Biomedical subjects

D Jezova

Publications and source records attributed to D Jezova.

48 records · Page 3Linked to original sources

PubMed1994

Activity of the hypothalamic pituitary adrenal axis and sympathoadrenal system during food and water deprivation in the rat.

It has been previously shown that chronic water deprivation or hypertonic saline intake, osmotic stress models with concomitant decrease in food intake, decrease hypothalamic CRH mRNA levels and ACTH responses to acute stimulation. To determine the contribution of food restriction to the effects of osmotic stimulation, the function of the hypothalamic pituitary adrenal axis was analyzed in rats subjected to food deprivation, water deprivation or their combination for 60 h. In all three groups, basal levels of plasma corticosterone were increased, while ACTH and catecholamines were unchanged. Basal plasma vasopressin levels were normal in food deprived rats, but significantly increased in water deprived and simultaneously food and water deprived rats. In contrast to the 25% reduction of plasma ACTH responses to 30 min immobilization by water deprivation, food deprivation had no inhibitory effect and prevented the decreased ACTH responsiveness caused by water deprivation. In control rats, plasma corticosterone levels increased 22.5-fold 30 min after immobilization, and this response was significantly potentiated in the water deprived, food deprived and combined food and water deprived groups. The elevation in plasma catecholamines in response to acute immobilization was also enhanced in both water deprived and food deprived rats. In situ hybridization studies showed a 35% increase in VP mRNA levels in the PVN after water deprivation, whereas food deprivation caused a slight decrease and prevented the stimulatory effect of water deprivation. CRH mRNA in the PVN was reduced by 27% after food deprivation and by 67% after water deprivation, but simultaneous food and water deprivation caused a significantly smaller reduction similar to that in food deprivation alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1993

Up-regulation of vasopressin mRNA in paraventricular hypophysiotrophic neurons after acute immobilization stress.

Cellular levels of vasopressin (VP) and corticotropin-releasing factor (CRF) mRNAs were determined in the rat hypothalamic paraventricular nucleus after acute immobilization stress. Messenger RNA levels were measured by in situ hybridization histochemistry using 35S-labeled synthetic DNA oligonucleotide probes and quantitative autoradiography. Analysis of histograms related to density values revealed that two hours after immobilization the average cellular VP and CRF mRNA levels were significantly increased (145 +/- 30.3 and 68 +/- 21.3%, respectively, above control values). Moreover, the number of VP-expressing parvicellular neurons was doubled in stressed rats relative to controls. These results indicate that single acute immobilization stress is sufficient to up-regulate VP as well as CRF mRNA production in the hypothalamic CRF-neurosecretory system.

Animals↗

PubMed1993

Stress-induced increase in vasopressin and corticotropin-releasing factor expression in hypophysiotrophic paraventricular neurons.

The concerted action of CRF and vasopressin (VP) plays a critical role in regulating ACTH release from anterior pituitary cells. In this study, we have explored the expression of these neurohormones in hypophysiotropic paraventricular neurons after repeated exposure of rats to immobilization stress. Cell by cell quantitative in situ hybridization was used to evaluate the steady state level of mRNAs coding for VP and CRF. We found that 16 daily stress exposures resulted in a significant increase in the average cellular level of CRF and VP mRNAs (150% and 200% of control levels, respectively). Moreover, in the repeatedly stressed group, the number of VP-expressing parvicellular neurons was approximately doubled relative to the control value. Using quantitative immunoelectron microscopy, VP- and CRF-immunoreactive sites were assessed in the dense core vesicle compartment of CRF axon terminals in the external zone of the median eminence. We found that after repeated stress, the immunolabeling of VP was augmented, while that of CRF was slightly decreased. Concurrently, we observed a significant increase in the proportion of CRF nerve terminals that were VP positive (from 50% in controls to 90% in stressed animals). We conclude that the observed changes in CRF neurons may represent a physiological response to increased functional demand and may lead to alterations in the composition of the ACTH-releasing signal.

Animals↗

PubMed1993

Hormonal changes with lower body negative pressure on the 6th day in microgravity in one cosmonaut.

We measured volume regulating and stress hormones (AVP, aldosterone, ANP, c-GMP, angiotensin II, PRA, epinephrine, norepinephrine, ACTH, cortisol) in venous blood twice during a lower body negative pressure (LBNP) maneuver in one cosmonaut (31 years, 75 kg, 180 cm) preflight (supine), inflight (6th d in orbit), and on the 4th d (supine) after a 10-d flight. Antecubital blood was taken at the beginning (3 min: "a") and after ceasing (2 min: "b") 40 min LBNP (-15/-30/-35 mm Hg for 15/15/10 min). At the beginning of LBNP, no big changes of resting hormone levels are to be expected. Comparison of "a" values: Inflight, there was a 4-5-fold increase in vasopressin and epinephrine, a slight increase in aldosterone, ANP, norepinephrine, cortisol and ACTH, and a decrease in PRA levels. Postflight, vasopressin was almost as much increased as inflight, and aldosterone and ANP levels were higher than pre- or inflight. PRA, epinephrine, norepinephrine, and cortisol were moderately increased, whereas ACTH and angiotensin II were diminished. Comparison of "b" to "a" values (2 min after LBNP to 3 min intra-LBNP): Preflight, ANP, PRA, and epinephrine rose more than 100%. The inflight response was higher for aldosterone but lower for all other volume active hormones. Postflight, the increase in PRA was pronounced, whereas little change occurred in other hormones. Cortisol and ACTH fell similarly during LBNP under all conditions. In summary, the data provide evidence that not only the endocrine status but also the neuroendocrine responsiveness to stimulation; i.e., the hormone response during cardiovascular load, are altered by the stay in microgravity and readaptation to normal conditions.

Adaptation, Physiological↗

PubMed1992

Repeated stress enhances vasopressin synthesis in corticotropin releasing factor neurons in the paraventricular nucleus.

The effect of repeated stress on corticotropin-releasing factor (CRF) and vasopressin (AVP) synthesis in parvocellular neurons of the paraventricular nucleus (PVN) was studied by means of double label immunocytochemistry. Once daily immobilization of male rats for 16 days leads to a 75% increase in the number of CRF immunoreactive neurons, but a 5-fold elevation in the number of AVP containing CRF cell bodies. These results demonstrate that repeated stress activates AVP synthesis in CRF neurons.

Animals↗

PubMed1992

Testing of neuroendocrine function in astronauts as related to fluid shifts.

We addressed the question of optimal conditions for neuroendocrine and cardiovascular testing in astronauts. We tested stress reactions during LBNP of < or = -50 mmHg. There was a mild transient elevation of plasma GH concentration and a nonsignificant rise of plasma ACTH, while PRL, insulin and glucose remained unchanged. Aldosterone was decreased 5 and 10 min after beginning of LBNP, thereafter rose significantly, and displayed further significant concentration increase 5 min post-LBNP. The endocrine and cardiovascular responses to submaximal exercise were tested at 8.00 am and 8.00 pm. Exercise-induced changes of heart rate and blood pressure remained unchanged with daytime whereas plasma concentrations of epinephrine, GH and PRL in response to work load were significantly higher in the evening than in the morning. As expected, basal resting values of plasma cortisol were significantly lower in the evening than in the morning but were similar one hour after cessation of exercise. Our findings demonstrate the importance of frequent sampling in case of transient physiological phenomena, and contribute to existing knowledge on circadian influences upon neuroendocrine stress responses.

Adult↗

PubMed1991

Repeated stress-induced activation of corticotropin-releasing factor neurons enhances vasopressin stores and colocalization with corticotropin-releasing factor in the median eminence of rats.

Stress-induced release of corticotropin-releasing factor (CRF) and vasopressin (AVP) was studied in rats by measuring the decline of CRF and AVP stores in the median eminence after blockade of fast axonal transport with colchicine (5 micrograms per rat intracisternally). Quantitative immunocytochemistry was used to detect changes in CRFi and AVPi in the external zone of the median eminence (ZEME) selectively. Immobilization stress induced a fast ACTH response to 1,000-2,000 pg/ml which was associated with a fall in both CRFi and AVPi of 34% during the first 30 min. This is followed by different time courses of further AVPi and CRFi depletion. In addition, we investigated the effect of repeated daily stress exposure on CRFi and AVPi in the ZEM 1 day after stress exposure. Repeated daily immobilization for 9 or 16 subsequent days did not affect the CRFi stores in the ZEME, but increased the AVPi stores to 161 +/- 13% and 218 +/- 11% respectively. Quantitative analysis of electron microphotographs of repeatedly handled rats showed a mean density of CRF positive profiles in the ZEME of 45.5 +/- 2.5 per 500 microns 2 of which 25% also stained for pro-AVP-derived peptides. After 9 subsequent days of immobilization the total density of CRF-positive profiles remained unchanged, but the fraction of CRF swellings that also stained for pro-AVP-derived peptides increased approximately 2-fold. We conclude that (1) the secretion of AVPi and CRFi from the ZEME are independently controlled, indicating differential activation of AVP containing and AVP deficient CRF neurons during acute immobilization, and (2) repeated stress leads to plastic changes in hypothalamic CRF neurons resulting in increased AVP stores and colocalization in CRF nerve terminals.

Adrenocorticotropic Hormone↗

PubMed1990

Epinephrine in rat hypophysial portal blood is derived mainly from the adrenal medulla.

This study was performed to determine if epinephrine (EPI) present in hypophysial portal blood has a peripheral or a central origin. Pituitary stalk and femoral arterial EPI plasma levels were simultaneously measured in rats anesthetized with thiopental or urethane. EPI was measured by two different methods: radioenzymatic assay or HPLC followed by electrochemical detection. In thiopental-anesthetized rats, levels were higher in hypophysial portal than in femoral arterial plasma with both methods. In urethane-anesthetized rats, no difference in EPI concentrations was found between peripheral and portal plasma. A rapid blood volume depletion (15 ml/kg in 3 min) evoked a marked elevation of pituitary stalk and arterial EPI plasma concentration while norepinephrine (NE) and dopamine (DA) levels were unaffected. Under both types of anesthesia, the increase of EPI levels was higher in peripheral than in portal plasma. After removal of the adrenal glands, EPI was undetectable or barely detectable in pituitary stalk and arterial plasma. The hemorrhage-induced stimulation of EPI secretion was blunted in portal and peripheral plasma of adrenalectomized rats. These findings indicate that: (1) hypophysial portal EPI plasma concentration is highly dependent on an adrenal source; (2) hypothalamic EPI is not released into portal circulation in response to acute hemorrhage, and (3) anesthesia markedly influences catecholamines plasma levels.

Adrenal Medulla↗

PubMed1989

Prior immobilization stress alters adrenal hormone responses to hemorrhage in rats.

The effect of prior immobilization stress (IMO) on the plasma epinephrine (EPI), norepinephrine (NE), adrenocorticotropic hormone (ACTH), and corticosterone (CS) responses to acute hemorrhage was studied in conscious male rats with chronic catheters in tail artery, using two combinations of IMO and hemorrhage. IMO per se led to significant increases of EPI, NE, ACTH, and CS in all animals. Hemorrhage of 25% of estimated blood volume (EBV) performed immediately after 150 min IMO caused exaggerated release of EPI and NE, whereas CS remained unchanged at the level previously elevated by IMO. ACTH response to initial blood loss of 12.5% was diminished in previously immobilized rats. Hemorrhage of 35% EBV after 60 min IMO and a 10-min recovery period also resulted in potentiated increases in EPI and NE, suppressed ACTH secretion, and no further change in stress-elevated CS concentration. No differences between groups were observed in relative mean arterial blood pressure, plasma protein, and lactate responses to 35% hemorrhage. Posthemorrhagic increase of plasma concentration of several tissue enzyme activities was significantly higher in prestressed rats. Furthermore, 24-h mortality rate increased by 49%. In summary, our results indicate that prior IMO potentiated activation of the sympathoadrenomedullary system and suppressed ACTH response to subsequent hemorrhage. Altered neuroendocrine responsiveness and stress-induced prehemorrhagic tissue damage may play roles in the increased susceptibility of the organism to blood loss.

Adrenocorticotropic Hormone↗

PubMed1988

Apomorphine injection stimulates beta-endorphin, adrenocorticotropin, and cortisol release in healthy man.

The effect of single injections of a dopaminergic agonist, apomorphine, on pituitary-adrenocortical function was investigated in healthy adult men by the measurement of plasma ACTH, beta-endorphin, cortisol and GH immunoreactivities. Single, subcutaneous injection of a subemetic dose of apomorphine (0.75 mg) resulted in a pronounced increase in plasma concentrations of GH, as well as ACTH, beta-endorphin, and cortisol, without induction of any serious adverse drug effects. These findings were confirmed in two separate experiments.

Adrenocorticotropic Hormone↗

PubMed1986

Plasma catecholamines do not participate in pituitary-adrenal activation by immobilization stress in rats with transection of nerve fibers to the median eminence.

The effect of immobilization stress was studied in rats in which the CRF and arginine vasopressin-containing innervation of the median eminence was destroyed by an anterolateral cut (ALC) around the medial basal hypothalamus. One week after surgery, the rats with ALC were subjected to immobilization and they showed a normal rise in plasma corticosterone, a smaller than normal rise of plasma ACTH, and an increased response of plasma epinephrine and norepinephrine. When in rats with an ALC the response of plasma catecholamines was prevented by guanethidine pretreatment and adrenal enucleation the small rise in plasma ACTH was unchanged during immobilization. In addition, the plasma corticosterone and ACTH rises during immobilization in the rats with ALC were not influenced by prior treatment with phentolamine (2.5 mg/kg ip) or propranolol (2.5 mg/kg ip). These findings suggest that the large rises in plasma epinephrine and norepinephrine levels during immobilization do not contribute to changes in plasma ACTH or corticosterone levels when hypothalamic regulation via CRF and/or arginine vasopressin is interrupted by ALC.

Adrenal Glands↗

PubMed1986

The patterns of endocrine response to surgical stress during different types of anesthesia and surgery in man.

The authors studied 123 patients undergoing minor (varicectomy) or major (cholecystectomy) surgery under diethyl ether, halothane, enflurane or hydroxydione anesthesia. The goal was to investigate the effects of emotional tension, anesthesia and surgical trauma, as well as glucose load, on the patterns of endocrine response under standardized clinical settings. The endocrine response (growth hormone, cortisol, insulin) was not modified significantly by emotional stress and the anesthetics used. Only prolactin was unique in that its release was markedly stimulated by halothane anesthesia. Neither the anesthetic drugs nor both types of surgical injury led to a constant hyperglycaemic response. Minor surgery failed to stimulate secretion of the studied hormones. However, major surgery stimulated growth hormone and cortisol secretion irrespective of the anesthetic used. Insulin secretion following glucose load was enhanced disproportionately. It is concluded that growth hormone level during surgical stress is determined by the extent and severity of surgical trauma, while neither anesthesia nor emotional tension exert any pronounced stimulative effect on its release. The observed changes in blood glucose levels and the lack of a proportionate insulin secretion are due to the effect of anesthesia rather than to that of surgery.

Adolescent↗