EFFECT OF STRESS ON THE CATECHOLAMINE CONTENT OF THE ADRENAL GLAND OF INTACT AND BURSECTOMIZED CHICKS

1. Bursa-intact and bursectomized chicks were exposed to cold-wet immobilization (CWI) stress for 1.5 min. The catecholamines (CA) from the adrenal gland were measured spectrofluorometrically 5, 15, 30 and 60 min after stress. 2. In bursa-intact chicks, the CWI stress caused decrease of both norepinephrine and epinephrine from the adrenal glands 5 min after stress. Resynthesis of epinephrine exceeded the control value 30 and 60 min after stress. 3. In bursectomized chicks, the CWI stress brought about a decrease of norepinephrine 15 and 30 min and of epinephrine 30 and 60 min after stress. 4. The findings suggest that bursa facilitates early (5 min) release of CA and also helps in quick resynthesis of epinephrine during stress.     

吸烟前后血浆儿茶酚胺和血流动力学的变化

检测２５名吸烟健康男性吸烟前后心率、血压、心输出量（ＣＯ）ｆｏ血浆儿茶酚胺的变化。结果发现，吸烟后１０ｍｉｎ，心率、血压和血浆儿茶酚胺均较前显著升高（Ｐ＜０．０５），每搏量、ＣＯ和射血速率指数均显著下降（Ｐ＜０．０５），体循环血管阻力的变化不明显。对照组上述参数无明显变化。     

Reduction in calcium concentration induces exocytotic secretion of catecholamines from the adrenal medulla in the absence of extracellular ions

Cat adrenal glands were perfused with a NaCl-free medium where all NaCl had been replaced by isotonic sucrose. Exocytotic secretion of catecholamines was evoked by a simple reduction in the concentration of Ca in the medium. The response required extracellular Ca and was blocked by Ca channel blockers. The results suggest that in the absence of most ions, Ca reduction itself increases permeability of the plasma membrane to Ca, thereby evoking secretion.     

A STUDY OF THE EFFECTS OF HYPOTHYROIDISM INDUCED BY PROPYLTHIOURACIL ON ADRENOCEPTORS AND NORADRENALINE LEVELS IN THE VAS DEFERENS OF THE RAT

1. The anti-thyroid drug, propylthiouracil (0.05% w/v in drinking water) was administered to rats for 3–4 weeks. This treatment decreased the rate at which rats gained body weight but did not affect the weight of the vasa deferentia. Circulating levels of thyroxine and triiodothyronine were markedly decreased. 2. The potencies of postjunctional α-adrenoceptor agonists, 1-noradrenaline and 1-phenylephrine, in eliciting contraction of the epididymal end of the vas deferens were unaffected by propylthiouracil treatment. In contrast, the potency of the β-adrenoceptor agonist, 1-isoprenaline, in inhibiting field stimulation-induced twitches of the prostatic end of the vas deferens was decreased in tissues from propylthiouracil-treated rats. Thus hypothyroidism induced by propylthiouracil produced an apparent change in the properties of postjunctional β-adrenoceptors without a concomitant reciprocal change in the properties of postjunctional α-adrenoceptors. 3. Treatment of rats with propylthiouracil led to a small increase in the concentration of noradrenaline in the vas deferens, and a concomitant small increase in the rate of accumulation of ³ H-noradrenaline in in vitro experiments. Extra-neuronal uptake of ³H-isoprenaline was unaffected by propylthiouracil treatment. 4. The potencies of the prejunctional α-adrenoceptor agonists, xylazine and 1-noradrenaline, in producing inhibition of twitches evoked by field stimulation of preparations of the prostatic end of the vas deferens, were similar in preparations from propylthiouracil-treated and control rats, although the slope of the log dose-response curve to xylazine was decreased in the former group. Thus unequivocal changes in the properties of prejunctional α-adrenoceptors did not accompany the other prejunctional effects of propylthiouracil upon endogenous noradrenaline levels and neuronal uptake of ³H-noradrenaline in this organ.     

Central nervous system effect of calcitonin: Stimulation of prolactin release in rats

Effect of [Asu^1,7]eel calcitonin (CT) on prolactin (PRL) release was examined in male rats under urethane anesthesia. Intravenous injection of 4–20 μg [Asu^1,7]eel CT did not modify plasma PRL levels. Injections of 0.5–2.5 μg [Asu^1,7]eel CT into the lateral ventricle produce a significant and dose-related increase of plasma PRL within 10 min of injection. When intraventricularly injected in an equimolar dose (0.74 nmol/10 μl), eel CT^11–32, eel CT^15–32, [Asu^1,7]eel CT^1–16 and [Asu^1,7]eel CT^1–9 showed 44.8, 25.7, 19.9 and 10.1% the potencies of [Asu^1,7]eel CT, respectively, in stimulating activity of PRL release. The rise of plasma PRL after [Asu^1,7]eel CT injection were significantly less or abolished not only in hypothalamic-lesioned rats but also in rats with complete deafferentation. Pretreatment with α-methyl-p-tyrosine (250 mg/kg, 12 h before) but not with p-chlorophenylalanine (300 mg/kg, 72 and 24 h before) resulted in a suppression of [Asu^1,7]eel CT-induced PRL release.These results suggest the following: first, PRL release is stimulated by centrally injected [Asu^1,7]eel CT, the action site of which may exist in the extrahypothalamic area; second, brain catecholamines may be involved in the mechanism of [Asu^1,7]eel CT-evoked PRL release; third, the C-terminal portion of the peptide may play an important role in stimulating PRL release.     

Characterization of substance P and somatostatin receptors on adrenal chromaffin cells using structural analogues

Substance P (SP) and somatostatin (SRIF) are known to inhibit the nicotine-induced release of catecholamines (CAs) from isolated adrenal chromaffin cells in culture^22,24. In order to characterize the receptors mediating this action, we have tested several SP and SRIF analogues for their effects on release of [³H]l-norepinephrine ([³H]NE) from chromaffin cell cultures. SP-free acid and a series of 11 SP analogues, in which each amino acid of SP is replaced in turn byl-alanine, all inhibited the nicotine-induced release of [³H]NE from these cultures. The rank order of potency of the analogues for this action was similar to their reported order of potency in other SP-responsive tissues. The least potent were SP-free acid, [Ala⁷]-SP, [Ala¹⁰]-SP, [Ala⁸]-SP and [Ala¹¹]-SP, while the potencies of the Ala 1 to 6 analogues and [Ala⁹]-SP were closer to that of SP. [Leu⁷]- and [Leu^7,8]-SP had potencies similar to that of SP. SP itself had no effect on basal [³H]NE release. The results suggest that adrenal chromaffin cells possess a specific SP receptor mediating inhibition of agonist-induced CA release and that the binding site of this receptor shares similar structural requirements with the binding site of the SP receptor on other tissues.Several SRIF analogues, which have been previously shown to be more potent than native SRIF at selective SRIF receptors^{2,3,31, 35}, were compared to SRIF for effects on [³H]NE release from chromaffin cell cultures. These analogues were found to be active but less potent than SRIF in inhibiting nicotine-induced [³H]NE release from these cultures, suggesting that the site mediating this action differs in its structural requirements from the SRIF receptor found in some other tissues.     

An electron microscopic study of degeneration of nerve terminals after administration of epinephrine

6-Hydroxydopamine (6-OHDA) has been used clinically to create a chemical sympathectomy and has been shown to cause acute, selective degeneration of sympathetic nerve terminals. Because epinephrine, an endogenous catecholamine, resembles 6-OHDA structurally, it was reasoned that some doses of epinephrine might cause similar degeneration. Supralethal doses of epinephrine were given to five cats pretreated with phenozybenzamine (an alpha receptor blocker known to protect animals from epinephrine's lethal effects) and the irises and spleen capsules were examined with the electron microscope and compared to control animals. In addition, high doses of epinephrine alone were given to three cats and specimens were taken and compared to controls. It appears systemic epinephrine administration can result in acute degeneration of nerve terminals while leaving other structures intact as has been reported for 6-OHDA.     

Plasma catecholamine levels during exposure to an environment of hyperbaric oxygen

Plasma catecholamine levels were measured before, during and after hyperbaric oxygen therapy in nine subjects. Adrenaline levels were elevated immediately prior to hyperbaric oxygen therapy, but then fell and stabilized once treatment commenced. No significant fluctuations in plasma dopamine or noradrenaline levels were noted during the treatment period.This study does not support the premise that there is a suppression of endogenous plasma catecholamine levels during hyperbaric oxygen as has been previously reported. The observed initial increase in adrenaline can be attributed to stress/anxiety and the subsequent decline in this stress, rather than the result of the hyperbaric oxygen treatment itself.     

Ultrastructure of the regenerating growth cones of catecholamine nerve terminals in rat hypothalamic nuclei after 5,7-dihydroxytryptamine administration

Ultrastructure of the regenerating growth cones of catecholamine axons is examined in the paraventricular nucleus and median eminence of the rat. Growth cones are observed during 1 to 4 months, and most frequently at 2 months, after the administration of 300 μg of 5,7-DHT in the lateral ventricle. The growth cones of catecholamine axons are characterized by an accumulation of branching smooth endoplasmic reticula which contain dense material.     

Agaridoxin: A fungal catecholamine which acts as an alpha 1 agonist of mammalian hypothalamic adenylate cyclase

Agaridoxin, a catecholamine isolated from mushrooms, and 4 synthetic analogues cause activation of adenylate cyclase in the presence of guanylyl imidodiphosphate (Gpp(NH)p) in membrane particles prepared from rat hypothalamus. These compounds also activate adenylate cyclase preparations from rat kidney, liver and cerebral cortex. In the presence of tyrosinase, these compounds are readily oxidized to quinones which lack agonist activity. Studies with selective adrenergic blockers suggest that agaridoxin acts at an alpha 1-type receptor. Agaridoxin-mediated adenylate cyclase stimulation is most effectively antagonized by WB-4101 and phenoxybenzamine, while propranolol and yohimbine are without inhibitory effect. Agaridoxin and the alpha 1 agonist methoxamine inhibited the binding of [3H]WB-4101 in rat hypothalamic and cerebral cortical membranes. The values of Ki for both compounds are lower than that of norepinephrine. The agaridoxin analogue, 4-aminocatechol hydrochloride, is a more effective and potent adenylate cyclase activator than agaridoxin or methoxamine.