Biomedical subjects

I Barna

Publications and source records attributed to I Barna.

At least 37 records · Page 2Linked to original sources

PubMed1997

Effects of anterolateral and posterolateral cuts around the medial hypothalamus on the immunoreactive ACTH and beta-endorphin levels in selected brain regions of the rat.

To evaluate the relative weight of the ACTH-ergic and beta-endorphin-ergic pathway(s) leaving the medial hypothalamus (MH) in anterior or posterior directions immunoreactive ACTH and beta-endorphin (ir-ACTH and ir-betaE) were quantified in selected brain regions of the rat 7-8 days after placing anterolateral (ALC) or posterolateral (PLC) cut around the MH. Retrograde accumulation of both peptides was observed in the MH after ALC, but not after PLC. ALC resulted in dramatic decrease in ir-ACTH/ir-betaE concentrations in all extra-MH brain regions tested (extra-MH hypothalamus, septum, thalamus, hippocampus, amygdala, and medulla oblongata). In contrast, ir-ACTH and ir-betaE levels decreased only in the thalamus and in the medulla oblongata after PLC. The present data indicate (a) ACTH- and betaE-like substances synthesized in the arcuate region of the hypothalamus are axonally transported to extrahypothalamic brain regions by neuronal pathways leaving the MH primarily anterolateral, anterodorsal, or anteromedial direction (even the fibers of certain posteromedial or posterolateral projections leave the MH some anterior directions); (b) the posterior ACTH-/betaE-ergic projections seem to be of minor importance except for the thalamus and the medulla oblongata where it contributes to about one-third of the peptide content. Our biochemical study provide quantitative complementary data to the detailed immunohistochemical picture of the ACTH/betaE-ergic projections in the rat brain described by Khachaturian et al.

Adrenocorticotropic Hormone↗

PubMed1997

Domperidone stimulates prolactin secretion in rats with complete destruction of the mediobasal hypothalamus.

The main objective of this study was to further elucidate the functional relationship between endogenous dopamine and the prolactin (PRL)-releasing effect of the dopamine antagonists domperidone and haloperidol. We studied the effect of the above dopamine antagonists on the PRL secretion in control and mediobasal hypothalamus (MBH)-lesioned rats. Significant increase in basal plasma PRL levels was detected 7 days after complete surgical destruction of the MBH. Haloperidol injection (0.5 mg/kg, i.v.) was followed by an increased plasma PRL concentration in the sham-operated animals; however, in the MBH-lesioned rats where the basal PRL levels were high haloperidol failed to produce additional PRL release. In contrast to haloperidol, domperidone (0.1 mg/kg, i.v.) was able to further elevate the MBH-lesion induced high plasma PRL concentration. Moreover, the change in plasma PRL levels of the MBH-lesioned rats was parallel with that in the sham-lesioned animals after domperidone injections. When haloperidol was given prior to the domperidone injection it did not influence the PRL releasing effect of domperidone in MBH-lesioned animals. The PRL stimulatory effect of domperidone (0.3 mg/kg, i.v.) in MBH-lesioned rats was antagonized by dopamine (20 micrograms/kg, i.v.) and bromocryptine (20 micrograms/kg, i.v.). The above results suggest that the stimulatory effect of domperidone on the pituitary PRL secretion is mediated--at least in part--through the pituitary D2 dopamine receptors, but not by the displacement of endogenous dopamine originating from the MBH and reaching the pituitary via portal vessels.

Animals↗

PubMed1997

Age-dependent muscarinic stimulation of beta-endorphin secretion from rat neurointermediate lobe in vitro.

The effect of acetylcholine on the neurointermediate lobe beta-endorphin secretion was studied in the neonatal and in the adult rat in vitro. Acetylcholine stimulated beta-endorphin secretion from the 2-day- and 5-day-old neurointermediate lobe, the effect was dose dependent and more pronounced in the presence of the cholinesterase inhibitor eserine. The 10-day-, the 21-day-old and the adult rat neurointermediate lobes did not respond to acetylcholine, even in the presence of eserine. Basal beta-endorphin secretion was elevated by the D2 receptor antagonist sulpiride, but acetylcholine was without effect in the 10-day-old and in the adult neurointermediate lobe even after dopamine receptor blockade. The beta-endorphin stimulatory response to acetylcholine was diminished by the M1 muscarinic receptor antagonist pirenzepine and blocked by the M3 > M1 antagonist 4-diamino-phenyl-piperidine (4-DAMP). The selective M2 antagonist methoctramine and nicotine had no effect. These data indicate that the neurointermediate lobe beta-endorphin secretion is under special muscarinic cholinergic regulation for a relatively short time after birth. The disappearance of this stimulatory cholinergic effect in later life might be due to changes in the intracellular secretory machinery in the IL and/or to the uncoupling of the cholinergic receptors from the intracellular signal transduction system(s) responsible for the stimulated secretion in the rat melanotrope cells.

Acetylcholine↗

PubMed1996

Compression of the pituitary stalk elicits chronic increases in CSF vasopressin, oxytocin as well as in social investigation and aggressiveness.

The neurochemical and behavioural effects of a novel stereotaxic surgical method developed for interrupting the nerve fibres running through the rat pituitary stalk to the posterior pituitary gland was studied. The cerebrospinal fluid (CSF) vasopressin (AVP) and oxytocin (OT) content as well as changes in aggressiveness were measured in rats one week and one month after the surgical intervention. The main results are as follows: (1) the compression of the pituitary stalk elicits a chronic increase in water consumption, as well as in CSF vasopressin and oxytocin content; (2) the surgical intervention increased the frequency of clinch fighting after one week. The increase in aggressiveness accentuated after one month and, in addition, operated animals showed reduced scores of resting while exploratory and social behaviours increased; (3) there was a strong positive correlation between water consumption, vasopressin, and aggressiveness; (4) oxytocin changes showed a positive correlation with variation in social behaviour. The surgical intervention may serve as a model for lesions of the pituitary stalk and formation of ectopic neurohypophyses in humans.

Aggression↗

PubMed1995

Hormonal and metabolic responses during psychosocial stimulation in aggressive and nonaggressive rats.

The physiological effects of a psychosocial threat (the mere presence of a potentially antagonist individual in the home cage) were studied in aggressive and nonaggressive rats. Aggressive animals spent a significantly longer time with the investigation of the opponent compared with the nonaggressive group. An increase in plasma epinephrine and corticosterone was noticed both in aggressive and nonaggressive animals. Ir beta-endorphin increased significantly only in nonfighters. Glycemia was slightly larger in nonaggressives, while lactaemia increased in both groups. The possibility is discussed that differences in psychosocial stress response may be involved in the regulation of behavior in a real encounter.

Adrenocorticotropic Hormone↗

PubMed1995

Adrenocorticotropin, prolactin and beta-endorphin stimulatory actions of alpha-2-adrenoceptor antagonists.

We studied the effect of glucocorticoid pretreatment, mediobasal hypothalamus lesion (MBHL) and the interaction between clonidine and yohimbine in male Wistar rats to elucidate the sites and/or mechanisms of endocrine actions of alpha 2-antagonists. The pretreatment of 1 mg/kg s.c. dexamethasone for 4 days effectively prevented the stimulatory effect of alpha 2-antagonists yohimbine (5 mg/kg i.p.) and CH-38083 (1 mg/kg i.p.) on adrenocorticotropin (ACTH) secretion, while the action of these antagonists on prolactin (PRL) and beta-endorphin (beta E) remained unchanged. The central (i.c.v.) pretreatment of 5 micrograms/rat clonidine failed to antagonize the prolactin (PRL) and beta E releasing effect of yohimbine. However, it inhibited the yohimbine-induced ACTH secretion. MBHL resulted in a significant enhancement in basal plasma PRL and beta-endorphin (beta E) levels. But basal plasma ACTH levels have not been changed. Yohimbine failed to stimulate ACTH secretion in MBH-lesions rats, while PRL and beta E response to the yohimbine was maintained in these animals. This study confirms that the alpha 2-antagonists stimulate ACTH secretion by a corticosteroid-sensitive mechanism which is located centrally. In contrast, alpha 2-antagonists affect PRL and beta E secretion via a corticosteroid-insensitive mechanism located at the periphery, possible within the pituitary gland.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1995

Effect of interleukin-1 beta on plasma ACTH, beta-endorphin, and corticosterone levels in infant and prepubertal rats.

IL-1 beta is known to enhance ACTH release from the anterior pituitary in the adult rat, mainly by simulating the hypothalamic ACTH-releasing hormone (CRH) release, but it seems to have a direct effect on the pituitary and on the adrenal hormone secretion, too. The effect of IL-1 beta on the beta-endorphin (beta E) secretion from the intermediate lobe is less well studied. There is very little information on the effect of IL-1 beta on the hypothalamic-pituitary-adrenal axis (HPAA) in the postnatal rat, which is a special period, because the reactivity of the HPAA is blunted. The effect of IL-1 beta in this period seemed to be of special interest, because neither the immune nor the endocrine system is fully developed. In the present study we tested the 30- and 120-min effect of intraperitoneally administered 0.5 and 100 ng/g body weight IL-1 beta on the plasma immunoreactive (ir) ACTH, beta E, and corticosterone (CS) levels in the 10-d-old (infant) and 30-d-old (prepubertal) rat. Generally, the ir-ACTH, ir-beta E, and ir-CS levels were significantly higher in prepubertal than in infant rats. Hormone levels were more enhanced by the higher dose of IL-1 beta, and changes were more pronounced at 120 min than at 30 min. The relative increase of ir-ACTH and ir-beta E was smaller in the infant than in the prepubertal rat. In contrast, the relative increase of ir-CS was more pronounced in the infant rat.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1994

[Comparative study of 24-hour ambulatory blood pressure monitors with standard zero and random zero sphygmomanometers].

The aim of the study was to evaluate the accuracy of the most widespread 24-hour ambulatory blood pressure monitor in Hungary. The test was based on simultaneous measurement on the same arm with the test device and standard zero or random zero sphygmomanometer in 100 patients. The difference between the blood pressure values measured by the test device and by the standard device was calculated in each case, and a relationship between this difference and the actual blood pressure of the patient was analysed. Actual blood pressure was considered as the average of the blood pressure measured by the test and that by the standard device. Regarding the diastolic values, the mean difference between the values obtained by the test device and the standard zero sphygmomanometer was -3.8 +/- 7.55 mm Hg (p > 0.05), and that between the test device and the random zero sphygmomanometer was -0.1 +/- 6.05 mm Hg (p > 0.05). This differences did not reach statistical significance. Regarding the systolic values, the difference showed significant positive correlation with the actual blood pressure level of the patient, meaning that at higher blood pressure values the difference between the data gained by the test and standard device is greater than at lower actual blood pressure levels. Finally, according to the criteria of the British Hypertension Society, our device could be graded "C" both for diastolic and systolic values against the standard zero sphygmomanometer, and "C" for systolic and "B" for diastolic blood pressure against the random zero sphygmomanometer.

Blood Pressure Determination↗

PubMed1994

Alpha 2-adrenoceptor blockade, pituitary-adrenal hormones, and agonistic interactions in rats.

The effects of adrenergic activation on aggressiveness and the aggression induced endocrine changes were tested in rats. Alpha 2 adrenoceptor blockers were used for enhancing activation of the adrenergic system, and changes in aggressiveness were tested in resident-intruder contests. Three experiments were conducted. In experiment 1, saline injected rats responded to the presence of an opponent by aggression and the increase in plasma ACTH and corticosterone. Intraperitoneal administration of 1 mg/kg CH-38083 (an alpha 2 adrenoceptor antagonist) produced a several fold increase in clinch fighting and mutual upright scores, and also further enhanced the plasma ACTH and corticosterone response. In experiment 2, the effect of three doses (0.5, 1 and 2 mg/kg) of three different alpha 2 adrenoceptor blockers CH-38083, idazoxan and yohimbine were tested. All the substances increased aggression at 0.5 and 1 mg/kg; at 2 mg/kg the effect of idazoxan and yohimbine disappeared, while with CH-38083 an additional increase was obtained. In yohimbine treated animals the enhancement of aggression was reduced already at 1 mg/kg. In experiment 3, indomethacin, a potent inhibitor of the catecholamine-induced ACTH release completely abolished the effects of the alpha 2 adrenoceptor antagonist CH-38083: the intensity of agonistic interactions, as well as ACTH and corticosterone plasma concentrations, returned to control levels. The possible role of catecholamines and the stress hormones in the activation of aggression is discussed.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1994

Atrial natriuretic peptide (ANP) responsiveness in patients with hypothyroidism.

Hypothyroidism is known to be associated with abnormalities of kidney function; recently, low atrial natriuretic peptide (ANP) plasma levels have been reported. Aim of the study was to asses ANP, sodium and water responsiveness to an acute saline load. Twelve patients with established primary hypothyroidism and 9 control subjects were studied. ANP was determined in plasma by RIA with extraction, prior to and after the infusion of saline, 500 ml/h for 4 hours. On a similar albeit liberal sodium diet hypothyroid patients excreted less sodium and water (74 +/- 33 (SD) mumol/min and 0.69 +/- 0.15 ml/min, respectively) than control subjects (110 +/- 52 mumol/min; P < 0.05 and 1.06 +/- 0.53 ml/min; P < 0.025, respectively). However, the infusion of saline resulted in a 3-fold increase of sodium output and more than 2-fold increase in urine flow. The exaggerated responsiveness in sodium excretion in patients with hypothyroidism was associated with significantly decreased pre-infusion ANP plasma levels (16.1 +/- 11.1 pg/ml vs. 44.4 +/- 14.4 pg/ml; P < 0.001) and also with sluggish response to the volume expansion (+24% vs. +48%). A significant correlation was found between serum T4 levels and plasma ANP concentrations in 8 patients (r = 0.689; P < 0.05). Although hypothyroid patients tend to retain sodium on a liberal salt diet, their kidney is capable of vigorously eliminating excess sodium when challenged with an acute saline load. This exaggerated responsiveness of sodium excretion can be demonstrated in spite of a sluggish response in ANP. Subnormal ANP levels in hypothyroidism are probably the result of thyroid deficiency.

Adult↗

PubMed1993

Effects of Hypnorm (fentanyl) on ACTH/beta-endorphin levels in plasma, pituitary and brain of 10-day old rats.

Administration of Hypnorm, an anaesthetic containing the known mu-opiate receptor agonist fentanyl, elicited dose- and time-related elevation of plasma ACTH, beta-endorphin and corticosterone levels in 10-day old rat pups. Pretreatment with specific antibodies (raised against CRH, AVP and ACTH resp.) revealed that Hypnorm administration activated the ACTH-corticosterone system in the 10-day old rat and its effect is mediated by CRH and/or AVP. Hypnorm anaesthesia was associated with significant decrease in the ACTH and beta-endorphin levels in the pituitary lobes as well as in beta-endorphin content of the hypothalamus and medulla oblongata. Latter results may indicate that the beta-endorphinergic system in the brain of the 10-day old rat is activated by Hypnorm, an effect most probably elicited by the opiate agonist fentanyl.

Adrenocorticotropic Hormone↗

PubMed1992

Effects of mediobasal hypothalamic lesion on immunoreactive ACTH/beta-endorphin levels in cerebrospinal fluid, in discrete brain regions, in plasma, and in pituitary of the rat.

One week after complete destruction of the mediobasal hypothalamus, immunoreactive adrenocorticotropin (ACTH) and beta-endorphin levels were determined in cerebrospinal fluid, trunk blood, as well as in brain and pituitary tissue samples collected from anaesthetized and cisternally cannulated rats. Control rats were sham operated. In lesioned rats we observed: (a) 60% decrease in the immunoreactive beta-endorphin concentrations in the cerebrospinal fluid, (b) decreased immunoreactive ACTH and beta-endorphin levels in the hypothalamus, in the thalamus and in the amygdala, (c) unaffected immunoreactive ACTH/beta-endorphin levels in the septum and in the hippocampus, (d) decreased immunoreactive beta-endorphin levels both in the anterior and neurointermediate pituitary but unchanged immunoreactive ACTH contents in the anterior lobe, and (e) unaffected immunoreactive ACTH and beta-endorphin levels in the plasma under stressful conditions. From these findings the following conclusions can be drawn: (1) more than 50% of the beta-endorphin-like peptide content of the cerebrospinal fluid originates from the periventricular nuclei of the hypothalamus and thalamus in the rat; (2) the loss of the hypothalamic control probably enhances the intracellular proteolytic degradation of beta-endorphin both in the anterior and neurointermediate pituitary lobe; (3) rats with mediobasal hypothalamic lesion cannot react to the stressful stimuli of ether anaesthesia or cisternal cannulation with elevated plasma immunoreactive ACTH and beta-endorphin levels.

Adrenocorticotropic Hormone↗

PubMed1992

Immunoreactive ACTH in the cerebrospinal fluid of the rat: decrease after mediobasal hypothalamic lesion and hypophysectomy, increase after adrenalectomy.

The effect of various anaesthetics and of the manipulations of the hypothalamo-pituitary-adrenocortical system (hypophysectomy, adrenalectomy and lesion of the mediobasal hypothalamus) was studied on immunoreactive-ACTH levels in the plasma and in the cerebrospinal fluid in the rat. The anaesthetics used (Hypnorm, pentobarbital, urethan and Ketanest) were without effect on immunoreactive-ACTH concentration in the cerebrospinal fluid. Immunoreactive-ACTH was significantly decreased after hypophysectomy and elevated after adrenalectomy in both cerebrospinal fluid and plasma. Destruction of the mediobasal hypothalamus resulted in reduced immunoreactive-ACTH content in the cerebrospinal fluid (about 20% of control) in both experiments, whereas immunoreactive-ACTH levels in the plasma of the lesioned rats were lower only in one of the two experiments performed. These data suggest that the main source of the immunoreactive-ACTH in the cerebrospinal fluid of the rat is the hypothalamus; the contribution of the pituitary gland being less than 50% of the radioimmunoassayable ACTH.

Adrenalectomy↗

PubMed1992

Body sodium, atrial natriuretic peptide and blood pressure in diabetes mellitus.

Diabetes mellitus (DM) is frequently associated with hypertension for which an independent pathomechanism has been suggested. We studied 26 patients with insulin-dependent (IDDM) and 18 patients with non-insulin-dependent (NIDDM) uncomplicated DM; all patients were in metabolic balance and none of them had hypertension. Exchangeable body sodium (NaE was estimated by isotope dilution, using appr. 1.1 Mbq 24NA. In a subset of 8 IDDM and 8 NIDDM patients atrial natriuretic peptide (ANP) plasma concentration was determined prior to and after the infusion of 2000 ml physiological saline over 2 hr. NaE was significantly increased both in IDDM and NIDDM patients (104.4 +/- 11.4% and 109.9 +/- 8.0% of the normal value for healthy subjects of identical body surface area; p < 0.05 and < 0.001 resp.). Mean blood pressure (MBP) correlated significantly with NaE in both groups (r = 0.364 and r = 0.520; p < 0.05 and < 0.025, resp.) but not in healthy control subjects (r = 0.112; N.S.). Resting ANP levels were not significantly different in IDDM (34.9 +/- 11.3 pg/ml), NIDDM (42.6 +/- 11.7 pg/ml) or control subjects (40.9 +/- 17.2 pg/ml) however the infusion of saline resulted in a significantly greater increase of plasma ANP in the NIDDM patients (to 82.9 +/- 43.2 pg/ml; P < 0.01) than in the controls (55.6 +/- 23.7 pg/ml; P < 0.01) which was associated with a significantly less increase in sodium excretion (UNAV) in the NIDDM patients (+86% vs. 3170%; P < 0.02) indicating down-regulation of ANP receptors in the kidney of NIDDM patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1991

Atrial natriuretic peptide (ANP) in patients with chronic renal failure on maintenance haemodialysis.

Atrial natriuretic peptide (ANP), a recently discovered cardiac hormone, is an important regulator of body fluid homeostasis. Twenty patients with established chronic renal failure and on maintenance haemodialysis were studied before and after dialysis with capillary dialysers. ANP was determined by RIA after extraction. Mean (+/- SD) pre-dialysis ANP concentration was 146 +/- 51 pg/ml and decreased significantly during dialysis to 68 +/- 38 pg/ml (p less than 0.001). Per cent and absolute changes in plasma ANP level correlated significantly with concomitant changes in body weight (r = 0.764; p less than 0.001 and r = 0.558; p less than 0.01, resp.) but not with changes in serum creatinine, blood pressure or serum electrolytes. The obtained results indicate that ANP levels in patients with chronic renal failure are elevated mainly due to fluid overload, and the rapid fall in ANP concentration observed during haemodialysis is caused by the removal of excess fluid from the body.

Adult↗

PubMed1991

Effect of anaesthetics on the release of beta-endorphin-immunoreactivity in rat plasma.

Analgesia and anaesthesia produced by fentanyl, urethane and ether, but not pentobarbital, occurred concomitantly with an increase in the concentration of plasma beta-endorphin like immunoreactivity (BEIR), probably of pituitary origin. This increase was not associated with significant changes in pituitary or brainstem beta-endorphin content. Pretreatment with naloxone caused a reduction in plasma BEIR increase following Hypnorm, ether and urethane; and in the analgesia following Hypnorm and urethane. Pentobarbital, alone or in combination with naloxone, did not increase the concentration of plasma beta-endorphin. These results may indicate participation of endogenous opioids in the mechanism of action of urethane.

Analgesics↗

PubMed1991

Relationship between exchangeable body sodium and urinary 6-keto-prostaglandin F1 alpha excretion in normal man.

The renal prostaglandins are involved in the regulation of sodium balance. In the present study exchangeable body sodium (NaE) and the urinary excretion of the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha (6-k-PGF1 alpha) were determined simultaneously in 10 hospitalized healthy individuals. NaE was 1461 +/- 107 mmol/m2 body surface area, or 98.5 +/- 6.9% when expressed as percent of the normal value assessed on the basis of measurements in 54 control subjects. The excretion of 6-k-PGF1 alpha amounted to 68.3 +/- 39.2 ng/4 hr. Statistical evaluation revealed significant correlation between NaE and PGF1 alpha excretion (r = 0.642; p less than 0.05) and between the serum Na concentration and the urinary excretion of 6-k-PGF1 alpha (r = 0.865; p less than 0.001). The obtained results indicate that urinary 6-k-PGF1 alpha excretion, hence the renal synthesis of prostacyclin, are regulated, among other factors, by body sodium stores. The increased production of prostacyclin with expanding sodium space might be regarded as a compensatory response contributing to the renal elimination of excess sodium from the body. The signal to this response could be the serum Na concentration.

6-Ketoprostaglandin F1 alpha↗

PubMed1990

[The role of exchangeable sodium content of the body in cases of hypertension of various etiology].

Measurement of exchangeable sodium by isotope dilution is a relatively simple, reliable method for the determination of body sodium contents, which can be used in the clinical practice without significant health hazard to the patient. When computed to body surface area, the values for exchangeable sodium can be compared in patients of different body build. Exchangeable sodium may be variably increased in different clinical conditions associated with hypertension, thus increased sodium contents of the body is of major importance in the pathogenesis of hypertension caused by all forms of mineralocorticoid excess, and in the majority of patients with chronic renal insufficiency. In several endocrine disorders, e. g., acromegaly, hypothyroidism, increased sodium space does not play any significant part in the pathogenesis of hypertension. In diabetes mellitus, exchangeable sodium may be increased already prior to the development of hypertension, however it is still a matter of debate whether this abnormality is involved in the pathogenesis of hypertension in these patients. It seems now beyond any doubt that body sodium is normal in patients with essential hypertension, including those with the low renin form of the disease; nevertheless, some data indicate that blood pressure may be volume dependent in elderly patients with essential hypertension.

Diabetes Mellitus, Type 1↗