A radioimmunoassay for epinephrine and norepinephrine in tissues and plasma.
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Animals↗
Biomedical subjects
W J Raum
Publications and source records attributed to W J Raum.
The role of hypothalamic adrenergic receptors in preventing testosterone-induced androgenization in the female rat brain.
Androgenization of the female neonatal rat brain by testosterone and the subsequent development of persistent estrus in the adult can be blocked by drugs which interfere with normal hypothalamic neuronal function. The mechanism of action of these drugs was studied. A 25-micrograms dose of testosterone propionate at 5 days of age produced a 69% incidence of persistent estrus at 90 days of age. alpha-Methyl-p-tyrosine given with testosterone propionate resulted in an 81% incidence of persistent estrus. Therefore, hypothalamic norepinephrine depletion did not prevent androgenization. Tyramine (100 micrograms) inhibited androgenization to an incidence of 27% by 90 days. Phenoxybenzamine (50 micrograms) and phentolamine (50 micrograms) each reduced the incidence to 0%. Combining the beta-antagonist propranolol with phenoxybenzamine or phentolamine reversed the block in androgenization, resulting in 37% and 50% incidences of persistent estrus, respectively. Tyramine causes the release of neuronal stores of norepinephrine which is turn stimulates alpha- and beta-adrenergic receptors. The action of tyramine implicates adrenergic stimulation as a mechanism for the inhibition of androgenization, but does not define which receptor type is involved. In addition to postsynaptic alpha-blockade, phenoxybenzamine and phentolamine can cause presynaptic alpha-blockade, resulting in increased neuronal norepinephrine release and beta-stimulation. When the beta-antagonist propranolol was added to the alpha-antagonists, the block in androgenization was reversed. Therefore, we conclude that beta-adrenergic receptor stimulation prevents androgenization of the neonatal rat brain.
Animals↗
Urinary metanephrine radioimmunoassay: comparison with the colorimetric assay.
A radioimmunoassay involving an 125I ligand has been developed and applied to the measurement of urinary metanephrine. To validate the clinical usefulness of this assay, we compared measurement of metanephrine by radioimmunoassay and of total urinary metanephrines by the Pisano colorimetric method. The radioimmunoassay is specific for metanephrine, whereas the colorimetric method measures both metanephrine and normetanephrine. We used both methods to determine urinary metanephrine or total metanephrines in subjects with essential hypertension, pheochromocytoma, the syndrome of multiple endocrine adenomatosis type 2, and normotensive volunteers. The mean and upper limit of normal (3 SD) for metanephrine by radioimmunoassay in our normotensive volunteers was 94.2 microgram/24 h and 229 microgram/24 h, respectively, which compares well with reported values of 87.6 microgram/24 h and 319 microgram/24 h by non-radioimmunoassay methods. Both radioimmunoassay and colorimetry accurately identified five patients with known pheochromocytoma. Good correlation (r = 0.993) was demonstrated between the two assays in a comparison of patients with essential hypertension and pheochromocytoma. We conclude that the radioimmunoassay is at least equivalent to the colorimetric methods in distinguishing pathological and normal catecholamine secretion, and is faster, more precise, and 1000-fold more sensitive.
Adrenal Gland Neoplasms↗
Changes in hypothalamic catecholamine neurotransmitters and pituitary gonadotropins in the immature female rat: relationships to the gonadostat theory of puberty onset.
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Aging↗
Comparison of two weeks versus one week of prenatal ethanol exposure in the rat on gonadal organ weights, sperm count, and onset of puberty.
Sprague-Dawley dams from Harlan Ind. (Indianapolis, IN) were administered a fortified ethanol liquid diet containing 35% ethanol derived calories for two weeks (E-2) beginning on day 7 or one week (E-1) beginning on day 13 of gestation and continuing through parturition. Control dams were pair-fed an isocaloric liquid diet containing no ethanol during these periods or remained on lab chow and water. E-2 dams consumed an average of 13.52 g ethanol/kg bwt during the first week of exposure (days 8-14) and 12.50 g ethanol/kg bwt the second week (days 14-20). E-1 dams consumed significantly less than E-2 dams during the second week (9.75 g/kg; p < 0.0001). Although the lower consumption in E-1 dams led to a significant decrease in maternal weight gained during the few days of pregnancy compared to E-2 dams, birthweights of E-1 offspring were significantly heavier than those of E-2 offspring (p < 0.05). No effect of ethanol was detected on anogenital distance at birth in either sex. Puberty was delayed in female offspring of both E-1 and E-2 dams (p < 0.01) as measured by age of vaginal opening. These data suggest that the primary teratogenic actions of ethanol in the rat on fetal growth, as well as delayed puberty in females, occur in the last week of gestation. In adult E-2 males, testis weight was significantly heavier than all other groups when indexed to body weight. No effect of prenatal ethanol exposure was observed on the indexed weights of prostate, epididymis, or seminal vesicles.(ABSTRACT TRUNCATED AT 250 WORDS)
Alcoholism↗
Ethanol exposure during the last week of gestation in the rat: inhibition of the prenatal testosterone surge in males without long-term alterations in sex behavior.
In utero ethanol exposure decreases the prenatal testosterone (T) surge in male rats. To determine the functional significance of this suppression, we measured sex behavior in adult litter representatives of pregnant rats that were administered a fortified liquid diet containing 35% ethanol-derived calories from day 15 of gestation through parturition. Control dams were pair-fed an isocaloric liquid diet with the ethanol calories replaced by sucrose. Results from the behavioral studies showed that gonadally intact fetal alcohol-exposed (FAE) males exhibited little masculine sex behavior in the first of four weekly sessions. However, their behavior in the subsequent three tests was indistinguishable from pair-fed controls. Lordosis quotients in the same males following castration and estrogen and progesterone treatment were under 10%. In castrated FAE females, no effects of prenatal ethanol exposure were observed in masculine behaviors following androgen replacement or feminine sex behaviors following estrogen and progesterone replacement. Additional studies measured the duration of prenatal ethanol exposure necessary to inhibit the prenatal T surge in order to determine whether the inhibition was due to a direct effect of the drug. Results revealed an inhibition of the surge in males exposed to ethanol from days 14 through 20 of pregnancy, days 14 through 16 of pregnancy, or days 17 through 20 of pregnancy. A normal surge of T was observed on days 18-19 of gestation in control fetuses. These findings indicate that ethanol does not have to be present in blood at the time of the surge to have an inhibitory effect. They also reveal that the surge can be inhibited with as little as 24-36 h of ethanol exposure prior to its normal appearance on day 18 of gestation. In spite of this inhibition of the prenatal T surge, the behavioral results indicate that normal masculinization and defeminization of sex behavior occurs in FAE males exposed to ethanol after the beginning of the period of differentiation of the hypothalamus and testes.
Animals↗