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Biomedical subjects

R Kvetnansky

Publications and source records attributed to R Kvetnansky.

At least 91 records · Page 5Linked to original sources

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↗

Neuroendocrine and immunologic effects of unemployment and job insecurity.

We prospectively followed a cohort of 354 blue-collar men and women, some of whom lost their jobs. Results show marked effects during the anticipatory and early unemployment phase on mental well-being, serum cortisol, prolactin, total cholesterol, HDL cholesterol, and phytohemagglutinin reactivity of lymphocytes. Most of these changes appear to be of short-term duration. However, changes in cardiovascular risk factors are observed at least 2 years following the loss of one's job. Coping style appears to be a major determinant whether or not and how people will react to unemployment.

Adaptation, Psychological↗

Prolactin response to immobilization stress and hemorrhage: the effect of hypothalamic deafferentations and posterior pituitary denervation.

The roles of posterior and anterolateral connections to the mediobasal hypothalamus (MBH) as well as innervation of the posterior pituitary in the PRL response to immobilization (IMO) and hemorrhage (HEM) were studied by means of surgical isolation, performed 6-9 days before stress exposure. Male rats bearing indwelling tail artery cannulae subjected to 120-min IMO reached peak PRL secretion in 5-20 min. HEM of 25% elicited a significant rise of PRL levels. A posterior cut in the MBH, performed without damaging the serotonergic fibers from the brain stem, attenuated the PRL response to 25% HEM, whereas the PRL elevation due to IMO remained unaffected. An anterolateral cut around the MBH eliminated both the IMO- and HEM-induced stimulation of PRL. Posterior lobe denervation reduced by about 27% the PRL response to IMO and eliminated the response to HEM. These results suggest the following conclusions. The neural structures located posteriorly to the MBH are involved in the transfer of signals triggering PRL secretion due to hypovolemia. Intact anterolateral pathways to the MBH and stalk-median eminence region are essential for the PRL-releasing activity under both stimuli. The posterior lobe may be an important link in the PRL stress response in male rats.

Animals↗

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↗

Plasma and urine catecholamine levels in cosmonauts during long-term stay on Space Station Salyut-7.

The activity of the sympathetic adrenal system in cosmonauts exposed to a stay in space lasting for about half a year has so far been studied only by measuring catecholamine levels in plasma and urine samples taken before space flight and after landing. The device "Plasma 01", specially designed for collecting and processing venous blood from subjects during space flight on board the station Salyut-7 rendered it possible for the first time to collect and freeze samples of blood from cosmonauts in the course of a long-term 237-day space flight. A physician-cosmonaut collected samples of blood and urine from two cosmonauts over the period of days 217-219 of their stay in space. The samples were transported to Earth frozen. As indicators of the sympathetic adrenal system activity, plasma and urine concentrations of epinephrine and norepinephrine as well as urine levels of the catecholamine metabolites metanephrine, normetanephrine, and vanillylmandelic acid were determined before, during and after space flight. On days 217-219 of space flight plasma epinephrine and norepinephrine levels were slightly increased, yet not substantially different from normal. During stress situations plasma norepinephrine and epinephrine levels usually exhibit a manifold increase. On days 217-219 of space flight norepinephrine and epinephrine levels in urine were comparable with pre-flight values and the levels of their metabolites were even significantly decreased. All the parameters studied, particularly plasma norepinephrine as well as urine norepinephrine, normetanephrine, and vanillylmandelic acid, reached the highest values 8 days after landing. The results obtained suggest that, in the period of days 217-219 of the cosmonauts stay in space in the state of weightlessness, the sympathetic adrenal system is either not activated at all or there is but a slight activation induced by specific activities of the cosmonauts, whereas in the process of re-adaptation after space flight on Earth this system is considerably more markedly activated.

Adrenal Glands↗

Opioid mu and delta and dopamine receptor number changes in rat striatum during stress.

The question whether acute and repeated immobilization stress is accompanied by changes in the number of opioid mu- and delta- -receptor and that of dopamine receptor in the rat corpus striatum was studied. The number of opioid mu- and delta-receptors as well as that of dopamine receptors was estimated in corpus striatum of rats subjected either to a single (acute) immobilization stress (IMO) for 150 min or to identical repeated stress exposure for 7 or 40 consecutive days. The number of mu-receptors was estimated by the use of 3H-dihydromorphine binding (an agonist) or 3H-naloxone binding (an antagonist). Increased number of mu-receptors was found after acute IMO as estimated from the binding of both mu-specific ligands. However, the binding of 3H-dihydromorphine showed no changes after 7x and elevated mu-receptor number after 40x repeated IMO, although the binding of 3H-naloxone after 7x and 40x IMO was decreased. This paradoxical pattern might be explained by different affinity of both ligands to mu-receptor subpopulations (i.e. mu1- and mu2-receptors). In addition, the number of delta-receptors (assayed by 3H-D-Ala2,D-Leu5-enkephalin binding) was increased after acute as well as repeated (7x and 40x) IMO. The changes of dopamine receptor number (as measured from 3H-spiroperidol saturation analysis) correlated well with delta-receptor changes after 1x and 7x repeated IMO, but not after 40x IMO, since in the latter group the number of dopamine receptors decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Sympathoadrenal activity facilitates beta-endorphin and alpha-MSH secretion but does not potentiate ACTH secretion during immobilization stress.

The potential involvement of the sympathoadrenal system in stress-induced secretion of peptides from the intermediate lobe of the pituitary gland and the activation of the pituitary-adrenal axis was studied. Male Wistar rats were subjected to control procedures, to sympathectomy by chronic administration (8 weeks) of guanethidine and/or to medullectomy by adrenal enucleation 9 weeks prior to exposure to forced immobilization stress for various periods of time. In intact or sham-operated rats, immobilization caused a prompt increase of circulating norepinephrine, epinephrine (EPI), corticosterone and of immunoreactive adrenocorticotropic hormone (ACTHi), alpha-melanocyte-stimulating hormone (alpha-MSHi) and beta-endorphin (beta-ENDi). Peak levels of pituitary hormones were found after 10 min of stress exposure, but fell to less than 30% of these levels after 2.5 h of immobilization. Adrenal medullectomy, which abolished the stress-induced release of EPI, reduced the acute increase of plasma alpha-MSHi and beta-ENDi, but did not influence the acute increase of plasma ACTHi during immobilization stress. Also in medullectomized plus sympathectomized rats, the initial stress response of circulating ACTHi was not different from that of controls. Adrenal medullectomy with or without additional sympathectomy caused a marked increase in plasma ACTHi concentrations after prolonged stress exposure. We conclude that: catecholamines originating from the adrenalmedulla facilitate the stress-induced secretion of intermediate lobe peptides (alpha-MSHi, beta-ENDi); catecholamines from the sympathoadrenomedullary system do not contribute to the acute release of ACTH during immobilization stress; the sympathoadrenomedullary system is involved in the secondary reduction of circulating ACTHi levels seen during prolonged stress.

Adrenal Medulla↗

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↗

Activity of the sympathetic-adrenomedullary system in rats after space flight on the Cosmos biosatellites.

The indicators of adrenomedullary activity (catecholamine content (CA) and the activity of the catecholamine-synthesizing enzymes tyrosine hydrozylase (TH) and dopamine-beta-hydrozylase (DBH) were measured in the adrenal glands of rats living in a state of weightlessness for 18.5-19.5 days on board the biosatellites COSMOS 936 and COSMOS 1129. None of these indicators was significantly changed by space flight, neither in the group living in a state of weightlessness nor in the group living in a centrifuge on board the spacecraft and exposed to artificial gravity of 1 g (COSMOS 936). Animals exposed after space flight to repeated immobilization stress on Earth showed a significant decrease of adrenal adrenaline and an appreciable increase in adrenal TH activity compared to stressed animals which were not in space. These results suggest that a prolonged state of weightlessness during space flight does not by itself represent an intensive stressful stimulus for the adrenomedullary system but potentiates the response of cosmonauts to stress after return to Earth.

Adrenal Medulla↗

Adrenaline, noradrenaline and dopamine levels in specific brain stem areas of acutely immobilized rats.

Catecholamines (adrenaline, noradrenaline and dopamine) have been measured in specific areas of the rat brain stem after acute immobilization stress. Adrenaline levels were significantly decreased after 240 min of immobilization in all areas studied: A1 area, nucleus commissuralis (NCO), A2 area, anterior part of the nucleus tractus solitarii (NTS), and the locus coeruleus. Noradrenaline concentrations in stressed rats were significantly reduced only in the NTS area. In contrast, during stress there were no significant changes in dopamine concentrations with respect to control values in any of the areas studied. These results implicate the participation of central adrenaline neurons, localized in specific brain stem areas, and noradrenaline neurons innervating the rostral part of the nucleus tractus solitarii, in the mechanism of central response to acute stress.

Animals↗

Sympatho-adrenal responses of spontaneously hypertensive rats to immobilization stress.

Blood pressure, heart rate, and circulating levels of norepinephrine, epinephrine, and corticosterone were measured before and during the first or seventh period of immobilization stress (150 min per day) in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive male rats. A catheter was inserted into the tail artery of each rat to permit direct measurement of blood pressure and heart rate and serial sampling of blood in conscious, unhandled animals. During the first immobilization, SHR rats had significantly higher circulating levels of norepinephrine, epinephrine, and corticosterone than did WKY rats. One day after the sixth immobilization, basal levels of norepinephrine and epinephrine were significantly higher and mean blood pressure was significantly lower in repeatedly stressed SHRs compared to unstressed SHRs. In addition, adaptation to the repeated stress in SHRs was attended by reduced adrenomedullary secretion and an increased blood pressure response. These results demonstrate that adaptive changes in the cardiovascular and sympatho-adrenal medullary systems of repeatedly immobilized rats are greater in SHR than in WKY rats.

Animals↗

Effect of handling and forced immobilization on rat plasma levels of epinephrine, norepinephrine, and dopamine-beta-hydroxylase.

Forced immobilization of rats triggers activation of adrenal-medullary discharge of epinephrine (EPI) and sympathetic neuronal release of norepinephrine (NE). Plasma levels of EPI reach peak values, which are about 40-fold greater than in undisturbed rats, at about 20 min and then decline to about one-third the peak levels. Plasma levels of NE are increased about 6-fold throughout the immobilization interval. Decapitation produces an 80-fold increase in plasma levels of EPI and an 8-fold increase in NE. These striking decapitation-induced increases are potentiated about 3-fold by immobilization, presumably as a consequence of an immobilization-induced alteration in the "set" of responsivity of spinal cord mechanisms controlling sympathoadrenal medullary discharge. Even minor disturbances produce highly significant increases in plasma EPI and NE and special precautions must be observed when studies involving plasma catecholamines or their effects are performed in animals.

Animals↗