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Biomedical subjects

J Antunes-Rodrigues

Publications and source records attributed to J Antunes-Rodrigues.

At least 109 records · Page 6Linked to original sources

Characterization of adrenergic control of the Leydig cell steroidogenesis: identification of both stimulatory and inhibitory components.

Percoll-purified Leydig cells were studied in vitro in order to evaluate the effect of adrenaline on testosterone (T) secretion. Adrenaline enhanced the basal and potentiated the hCG-induced T release. A similar effect was also obtained with the beta 2-agonist, salbutamol. Although phenylephrine, an alpha 1-agonist, did not alter the basal T secretion, it enhanced hCG-mediated T secretion. Para-aminoclonidine, an alpha 2-agonist, decreased the basal T release without altering the hCG-stimulated T release. These data demonstrate that either inhibitory or stimulatory effects on T release can be obtained and that they depend on the adrenoreceptor subtype involved.

Animals↗

Acute effects of human growth hormone on zinc, copper, calcium and magnesium metabolism in normal subjects.

The acute effects of human growth hormone (hGH) on the metabolism of zinc, copper, calcium and magnesium ions was studied. Seven normal subjects were perfused iv with doses of 0.2 or 1.0 mg hGH over a period of 60 min. An increase in plasma zinc, calcium and magnesium, and a decrease in plasma copper levels was noted for the 0.2 mg dose, and these effects were reversed for the 1.0 mg dose although no urine changes occurred. Plasma mobilization of these ions appears to be related to their roles as essential physiological modulators for the action of hGH.

Adolescent↗

Metabolic effects of glucagon on plasma and urine zinc, copper, calcium and magnesium levels.

The present study determines the effect of glucagon on the behavior of zinc, copper, calcium and magnesium ions in human plasma and urine. Five normal adults were submitted to intravenous infusion of 2.0 mg glucagon over a period of 120 min. A decrease in plasma magnesium and copper was observed with no significant change in urine ion concentrations. We related plasma magnesium mobilization to glucagon, and copper mobilization to plasma variation in free fatty acids and albumin.

Adult↗

Effect of copper on the secretion of human growth hormone.

The response of human growth hormone to the oral administration of 5.0 mg copper was studied in plasma from 12 normal adults. Blood samples were collected at 30 min intervals over a period of 240 min after two basal measurements taken at time = -30 and time = 0 min. Six subjects responded to the stimulus with increased growth hormone secretion, revealing a positive correlation with plasma copper levels. The other six subjects presented a similar rise in plasma copper levels but no increase in plasma growth hormone levels. These results suggest that acute, high blood copper levels can increase basal growth hormone secretion in normal individuals, presumably by acting on the hypothalamic center.

Adult↗

Central histaminergic effect on basal and opioid-induced prolactin secretion.

1. The participation of the central histaminergic system in basal and opioid-induced prolactin secretion in male rats was investigated. 2. Central injections of cimetidine, an H2 antihistaminic, reduced basal plasma prolactin levels from 5.08 +/- 0.76 to 3.11 +/- 0.50 ng/ml (N = 10) while diphenhydramine, an H1 antihistaminic, had no effect. 3. Intracerebroventricular injections of FK 33824, a synthetic opioid peptide, produced a dose-dependent increase of prolactin secretion. This effect was partially blocked (-50%) by pretreatment with 20 ng diphenhydramine 15 min before administration of the opioid peptide. Cimetidine pretreatment failed to modify the prolactin rise in this case. 4. We conclude that brain histaminergic pathways exert a stimulatory tone on basal prolactin secretion which is mediated by H2 receptors and that the opioid-induced prolactin rise depends at least in part on activation of H1-histamine receptors.

Animals↗

Effect of atropine injection into the medial septal area on food-associated drinking.

The effect of atropine injection into the medial septal area (MSA) or medial preoptic area (MPOA) on carbachol-induced drinking was evaluated in conscious unrestrained rats during a food-associated drinking test reinforced by 14 h of food deprivation. Atropine did not alter food intake when injected into either area, nor did it affect drinking after its injection into the MPOA. However, atropine markedly reduced water intake after its injection into the MSA. These results suggest that the central cholinergic system in the MSA can participate in the regulation of food-associated drinking.

Animals↗

Role of opiates in the regulation of water and salt metabolism: effects of the FK 33-824 injection into the subfornical organ of both normal and hypophysectomized rats.

The present study was performed to evaluate the participation of the subfornical organ (SFO) in the opioid modulation of urinary volume (Uv), and of sodium and potassium excretion. Intact and hypophysectomized (HYPOX) adult male rats were implanted with a cannula into the SFO, and injected with the opiate agonist FK 33-824 (FK). FK induced a significant decrease in Uv and in Na+ and K+ excretion in both intact and HYPOX rats. The data show that opioids play an important role in the regulation of hydromineral metabolism by the SFO.

Animals↗

Evidence for interaction between central beta-2 adrenoceptors and epinephrine pathways in the opioid-induced prolactin rise in the rat.

1. The possible role of central beta-2 adrenoceptors and epinephrine pathways in opioid-induced prolactin (PRL) rise was investigated. 2. FK 33824, a synthetic opioid peptide injected into the third ventricle of Wistar male rats, generated a PRL rise that was significantly reduced by pretreatment with IPS 339, a potent and selective beta-2 antagonist. 3. Inhibition of central epinephrine synthesis with SKF 64 139, which selectively blocks phenylethanolamine-N-methyltransferase, partially decreased the PRL release induced by FK 33824. 4. Practolol, a selective beta-1 adrenoceptor blocker, did not modify the PRL secretion induced by FK 33824. 5. The results indicate that this FK 33824-induced PRL rise depends in part on the functional integrity of central beta-2 adrenoceptors and that epinephrine pathways in the brain may play an important role in the mechanisms by which opioid peptides increase PRL secretion.

Animals↗

Factors controlling adrenal weight and corticosterone secretion in male rats as revealed by median eminence lesions and pharmacological alteration of prolactin secretion.

To determine whether or not prolactin, as well as ACTH, was involved in the control of adrenal weight and steroid release, lesions in the median eminence which had previously resulted in impaired steroid release and atrophy of the adrenal were placed in animals in which the plasma prolactin was allowed to rise as a result of the lesions or prevented from rising by the administration of the dopamine agonist, CB-154. As previously reported, as the severity of diabetes insipidus (DI) increased as a result of interruption of the supraoptico-hypophyseal tract, adrenal weight declined reaching a nadir at water intakes of approximately 100-150 ml/day. This was followed by a reversal of this trend and an increase in adrenal weight as water intakes increased further. These effects were not modified by CB-154 which was effective to lower the elevated prolactin levels in the animals. In general, adrenal weight correlated with levels of plasma corticosterone and progesterone. The ability of the animals to undergo compensatory adrenal hypertrophy was also impaired by median eminence lesions in the presence or absence of CB-154. Exceptional animals were encountered in which adrenal weight was high and yet plasma corticosterone was low. Treatment of hypophysectomized animals with long-acting ACTH plus maintenance doses of triiodothyronine prevented the adrenal atrophy characteristic of the hypophysectomized animal, thus confirming that ACTH is the most important hormone in the control of adrenal weight.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

Leydig cell hypertrophy and hyperplasia in adult rats treated with an excess of human chorionic gonadotrophin (hCG).

A morphometric study was undertaken to determine to what extent the increase in LEYDIG cell activity is related to an increase in their number and/or size. An attempt was also made to consider the morphological characteristics of the cells in terms of their probable functional capacity. Following 8 h to 3 d of excess hCG treatment, LEYDIG cells nuclear volume exhibited an increase of 16 to 18% while no significant increase in cells number was observed. By 7 d of hCG treatment, the nuclear hypertrophy (42%) coexisted with hyperplasia (33%). After 14 d of stimulation, a 41% augment in cells number and 31% increase in nuclear volumes were found. Such morphometric parameters were correlated with plasma levels of testosterone. The results suggest that hypertrophy plays a more important role in the enhancement of LEYDIG cells secretory activity in the initial phase of hCG stimulation. A subsequent hyperplasia seems to become relatively more important in longer periods of treatment. Our findings support the statement that both hCG dose and time of treatment, and consequently the plasma level of testosterone, are important parameters to be considered when the functional activity of LEYDIG cells is been evaluated by morphometric techniques.

Animals↗

Central administration of atrial natriuretic factor inhibits saline preference in the rat.

Atrial natriuretic factors (ANFs), produced in myocytes of mammalian atria, exert potent natriuretic and diuretic actions in the kidney as well as a variety of other actions coordinated to normalize extracellular fluid volume. Recently, ANF-like immunoreactivity has been detected in the hypothalamus of the rat, and central administration of ANF has been shown to block dehydration-induced water intake. We describe here the ability of 0.2 and 2.0 nmol atriopeptin III to inhibit saline intake when infused into the third ventricle of conscious, salt-depleted rats; an effect that was dose-related and long-lasting (24 h). These studies provide further evidence for a central nervous system action of ANF, which, together with its established renal and adrenal actions, might be an important feature of the coordinated physiological control of fluid volume.

Animals↗

Effect of a selective inhibitor of epinephrine synthesis, SK&F 64 139, on prolactin secretion in the rat.

The participation of central epinephrine in prolactin secretion was investigated in rats by testing the effects of SK&F 64 139, a selective inhibitor of phenylethanolamine-N-methyltransferase. The drug is reported to dramatically reduce brain epinephrine concentration without affecting norepinephrine or dopamine levels. When SK&F 64 139 was administered (40 mg/kg, ip) to male rats or to female rats during diestrus or proestrus, plasma prolactin levels were not different from those of control groups. Lactating and ovariectomized rats, however, responded to the same SK&F 64 139 dose with an increase in plasma prolactin levels: 210.02 +/- 22.72 vs 378.66 +/- 42.57 (mean +/- SEM) for control of lactating rats, and 4.35 +/- 0.52 vs 6.21 +/- 0.60 ng/ml for control ovariectomized rat. These results suggest that epinephrine may play a functional inhibitory role in prolactin secretion in the lactating and ovariectomized rat.

Animals↗

Effect of spermatic cord phenolization on the spermatogenetic and secretory activities of adult rat testes.

We evaluated the effect of testicular denervation on the spermatogenetic and secretory activities of the adult rat testis. Testes were denervated by applying 20% (v/v) phenol to the spermatic cord and measurements were made 30 days thereafter. There was an increase in the frequency of stages VII-VIII of the seminiferous epithelium cycle, indicating an increase in the relative amount of mature elongated spermatids present in the seminiferous tubules. The frequency of stage XIV remained unchanged, suggesting that the rate of reductional divisions was constant. A decrease in the nuclear volume of Leydig cells paralleled increased plasma LH and testosterone levels. The results are discussed in terms of a possible role of phenol-sensitive neural elements which affect testicular spermatogenetic and secretory functions.

Animals↗

Mechanism of the CNS-mediated pressor response to intracerebroventricular injection of noradrenaline in unanaesthetized rats.

Catecholamines administered intracerebroventricularly (i.c.v.) have cardiovascular effects mediated by the CNS. Although hypotension constitutes the more prominent response, an increase in blood pressure has also been reported after the intracerebroventricular injection of these amines. Anaesthesia interferes with pressor responses mediated by the CNS to a larger extent than with depressor mechanisms and constitutes one of the major factors influencing the pattern of response to the amines. The depressor response observed after the intracerebroventricular administration of noradrenaline is reversed into increases in blood pressure in awake animals. In the present experiment, the action of intracerebroventricularly injected noradrenaline was compared in anaesthetized and conscious rats. The results indicated that the pressor response in awake rats was not mediated by the sympathetic nervous system and involved the release of a pituitary humoral-factor, most probably vasopressin, whereas the depressor response observed in anaesthetized animals was not dependent on pituitary mediation. The involvement of histaminergic mechanisms in the CNS in the control of the pressor response to intracerebroventricularly administered noradrenaline in the rat is proposed.

Anesthesia↗

Participation of cholinergic and adrenergic synapses of the medial septal area (MSA) in the natriuretic and kaliuretic responses to intraventricular hypertonic saline (NaCl).

The microinjection of hypertonic sodium chloride into the third ventricle elicits natriuresis and kaliuresis in rats following water loading. These responses were blocked by atropine or phentolamine microinjection into the MSA. The data suggest the interaction between periventricular areas sensible to changes of sodium concentration in the cerebrospinal fluid (CSF) and MSA. Cholinergic and alpha-adrenergic synapses of MSA are involved in this interaction which regulates renal sodium excretion.

Adrenergic Fibers↗

Blockade of adrenal compensatory hypertrophy by unilateral hypothalamic lesions.

To determine if unilateral hypothalamic lesions block adrenal compensatory hypertrophy (ACH), such lesions were produced unilaterally under stereotaxic guidance using direct cathodal current in rats just after the left adrenal gland was removed. The animals were sacrificed one week later and the degree of the ACH of the remaining adrenal gland was determined. Animals without lesions uniformly showed ACH in terms of an absolute increase in adrenal weight of the remaining gland as compared to the one excised or if calculated as mg adrenal weight/100 g body weight. On the other hand, lesions in the region lateral to the paraventricular nucleus, lateral to the median eminence or in the region between these two loci prevented ACH in roughly 50% of the animals whether the lesion was placed on the same or opposite side of the hypothalamus. Some lesions in the mid-line in the vicinity of the paraventricular nucleus also resulted in blockade of ACH. We speculate that the blockade is due to a partial elimination of CRF and/or vasopressin/oxytocinergic pathways which are activated by the fall in plasma corticosterone after removal of an adrenal gland.

Adaptation, Physiological↗