Biomedical subjects

C Ariznavarreta

Publications and source records attributed to C Ariznavarreta.

10 recordsLinked to original sources

PubMed1991

Stress induced changes in testis function.

The mechanism through which chronic stress inhibits the hypothalamic-pituitary-testicular axis has been investigated. Chronic restraint stress decreases testosterone secretion, an effect that is associated with a decrease in plasma gonadotropin levels. In chronically stressed rats there was a decrease in hypothalamic luteinizing hormone-releasing hormone (LHRH) content and the response on plasma gonadotropins to LHRH administration was enhanced. Thus the inhibitory effect of chronic stress on plasma LH and FSH levels seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a modification in LHRH secretion. It has been suggested that beta-endorphin might interfere with hypothalamic LHRH secretion during stress. Chronic immobilization did not modify hypothalamic beta-endorphin, while an increase in pituitary beta-endorphin secretion was observed. Since we cannot exclude that changes in beta-endorphin secreted by the pituitary or other opioids may play some role in the stress-induced decrease in LHRH secretion, the effect of naltrexone administration on plasma gonadotropin was studied in chronically stressed rats. Naltrexone treatment did not modify the decrease in plasma concentrations of LH or FSH. These findings suggest that the inhibitory effect of restraint on the testicular axis is exerted at hypothalamic level by some mechanism other than opioids.

Adrenal Glands↗

PubMed1991

Naltrexone does not reverse the inhibitory effect of chronic restraint on gonadotropin secretion in the intact male rat.

There is considerable evidence suggesting that endogenous opioids may play an important role in acute stress-induced decreases in luteinizing hormone (LH) release. Studies were undertaken to analyze the role of endogenous opioids in chronic stress-induced decrease in circulating LH and follicle-stimulating hormone (FSH). Chronic restraint (6 h daily over 4 days) evoked a decrease in circulating LH and FSH. Naltrexone treatment, (2 mg/kg three times daily) during the 4 days of restraint, caused an increase in plasma concentrations of LH and FSH, and antagonized the LH suppressory effect of morphine (10 mg/kg) administration. Despite this, naltrexone treatment was ineffective in preventing the inhibitory effect of chronic restraint stress on circulating LH and FSH. Chronic restraint also induced a decrease in hypothalamic LH-releasing hormone (LHRH) content in saline-treated rats. On the contrary, in naltrexone-treated rats, chronic restraint evoked an increase in hypothalamic LHRH content. Thus endogenous opioids and chronic stress seem to act by different mechanisms on the hypothalamic LHRH neuron. In unstressed orchidectomized rats, naltrexone administration did not modify circulating LH, but increased plasma concentrations of LH in acutely restrained rats. These data suggest that endogenous opioids may mediate gonadotropin secretion during acute stress, but not during chronic stress.

Animals↗

PubMed1991

Influence of chronic restraint stress on pro-opiomelanocortin mRNA and beta-endorphin in the rat hypothalamus.

It has been postulated that some endocrine responses to stressful stimuli are mediated through the activation of hypothalamic pro-opiomelanocortin (POMC)-derived peptides. The aim of the present study was to analyse the effect of chronic stress on expression of the POMC gene in the medial basal hypothalamus and pituitary, and on serum concentrations of LH, beta-endorphin and corticosterone. Adult male rats were killed after being subjected to restraint stress for 6 h/day over 2, 3 or 4 days. Chronic restraint induced an increase in serum concentrations of beta-endorphin and corticosterone and a decrease in serum LH levels. To determine whether chronic stress induced any change in POMC synthesis, a dot-blot method was used to measure POMC mRNA levels. No significant changes were detected either in the beta-endorphin content or in POMC mRNA levels in the medial basal hypothalamus after 2, 3 or 4 days of chronic restraint. This observation contrasts with the stimulation of POMC mRNA levels in both lobes of the pituitary. The data suggest that although chronic restraint induces an increase in POMC synthesis and secretion in the pituitary and a decrease in LH secretion, it has no effect on hypothalamic POMC neurones.

Animals↗

PubMed1990

Role of LHRH in the gonadotrophin response to restraint stress in intact male rats.

A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20-45 min of stress there was an increase in plasma concentrations of LH (P less than 0.01) and a decrease in hypothalamic LHRH content (P less than 0.01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion.

Animals↗

PubMed1989

Role of the adrenal cortex in chronic stress-induced inhibition of prolactin secretion in male rats.

The response of prolactin to chronic stress in intact, adrenalectomized and adrenomedullectomized male rats was studied. Immobilization stress in intact animals induced a significant increase in plasma concentrations of prolactin after 20 and 45 min and a significant decrease when the rats were submitted to chronic restraint (6 h daily for 4 days). Five weeks after adrenomedullectomy, plasma prolactin and corticosterone responses to chronic stress were not modified. In contrast, the inhibitory effect of chronic stress on prolactin secretion was totally suppressed by adrenalectomy. When treated with dexamethasone during the 4 days of restraint, adrenalectomized stressed rats showed similar plasma concentrations of prolactin to the intact stressed rats. These data indicate that the adrenal cortex is able to play an inhibitory role on prolactin secretion during stress only through a prolonged release of glucocorticoids.

Adrenal Cortex↗

PubMed1989

Effect of adrenomedullectomy and propranolol treatment on the response of gonadotrophins to chronic stress in male rats.

In order to study the involvement of the adrenal medulla in stress-induced inhibition of gonadotrophin secretion, we measured plasma concentrations of LH, FSH and corticosterone in adult male rats subjected to chronic restraint after surgical ablation of the adrenal medulla. In intact animals, chronic restraint (6 h daily over 4 days) induced a significant (P less than 0.05) decrease in plasma concentrations of LH, whereas plasma concentrations of corticosterone showed the expected significant (P less than 0.01) increase. Adrenomedullectomy did not significantly modify basal plasma concentrations of LH or corticosterone. In these rats, there was no significant decrease of LH after stress, while the increase in corticosterone was as significant as in sham-operated animals (P less than 0.01). In order to confirm the role of adrenomedullary catecholamines in stress-induced gonadotrophin inhibition another group of rats was treated s.c. with the beta-adrenergic blocker propranolol (2 mg/kg twice daily). These rats showed an attenuated inhibition of LH during stress similar to that observed in adrenomedullectomized rats. Levels of FSH were significantly reduced after stress in the saline-treated group, while there were no differences between stressed or unstressed rats in the propranolol-treated group. These results may be considered as evidence that medullary catecholamines, acting through beta-receptors, are factors involved in gonadotrophin inhibition during chronic stress.

Adrenal Medulla↗

PubMed1989

[Response of plasma and retinal somatostatin to insulin-induced hypoglycemia in diabetic and control rats].

Changes in plasmatic levels and retinal content of somatostatin after insulin-induced hypoglycemia were investigated in three different groups of animals: Control group (C), Diabetic untreated group (D); and, Insulin-treated diabetic group (DI). In addition, another group of animals, not submitted to hypoglycemia, was used as control reference of retinal prehypoglycemic content of somatostatin (group B). Plasmatic basal levels of somatostatin were slightly higher in group DI, and significantly higher in group C, whereas they did not show any differences in group D and DI after hypoglycemia, being significantly higher in group C. The somatostatin retinal content is similar in animals not subjected to hypoglycemia and in the C and DI groups after hypoglycemia, where the rats of the D groups showed significantly higher values than the remainder of the experimental groups, an effect that is also evident in nontreated diabetic animals, even if they are not subjected to hypoglycemia, Summing up, the plasmatic somatostatin response to insulin-induced hypoglycemia is impaired in diabetic rats. Retinal somatostatin content is unchanged after hypoglycemia.

Animals↗

PubMed1987

Gonadotropin inhibition during chronic stress: role of the adrenal gland.

The effect of adrenalectomy, metyrapone and dexamethasone treatments on gonadotropin response to chronic stress were studied. Adult male rats were submitted to chronic restraint (6 h daily over 4 days). At the end of the last stress period animals were decapitated and trunk blood was collected. Chronic restraint evoked a decrease in plasma LH and to a lesser degree in plasma FSH in the intact rat. Adrenalectomy did not prevent the LH reduction induced by stress and magnified the inhibitory effect of restraint on FSH secretion. Administration of the corticosterone synthesis blocker metyrapone increased the inhibitory effect of restraint on plasma LH and to a lesser degree on plasma FSH. Dexamethasone treatment did not significantly modify plasma gonadotropin levels in adrenalectomized unstressed rats, but this treatment totally blocked plasma LH and FSH reduction after chronic restraint. These results indicate that plasma LH and FSH reduction during chronic restraint is not due to the increase in glucocorticoid secretion, but seems to be mediated by the increase of the hypothalamic-pituitary components of the adrenal axis.

Adrenal Glands↗

PubMed1987

Influence of streptozotocin-induced diabetes on the concentration of immunoreactive somatostatin in the retina and peripheral blood of the rat: effect of insulin treatment.

Changes in somatostatin-like immunoreactivity (SLI) were examined in the retina and peripheral blood of diabetic rats treated with streptozotocin (STZ) and insulin. There was no change in retinal SLI content at 4 and 11 days after administration of STZ but, thereafter, SLI increased progressively in the diabetic animals by 220% at 18 days and 300% at 27 days. Plasma SLI levels increased by 500% at 11 days and maintained similar levels thereafter. Diabetic animals treated with insulin (3-5 i.u. daily) for 27 days showed a significant (P less than 0.01) decrease of retinal and plasma SLI levels compared with untreated diabetic animals. It is concluded that there is a significant increase of retinal and plasma SLI levels in diabetic rats which tends to normalize after several days of insulin treatment.

Animals↗

PubMed1987

Gastric mucosal somatostatin-like immunoreactivity in peptic ulcer.

Somatostatin (SS) has been reported to exert potent inhibitory effects on gastric acid, pepsin and gastrin secretion. Although still controversial, the results of several studies have shown a possible influence of a local decrease in gastric somatostatin in the physiopathologic characteristics of peptic ulcer disease. In the present study, immunoreactive SS content (SLI) of antral (SLI-a), corpal (SLI-c) and fundic (SLI-f) mucosal extracts was measured by radioimmunoassay (RIA) in control patients (C) and in those patients with duodenal ulcer (DU) or gastric ulcer (GU) to further study a possible role of SS in peptic ulcer disease. Fifty-five patients (C = 20, DU = 21 and GU = 14) were included in the study. Gastric mucosal samples were obtained either by endoscopic biopsy (4.6 +/- 0.2 milligrams of weight) or operation (52.3 +/- 3.8 milligrams of weight). RIA was performed after a modified Arimura's method and results were expressed as nanograms per milligram of tissue plus or minus standard error of the mean. Chromatographic analysis of gastric mucosal extracts was performed on a Sephadex G-25 fine column. A great interindividual variation in SLI levels was observed (a range of 0.02 to 5.30 nanograms per milligram of weight). The mean SLI concentrations were: C (SLI-a, 2.55 +/- 0.45, SLI-c, 0.99 +/- 0.46 and SLI-f, 1.03 +/- 0.21); DU (SLI-a, 0.48 +/- 0.16, SLI-c, 0.43 +/- 0.13, and SLI-f, 0.58 +/- 0.12), and GU (SLI-a, 1.10 +/- 0.25, SLI-c, 0.40 +/- 0.10, and SLI-f, 0.81 +/- 0.24). Significantly greater amounts of SLI contents were found in the antrum of control patients as compared with those found in the corpus or fundus (p less than 0.05 and p less than 0.01, respectively). SLI-a levels were lower in peptic ulcer patients (DU, p less than 0.001 and GU, p less than 0.05) than in control patients. There was also a significant difference between SLI-a levels in DU versus GU patients (p less than 0.05). No significant differences were found in SLI-c and SLI-f contents in all three groups studied. In conclusion, these results suggest that decreased SS levels in antral gastric mucosa could be the alteration underlying the various physiopathologic mechanisms involved in the development of peptic ulcer disease.

Adult↗