was also tested. Deoxycorticosterone acetate increased urinary kallikrein more in normal than in thyroidectomized rats. These results suggest that thyroidectomy decreases renal kallikrein synthesis and lowers the turnover rate of the enzyme, changes not detectable by a single measurement of the renal kallikrein content but reflected by an alteration in the urinary excretion of the enzyme. Thyroid hormones participate in the control of urinary kallikrein. This effect, however, is probably indirect and may be mediated by mineralocorticoids since thyroid function affects both the plasma level of aldosterone, which is known to influence renal kallikrein, and the kallikrein response to exogenous mineralocorticoids.

Differential impairment of thermogenesis in the pigeon after chemical sympathectomy

1978 ◽  
Vol 56 (4) ◽  
pp. 578-584 ◽  
Author(s):  
E. Hohtola ◽  
H. Rintamäki ◽  
R. Hissa
Keyword(s):  
Oxygen Consumption ◽  
Electrical Activity ◽  
Plasma Free Fatty Acid ◽  
Lower Body ◽  
Plasma Lactate ◽  
Chemical Sympathectomy ◽  
Ffa Metabolism ◽  
Lactate Levels ◽  
The Stability ◽  
6 Hydroxydopamine

A dose-controlled chemical sympathectomy with 6-hydroxydopamine (6-OHDA) did not disrupt thermostasis in the pigeon at +38 °C. At +6 °C, thermogenesis was impaired, but the lower body temperature and oxygen consumption were stable and vasoconstriction was normal. The stability may partly be explained by a massive release of adrenaline from the adrenals (50% in 20 min). Despite a deficit in heat production both after sympathectomy and after acute 6-OHDA, no change in muscle electrical activity was observed. Plasma free fatty acid (FFA) concentration was significantly elevated after sympathectomy, but no changes occurred in blood glucose or plasma lactate levels. The results indicate a major compensatory role for the adrenals in avian thermogenesis. They also suggest a sympathetically mediated auxiliary thermogenic mechanism independent of muscle electrical activity and coupled to FFA metabolism.

Pulmonary hypoxic vasoconstriction: not affected by chemical sympathectomy

1979 ◽  
Vol 46 (3) ◽  
pp. 529-533 ◽  
Author(s):  
C. A. Hales ◽  
D. M. Westphal
Keyword(s):  
Hypoxic Pulmonary Vasoconstriction ◽  
Systemic Blood Pressure ◽  
Lung Perfusion ◽  
Chemical Sympathectomy ◽  
Test Lung ◽  
Systemic Blood ◽  
Pulmonary Vasoconstriction ◽  
Hypoxic Vasoconstriction ◽  
Alveolar Hypoxia ◽  
6 Hydroxydopamine

The influence of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on regional alveolar hypoxic vasconstriction and on global hypoxic pulmonary vasoconstriction was investigated. In eight dogs a double-lumened endotracheal tube allowed ventilation of one lung with nitrogen as an alveolar hypoxic challenge while ventilation of the other lung with 100% O2 maintained adequate systemic oxygenation. Distribution of perfusion to the two lungs was determined with 133Xe and external counters. Mean perfusion to the test lung was 50.9 +/- 4.9% of total lung perfusion on room air and decreased by 32.4% (P smaller than 0.01) during alveolar hypoxia. Following 6-OHDA the test lung continued to reduce perfusion during alveolar hypoxia by 27.3%. In five dogs global hypoxia induced a 106% increase in pulmonary vascular resistance (PVR) prior to 6-OHDA and a 90% increase in PVR after 6-OHDA. After 6-OHDA no rise in PRV or systemic blood pressure occurred in response to tyramine, confirming effective sympathectomy by the 6-OHDA. Thus, sympathectomy with 6-OHDA failed to substantially block regional alveolar hypoxic vasoconstriction or global hypoxic pulmonary vasconstriction.

The Relation Between Urinary Excretion and Tissue Concentrations of Thiamine in Rats

1948 ◽  
Vol 36 (2) ◽  
pp. 307-313 ◽  
Author(s):  
Juan Salcedo ◽  
Victor A. Najjar ◽  
L. Emmett Holt ◽  
Elsa W. Hutzler
Keyword(s):  
Urinary Excretion ◽  
Tissue Concentrations

Cat retinal ganglion cell receptive-field alterations after 6-hydroxydopamine induced dopaminergic amacrine cell lesions

1985 ◽  
Vol 53 (6) ◽  
pp. 1431-1443 ◽  
Author(s):  
G. W. Maguire ◽  
E. L. Smith
Keyword(s):  
Receptive Field ◽  
Ganglion Cell ◽  
Cell Response ◽  
Amacrine Cell ◽  
Ganglion Cells ◽  
Response Functions ◽  
Endogenous Dopamine ◽  
Dopamine Content ◽  
Intensity Response ◽  
6 Hydroxydopamine

Optic tract single-unit recordings were used to study ganglion cell response functions of the intact cat eye after 6-hydroxydopamine (6-OHDA) lesioning of the dopaminergic amacrine cell (AC) population of the inner retina. The impairment of the dopaminergic AC was verified by high pressure-liquid chromatography (HPLC) with electrochemical detection of endogenous dopamine content and by [3H]dopamine high-affinity uptake; the dopaminergic ACs of the treated eyes demonstrated reduced endogenous dopamine content and reduced [3H]dopamine uptake compared with that of their matched controls. Normal appearing [3H]GABA and [3H]-glycine uptake in the treated retinas suggests the absence of any nonspecific action of the 6-OHDA on the neural retina. The impairment of the dopaminergic AC population was found to alter a number of response properties in off-center ganglion cells, but this impairment had only a modest effect on the on-center cells. An abnormally high proportion of the off-center ganglion cells in the 6-OHDA treated eyes possessed nonlinear, Y-type receptive fields. These cells also possessed shift-responses of greater than normal amplitude, altered intensity-response functions, reduced maintained activities, and more transient center responses. Of the on-center type cells, only the Y-type on-center cells were affected by 6-OHDA, possessing higher than normal maintained activities and altered intensity-response functions. The on-center X-cells were unaffected by 6-OHDA treatment. The dopaminergic AC of the photopically adapted cat retina therefore modulates a number of ganglion cell response properties and within the limits of this study is most prominent in off-center ganglion cell circuitry. When functioning normally, the dopaminergic AC of the cat's retina appears to make the receptive field of the off-center cell more sustained and may make its spatial summation characteristics more linear while adjusting the intensitive properties of neurons in both the on- and off-center pathways.

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