�ber das sympathicomimetische pressorische Prinzip des Harns (?Urosympathin?)

Holtz, Peter; Credner, Karl; Kroneberg, G.

doi:10.1007/bf00738347

Cited by 180 publications

(19 citation statements)

References 21 publications

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“…Previous studies on the significance of the urinary excretion of catecholamines and their metabolites in hypertensive diseases have been negative or contradictory (2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13). However, such studies may be misleading since they reflect a summation of events occurring in the entire body.…”

mentioning

confidence: 97%

Catecholamine Metabolism in Experimental Hypertension in the Rat

Champlain

Krakoff

Axelrod

1967

Circulation Research

141

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The role of catecholamines was investigated in uninephrectomized SpragueDawley male rats made hypertensive by administration of desoxycorticosterone and a high salt diet. The accumulation of tritiated norepinephrine and the endogenous norepinephrine levels were measured in the various organs. The content of endogenous norepinephrine and the accumulation of 8 H-norepinephrine 1 hour after its injection were reduced in the heart, spleen, intestine, skeletal muscle, and kidney of hypertensive rats as compared to controls. Simultaneously, an increase in total s H-metabolites was also found in the hypertensive animals.A highly significant inverse relation was established between the level of blood pressure and the accumulation of 8 H-norepinephrine or endogenous norepinephrine levels in the heart.The abnormalities observed in the disposition of exogenously administered and endogenous norepinephrine do not appear to be secondary to a change in the distribution of cardiac output to the various organs. Since the initial uptake was normal in the hypertensive rats, the reduced capacity to accumulate norepinephrine seems to be related to a defect in the storage of norepinephrine.

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mentioning

confidence: 97%

Catecholamine Metabolism in Experimental Hypertension in the Rat

Champlain

Krakoff

Axelrod

1967

Circulation Research

141

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“…However, it was not until 1950 that this amine was found in mammalian tissue, at which time Goodall demonstrated its presence in the heart (2, 3) and in the adrenal gland along with L-DOPA (3,4-dihydroxyphenylalanine) (3,4). Since then dopamine has been demonstrated in multiple tissues (5)(6)(7)(8)(9)(10)(11)(12), urine (13)(14)(15)(16), and brain (17,18). In 1959, Bertler and Rosengren (19), Sano et al (20), and later others (21)(22)(23) showed that dopamine existed in relatively high 1Dopamine-2-1'C HCI (3,4-dihydroxyphenylethylamine, 3-hydroxytyramine), Nuclear-Chicago Corporation, Des Plaines, I11.…”

mentioning

confidence: 99%

Dopamine (3-Hydroxytyramine) metabolism in parkinsonism

Goodall¹,

Alton²

1969

J. Clin. Invest.

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A B S T R A C T Three patients with idiopathic parkinsonism and six normal subjects were infused over a 4 hr period with 104.6 sc of dopamine-2'C (3,4-dihydroxyphenylethylamine, 3-hydroxytyramine) ,' the immediate precursor in the synthesis of the sympathetic neurohormone, noradrenaline (norepinephrine). Urine was collected during the infusion period, 0-2 hr, 2-4 hr, 4-8 hr, 8-24 hr, and thereafter for 4 additional days. Using a technique herein described, the various metabolic and biosynthetic products of dopamine, including noradrenaline and its metabolic products, were separated, identified, and their radioactivity measured.The metabolic pattern of dopamine in the normal subject was compared to that of the three parkinsonism patients. The results indicate that in idiopathic parkinsonism there is a decrease in the recovery of free radioactive noradrenaline in the urine following an infusion of dopamine-2-"'C and a slight shift toward dopamine metabolism. The latter is reflected by an increase in the following metabolites of dopamine: 3,4-dihydroxyphenylacetic acid and the conjugates of 3-methoxy-4-hydroxyphenylacetic acid, 3,4-dihydroxyphenylacetic acid, 3-methoxy-4-hydroxyphenylethanol and dopamine.

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“…In both the cat and the dog the adrenal glands release a mixture of adrenaline and noradrenaline into the bloodstream (Holtz et al 1947;Bulbring & Burn, 1949). Many authors have argued for and against the independent control of the release of the two catecholamines.…”

Section: Introductionmentioning

confidence: 99%

The reflex release of adrenaline and noradrenaline from the adrenal glands of cats and dogs.

Critchley¹,

Ellis²,

Ungar³

1980

The Journal of Physiology

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SUMMARY1. We have studied the release of noradrenaline and adrenaline from the adrenal glands of dogs and cats in response to the lowering of carotid sinus pressure (baroreceptor tests) and to the perfusion of the vascularly isolated carotid bifurcations with hypoxic blood (chemoreceptor tests).2. In cats, the resting output of catecholamines had a ratio of noradrenaline to adrenaline of 1:1. The ratio in the incremental release during baroreceptor tests rose to 3: 1, and during chemoreceptor tests it fell to 1: 6. 3. In dogs, the ratio of noradrenaline to adrenaline at rest was 1:4. The ratio did not change over a wide range of outputs during baroreceptor tests, chemoreceptor tests and splanchnic nerve stimulation.4. The release of catecholamines in response to baroreceptor tests in the cat was abolished by hexamethomium bromide at doses that did not diminish the response to chemoreceptor tests.

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�ber das sympathicomimetische pressorische Prinzip des Harns (?Urosympathin?)

Cited by 180 publications

References 21 publications

Catecholamine Metabolism in Experimental Hypertension in the Rat

Catecholamine Metabolism in Experimental Hypertension in the Rat

Dopamine (3-Hydroxytyramine) metabolism in parkinsonism

The reflex release of adrenaline and noradrenaline from the adrenal glands of cats and dogs.

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