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Biomedical subjects

R Kvetnansky

Publications and source records attributed to R Kvetnansky.

At least 55 records · Page 3Linked to original sources

Effect of microgravity on plasma catecholamine responses to stressors during space flight.

The effect of microgravity on the sympathicoadrenal system (SAS) activity in humans and animals has not yet been clarified. Our previous studies suggested that the SAS activity, evaluated by circulating and/or urinary catecholamine (CA) levels in astronauts during space flights, was found to be rather unchanged. However, CA levels were measured in astronauts only at rest conditions. The aim of the present study was to investigate effect of microgravity during space flight and post-flight readaptation on responsiveness of the SAS to somatic and psychic stressors evaluated by levels of catecholamines and their metabolite in the blood of the Slovak cosmonaut during his stay on board the space station Mir.

Adaptation, Physiological↗

Plasma hormone levels in human subject during stress loads in microgravity and at readaptation to Earth's gravity.

In great part of the investigations of endocrine system functions in astronauts during space flights the plasma levels of hormones and metabolites were determined only in resting conditions, usually from one blood sample collection. Such levels reflected the psychical and physical state and new hormonal homeostasis of organism at the time of blood collection, however, the functional capacity of neuroendocrine system to respond to various stress stimuli during space flight remained unknown. The aim of present investigations was to study dynamic changes of hormone levels during the stress and metabolic loads (insulin induced hypoglycemia, physical exercise and oral glucose tolerance test) at the exposure of human subject to microgravity on the space station MIR. The responses of sympatico-adrenomedullary system to these stress and workloads were presented by Kvetnansky et al.

Adaptation, Physiological↗

Increased expression of the Na(+)/Ca(2+) exchanger in the rat heart after immobilization stress is not induced by cortisol.

Calcium homeostasis is crucial for the proper function of cardiac cells. Since the Na(+)/Ca(2+) exchanger is an important modulator of calcium homeostasis especially in the heart, the objective of this study was to investigate the effect of immobilization stress on the high capacity Na(+)/Ca(2+) exchanger in rat heart ventricles and atria. Repeated immobilization stress increased both the mRNA and the protein level and the activity of the Na(+)/Ca(2+) exchanger in the left, but not the right ventricle of rat heart. Since corticosterone is rapidly increased during the stress stimulus, it might be assumed that mRNA of the Na(+)/Ca(2+) exchanger is increased through a glucocorticoid responsive element. However, we have found that cortisol did not change the Na(+)/Ca(2+) exchanger at the mRNA or protein levels. These results clearly show that this effect of stress is not mediated via cortisol.

Animals↗

Malondialdehyde, lipofuscin and activity of antioxidant enzymes during physical exercise in patients with essential hypertension.

DESIGN: To clarify the role of oxidative damage in essential hypertension, levels of lipid peroxidation products (malondialdehyde and lipofuscin) and activity of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) were examined during a short period of physical exercise. PATIENTS AND METHODS: We studied 11 male patients with mild to moderate essential hypertension in World Health Organization classes I or II and 10 healthy male controls. Physical exercise was performed on a bicycle ergometer at graded intensities of 1.0, 1.5 and 2.0 W/kg body weight Plasma concentrations of lipofuscin, malondialdehyde, epinephrine, norepinephrine, insulin, free fatty acids and glucose were determined. Superoxide dismutase activity was analysed in erythrocytes and glutathione peroxidase activity in whole blood. RESULTS: Concentrations of lipofuscin and malondialdehyde were significantly elevated in hypertensive patients. Superoxide dismutase activity was not different between groups, while glutathione peroxidase activity was significantly decreased in hypertensive subjects. During exercise, the concentration of malondialdehyde and antioxidant enzyme activities increased significantly in both groups. No differences were found in absolute increases between the normotensive and hypertensive subjects. The levels of glucose, insulin and free fatty acids were similar in both groups. Basal concentrations of catecholamines and also the exercise-induced increases were lower in hypertensive patients. CONCLUSIONS: Our results indicate increased oxidative damage in patients with essential hypertension, which might be caused by a decrease in the activity of glutathione peroxidase. The ability of superoxide dismutase and glutathione peroxidase to respond to increased production of reactive oxygen species during a short period of physical exercise was not impaired in hypertensive subjects.

Adult↗

Changes in plasma catecholamine and corticosterone levels and gene expression of key enzymes of catecholamine biosynthesis in partially hepatectomized rats.

OBJECTIVE: To reexamine the possible role of catecholamines and corticosterone in the early period of liver regeneration after partial hepatectomy (PH)in conscious cannulated rats under carefully controlled conditions which would allow to obtain reliable information about sympathetic-adrenomedullary function after PH in the rat in vivo. METHODS: Plasma levels catecholamines (epinephrine - EPI, norepinephrine - NE) were estimated by radioenzymatic assay and these of corticosterone by competitive protein binding assay. The total RNA was isolated from the adrenals and tyrosine hydroxylase (TH) mRNA expression was estimated by hybridisation with cDNA after Northern blot. The level of immunoreactive protein was measured by using a monoclonal antibody to rat TH, visualized by Western light chemiluminescent detection system and analyzed by densitometry. The level of TH in adrenals was estimated with the aid of 3H-tyrosine and TH cofactor DL-6-methyl-5,6,7,8-tetrahydropterine and the formed radioactive water was measured by scintillation spectometry. RESULTS: The plasma level of norepinephrine (NE), epinephrine (EPI) and corticosterone rapidly increased 20 min. after PH or sham operation (laparotomy). Although the increase of plasma NE was about the same after both PH and laparotomy, that of EPI and corticosterone in PH rats was significantly higher as compared to the laparotomy. One hour after the surgery plasma NE levels in both groups decreased to the basal value and remained still unchanged 4 and 24 h later. At the interval of 4h the plasma level of EPI was higher than in laparotomized controls, but after 24 h the EPI levels returned to basal values. Adrenal tyrosine hydroxylase (TH) mRNA level was significantly elevated in both PH and laparotomized rats, however 24 h after the surgery they returned to the baseline. Adrenal TH immunoprotein levels and TH activity were significantly elevated in both groups 4 h after the surgery, while 24 h later they returned to the baseline in laparotomized rats bur remained elevated in PH rats. Adrenal phenylethanolamine N-methyl-transferase (PNMT) mRNA levels were increased 4 h after both the PH and laparotomy and declined within 24 h. CONCLUSIONS: The first peak of catecholamine and corticosterone levels might result from unspecific stressor associated with the surgery. These levels could be accompanied with the mechanism of the rat liver regeneration. Prolonged elevations of EPI found after PH seems to be specific for liver regeneration indicating that the rise in the adrenal TH mRNA appears to be translated into immunoreactive protein which further leads to the elevation of TH activity. These results contrast markedly with previous studies indicating that the regeneration is modulated predominantly by norepinephrine.

Anesthesia↗

Expression of cardiac renin and its modulation by stress in normotensive and hypertensive rats.

Renin is the rate-limiting step in angiotensin II production. Existence of the cardiac renin is still ambiguous in healthy animals, although there is evidence that under some pathological conditions the heart might express mRNA for renin. Therefore, the aim of the present study was to (i) detect the renin gene expression in the whole rat heart, ventricles, atria and in isolated and purified myocytes, (ii) determine the effect of stress on renin mRNA and protein levels, and (iii) compare the response of renin gene expression to stress in normotensive and spontaneously hypertensive rats. Renin mRNA was determined by reverse transcription and polymerase chain reaction and quantified relatively to beta-actin and glyceraldehyde-3-phosphate dehydrogenase. Protein message was detected by monoclonal antibody against renin. Renin mRNA was found in all parts of the heart and in myocytes. Renin protein was found in the heart ventricles and atria, but not in cardiomyocytes. Immobilization stress affected renin on both, the mRNA and the protein level. The effect of stress was observed in the hearts of normotensive, but not in genetically hypertensive rats. Thus, renin might be involved in the development of the pathophysiological state in rat heart.

Animals↗

Endocrine status and LBNP-induced hormone changes during a 438-day spaceflight: a case study.

We investigated basal levels and lower body negative pressure (LBNP)-induced changes of volume regulating (PRA, aldosterone, AVP, ANP99-126) and other stress-sensitive hormones (catecholamines, cortisol, ACTH) in venous plasma from one cosmonaut before (-45 d), during (3, 170, 287, 430 d) and after (+4, +90 d) a record-breaking long-term (438 d) spaceflight. Blood was taken at the beginning and immediately after ending LBNP (-15/-30/-35 mm Hg for 15/15/10 min, respectively) preflight supine, inflight, and postflight supine. PRA, aldosterone, and vasopressin levels stayed within normal boundaries during the entire flight and after landing. Catecholamines exceeded reference limits (epinephrine > 140 pg x ml(-1), norepinephrine >1000 pg x ml(-1) 5 and 9 mo inflight, and 4 d postflight. ANP and cGMP were lower inflight (p<0.04) than pre- or postflight. Cortisol and ACTH were not consistently altered. LBNP-induced hormonal changes were not different (p>0.05) in microgravity and 1-G. Based on data from one cosmonaut, we conclude that long-term spaceflight up to 430 d duration appeared to lower plasma ANP and cGMP during flight and occasionally elevate catecholamine levels, without significantly altering LBNP-induced relative hormone changes as compared with those observed on the ground.

Adaptation, Physiological↗

Heterogeneous neurochemical responses to different stressors: a test of Selye's doctrine of nonspecificity.

Selye defined stress as the nonspecific response of the body to any demand. Stressors elicit both pituitary-adrenocortical and sympathoadrenomedullary responses. One can test Selye's concept by comparing magnitudes of responses at different stress intensities and assuming that the magnitudes vary with stress intensity, with the prediction that, at different stress intensities, ratios of increments neuroendocrine responses should be the same. We measured arterial plasma ACTH, norepinephrine, and epinephrine in conscious rats after hemorrhage, intravenous insulin, subctaneous formaldehyde solution, cold, or immobilization. Relative to ACTH increments, cold evoked large norepinephrine responses, insulin large epinephrine responses, and hemorrhage small norepinephrine and epinephrine responses, whereas immobilization elicited large increases in levels of all three compounds. The ACTH response to 25% hemorrhage exceeded five times that to 10%, and the epinephrine response to 25% hemorrhage was two times that to 10%. The ACTH response to 4% formaldehyde solution was two times that to 1%, and the epinephrine response to 4% formaldehyde solution exceeded four times that to 1%. These results are inconsistent with Selye's doctrine of nonspecificity and the existence of a unitary "stress syndrome," and they are more consistent with the concept that each stressor has its own central neurochemical and peripheral neuroendocrine "signature."

Adrenocorticotropic Hormone↗

Glucocorticoids elevate GTP cyclohydrolase I mRNA levels in vivo and in PC12 cells.

GTP cyclohydrolase I (GTPCH) is the rate-limiting enzyme in the formation of tetrahydrobiopterin, the cofactor for catecholamine, indolamine and nitric oxide biosynthesis. The effect of glucocorticoids on GTPCH gene expression was examined by direct infusion of cortisol to rats and by incubation of PC12 cells with glucocorticoids. Northern blot analysis revealed that infusion of cortisol for 1 or 7 days elevated levels of the 3.6 kb GTPCH mRNA species in rat adrenal medulla, while the 1.2 kb mRNA species were only increased by 1 day cortisol. Cortisol administration to hypophysectomized animals elicited a 4-5-fold elevation in both forms of GTPCH mRNA. These results indicate that glucocorticoids may be directly involved in the regulation of adrenomedullary GTPCH mRNA levels by physiological stress. Incubation of PC12 cells with plasma from immobilized, but not control, animals increased the level of the 3.6 kb mRNA. Treatment of PC12 cells with dexamethasone for 12-48 h elicited a 4-6-fold elevation in both GTPCH mRNAs. Using the nuclear run-on assay, increased transcription of the GTPCH gene was observed in the rat adrenal medulla with immobilization stress, or in PC12 cells treated with dexamethasone. This is the first report that glucocorticoids can alter GTPCH expression.

Adrenal Medulla↗

Immobilization Stress Elevates GTP Cyclohydrolase I mRNA Levels in Rat Adrenals Predominantly by Hormonally Mediated Mechanisms.

GTP cyclohydrolase I (GTPCH) is the rate-limiting enzyme in the biosynthesis of tetrahydrobiopterin, the cofactor for catecholamine, indolamine and nitric oxide biosynthesis. In this study we examined the effect of immobilization stress on GTPCH mRNA levels and the mechanism(s) of stress-induced changes in adrenomedullary GTPCH mRNA levels. We used reverse-polymerase chain reaction to isolate and clone a cDNA corresponding to nucleotides 269 to 570 of rat GTPCH. Northern blot analysis with a cRNA probe revealed two species of GTPCH mRNA (about 3.6 and 1.2 kb) in rat adrenal medulla and cortex, and in PC12 cells. The levels of both forms of GTPCH mRNA were significantly increased 3-5 fold in adrenal medulla by a single 2 hour immobilization and by repeated immobilizations (2 hours a day for 2 days). Hypophysectomy had little effect on their basal levels but prevented the stress elicited rise in both GTPCH mRNAs. In contrast, unilateral transection of the splanchnic nerve did not affect induction of the 3.6 kb GTPCH mRNA by stress. Combined denervation with hypophysectomy completely blocked the induction of both GTPCH mRNA species by immobilization stress. Thus, stress elicits elevation of both forms of GTPCH mRNA by a mechanism requiring an intact pituitary-adrenocortical axis.

Journal Article↗

Glucoprivation by insulin leads to trans-synaptic increase in rat adrenal tyrosine hydroxylase mRNA levels.

Effects of single or repeated insulin or 2-deoxy-D-glucose administration on adrenal tyrosine hydroxylase mRNA and protein levels were examined in rats. Insulin produced hypoglycemia and an elevation in plasma epinephrine and norepinephrine levels. A significant increase (3-5-fold) in tyrosine hydroxylase mRNA levels was found at 5 h, decreasing to near basal levels at 24 h following the first and also the sixth consecutive injection of insulin or 2-deoxy-D-glucose. Whereas insulin treatment raised tyrosine hydroxylase mRNA levels in intact adrenals, no increase in tyrosine hydroxylase mRNA levels occurred following adrenal denervation by splanchnic nerve transection. Western blot analysis showed that although a single insulin treatment did not affect tyrosine hydroxylase protein levels, a significant increase was observed following the seventh administration. This study shows that insulin-induced hypoglycemia increases tyrosine hydroxylase gene expression and that this process is regulated by a central mechanism via the splanchnic nerve.

Adrenal Medulla↗

Interrelations between sympathoadrenal system and hypothalamo-pituitary-adrenocortical/thyroid systems in rats exposed to cold stress.

The interrelations between sympathoadrenal (SA) system and hypothalamo-pituitary-adrenocortical (HPA) or hypothalamo-pituitary-thyroid (HPT) system during cold stress were examined by measuring plasma levels of dihydroxyphenylalanine (DOPA), catecholamine and their metabolites in adrenalectomized (ADX) and thyroidectomized (TX) rats exposed to cold stress (-3 degrees C). Plasma levels of adrenocorticotropic hormone (ACTH), corticosterone (CORT), thyroid-stimulating hormone (TSH) and thyroid hormones in cold-stressed rats were measured also. Plasma ACTH levels were increased transiently after 1 h of cold exposure, after which the circadian rhythm and plasma levels of ACTH were similar to those of normal rats. Plasma CORT levels were also elevated after 1 h of cold exposure; the increased levels of CORT tended to return to normal levels after 9 h of cold, but remained higher than those of normal rats during at least 24 h of cold exposure. Plasma ACTH levels of 5 day cold-stressed rats were no longer elevated above those of control rats and plasma CORT levels were only slightly higher than in control animals. However, plasma levels of TSH and free thyroid hormones were elevated after 1 day and remained elevated after 5 days of cold exposure. Thus, cold stress appears to activate chronically the HPT system, but only transiently activates the HPA system. ADX rats had higher basal plasma levels of dihydroxyphenylglycol (DHPG), methoxyhydroxyphenylglycol (MHPG), DOPA and homovanillic acid (HVA) than those of sham-operated (SHAM) rats, but norepinephrine (NE) levels were not significantly greater than in SHAM animals. TX rats had higher basal plasma levels of NE, epinephrine (EPI) and dopamine (DA), as well as much higher plasma levels of the metabolites. Exposure to cold increased plasma NE levels in both ADX and TX rats, but the increments in TX rats were much greater than in SHAM and ADX groups. Plasma EPI levels were not significantly elevated during cold exposure in SHAM rats, but were highly elevated in TX rats exposed to cold. TX rats had much larger increments in plasma levels of DHPG, MHPG, DA, dihydroxyphenylacetic acid (DOPAC) and HVA during cold exposure than those of SHAM and ADX rats. These results are consistent with the view that endogenous glucocorticoids restrain responses of catecholamine synthesis, release, reuptake, and metabolism in sympathetic nervous system of cold-stressed animals, but that in the absence of an effective HPT system, there is enhanced sympathoadrenal medullary function and augmentation of their responses to cold as a means for maintaining body temperature when the HPT thermogenesis system is impaired.

Adrenal Glands↗

Effects of continuous and intermittent cold (SART) stress on sympathoadrenal system activity in rats.

We compared sympathoadrenal responses to intermittent cold (SART) stress (in which cold exposure is interrupted by 4-hourly intervals daily at room temperature) with those to continuous cold (-3 degrees C) stress. Plasma levels of dihydroxyphenylalanine (DOPA), catecholamines and their metabolites as well as tyrosine hydroxylase (TH) activities in sympathetically innervated tissues were examined in rats exposed to each stressor for 1 day or for 5 days. Neither SART nor continuous exposure to cold for 1 day or 5 days altered plasma epinephrine (EPI) levels. However, norepinephrine (NE) and dihydroxyphenylglycol (DHPG) levels increased markedly during exposure to these stressors. On the first day of SART or continuous cold stress, NE levels were increased similarly, but the increments in DHPG levels were greater during SART stress. Since DHPG is formed in neurons, neural reuptake of NE may be more enhanced on the first day of SART stress than on the first day of continuous cold stress. After 5 days of SART stress plasma NE levels were significantly higher than those found after 5 days of continuous cold exposure. Plasma levels of DHPG were elevated to the same extent in both 5 days SART- and continuously cold-stressed rats, whereas plasma levels of methoxyhydroxyphenylglycol (MHPG) increased only by 5 days SART stress. Even at 1 h after the removal from 5 days SART stress, increased plasma levels of NE, DHPG and MHPG were still evident. These results suggest that 5 days SART stress elevates extraneuronal O-methylation of DHPG, and that NE turnover is more greatly increased by SART stress than by continuous cold stress. Plasma levels of DOPA, dopamine, dihydroxyphenylacetic acid and homovanillic acid also increased after either SART or continuous cold stress for 1 day and 5 days. Adrenal TH activities were significantly increased in rats exposed to SART or continuous cold stress for 1 day and 5 days, but in brown fat TH activity was elevated only in rats exposed to 5 days of continuous cold. Both SART and continuous cold stress are selective and potent stimuli for activation of the sympathoneural system, apparently without significant adrenomedullary EPI release. The increase of TH activity in the brown fat pad as well as of plasma NE and its metabolites is probably a result of adaptation to cold. It appears that even short intervals of return to a normal environmental temperature, as in SART, are sufficient to diminish sympathetic adaptation to cold.

3-Methoxy-4-hydroxyphenylethanol↗

Immobilization stress elevates gene expression for catecholamine biosynthetic enzymes and some neuropeptides in rat sympathetic ganglia: effects of adrenocorticotropin and glucocorticoids.

Sympathetic ganglia are the major contributors to the stress-elicited rise in circulating norepinephrine, enkephalins, and neuropeptide Y. Here we examined the effect of immobilization stress and treatment with ACTH and glucocorticoids on messenger RNA (mRNA) levels for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (DBH), preproneuropeptide Y (pre-NPY), and proenkephalin in rat superior cervical ganglia (SCG) and in stellate ganglia. Our results show a severalfold increase in the relative abundance of TH and NPY mRNAs in response to a single immobilization. Repeated stress elevated expression of all the genes studied and increased TH immunoreactivity in both ganglia. The effect of stress was more pronounced in SCG. Prolonged cortisol administration failed to alter the mRNA levels of TH, DBH, and NPY in control animals but attenuated the response to stress. In contrast, TH and DBH mRNA levels in the SCG, but not in adrenal medulla, were elevated by ACTH administration, similar to the levels attained after immobilization. The results revealed that the regulation of gene expression in response to immobilization stress in sympathetic neurons differs from the regulation in adrenal medulla. The study implicates hormonal involvement in the stress-induced changes in TH, DBH, NPY, and proenkephalin gene expression in sympathetic ganglia.

Adrenocorticotropic Hormone↗

Effects of space flight on endocrine system function in experimental animals.

The effects exposing rats to space flights of various lengths in a series of COSMOS satellites are reported based on an evaluation of plasma hormone levels and several enzyme activities in the tissues. The results after space flights are compared with those obtained from rats exposed to acute or repeated stress. Space flight induced selective morphological responses in the corticotrophs and gonadotrophs of the pituitary. Plasma levels of ACTH did not change, but plasma growth hormone and TSH levels decreased after longer space flights (>14 days), while prolactin in the plasma increased after short flights (5-7 days). Plasma corticosterone was higher after all flights. Catecholamine levels in plasma increased only after long space flights. These changes in plasma hormone levels affected the activities of enzymes involved in the amino acid metabolism of the liver and lipolysis in the adipose tissues. Norepinephrine level and catecholamine synthesizing enzyme activity in the hypothalamus did not change in flight rats. The norepinephrine content, however, decreased in several nuclei selected from the hypothalamus of flight rats. Increases in plasma insulin and glucose were noted in rats after space flight. Glucagone values in plasma remained unchanged. Comparing these results from flight rats against rats exposed to acute or repeated stress indicate that long stays in microgravity do not represent intensive stressogenic stimulus of the adrenocortical and sympathetic adrenomedullar systems, and hormone alterations observed after space flight may be due primarily to acute stressor activity resulting from a return to Earth's gravity (gravitational stress).

Adaptation, Physiological↗

Stress and antidepressants differentially regulate neurotrophin 3 mRNA expression in the locus coeruleus.

The mechanisms by which stress and anti-depressants exert opposite effects on the course of clinical depression are not known. However, potential candidates might include neurotrophic factors that regulate the development, plasticity, and survival of neurons. To explore this hypothesis, we examined the effects of stress and antidepressants on neurotrophin expression in the locus coeruleus (LC), which modulates many of the behavioral and physiological responses to stress and has been implicated in mood disorders. Using in situ hybridization, we demonstrate that neurotrophin 3 (NT-3) is expressed in noradrenergic neurons of the LC. Recurrent, but not acute, immobilization stress increased NT-3 mRNA levels in the LC. In contrast, chronic treatment with antidepressants decreased NT-3 mRNA levels. The effect occurred in response to antidepressants that blocked norepinephrine uptake, whereas serotonin-specific reuptake inhibitors did not alter NT-3 levels. Electroconvulsive seizures also decreased NT-3 expression in the LC as well as the hippocampus. Ntrk3 (neurotrophic tyrosine kinase receptor type 3; formerly TrkC), the receptor for NT-3, is expressed in the LC, but its mRNA levels did not change with stress or antidepressant treatments. Because, NT-3 is known to be trophic for LC neurons, our results raise the possibility that some of the effects of stress and antidepressants on LC function and plasticity could be mediated through NT-3. Moreover, the coexpression of NT-3 and its receptor in the LC suggests the potential for autocrine mechanisms of action.

Animals↗

Aging and acute stress decrease corticotropin releasing hormone in the ovary of the Fischer 344/N rat.

Corticotropin-releasing hormone (CRH), originally isolated from the hypothalamus, is widely distributed in many extrahypothalamic central nervous system sites, and in the periphery. Immunoreactive (ir)-CRH has been identified in rat and human inflammatory sites, in rat testicular Leydig cells, and in rat thecal and stromal ovarian cells. In the current study, we investigated whether aging and stress are associated with changes in ovarian ir-CRH in the rat. Healthy young (3-4 mo) and old (24 mo) female Fischer 344/N rats (6 per group) were studied in the morning, before and after being stressed by 120 min of immobilization, and were sacrificed by decapitation. Young females were all in proestrous, and old females were in constant anestrous. Pre-immobilization corticosterone (CORT) levels were similar in both age groups; immobilization produced a dramatic increase in CORT in both groups; however, the increase was smaller in the old rats, although this did not reach statistical significance (P < 0.06). Immunoreactive CRH was detected in the ovaries of all rats, and its distribution and intensity were quantified masked to the age and treatment group, in the theca, granulosa, stroma, and corpus luteum. At baseline, ir-CRH was 50% lower in old than in young rats in the theca and stroma by both distribution and intensity. Stress was associated with a decrease of ir-CRH levels in the theca in both age groups, albeit to a significantly lesser extent in old rats (old 35% versus young 70%). These data suggest a functional and, perhaps, developmental role for ovarian CRH.

Acute Disease↗

Temporary increase of plasma epinephrine affects stress responses 24 h later.

The impact of temporary (24 h) implantation of epinephrine tables on catecholamine responses to handling and immobilization 24 h later was investigated in rats. Free plasma epinephrine responded with an increase to both types of stress (77% and 326%, respectively) while controls showed a weaker response to immobilization. The basal level of free plasma norepinephrine was reduced (46% vs. controls) after epinephrine pretreatment, but neither handling nor immobilization had a specific effect on this parameter. In contrast, the basal level of free plasma dopamine was increased after epinephrine pretreatment (183%); however, as with free norepinephrine, there was no specific effect of handling or immobilization. Conjugated plasma epinephrine was significantly lowered after epinephrine pretreatment (44% vs. controls). It did not respond specifically to handling or immobilization except for a stronger response after 20 min of immobilization. Conjugated norepinephrine showed no specific response, but increased nonspecifically after extended immobilization. Conjugated dopamine was lowered (30%-48%) in the E-treated group and did not respond to stress at any time. Thus, a temporary elevation of free plasma epinephrine affected, differentially, basal levels and stress responses of free and conjugated catecholamines 24 h later.

Adrenergic Agonists↗