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Biomedical subjects

F Laczi

Publications and source records attributed to F Laczi.

At least 37 records · Page 2Linked to original sources
PubMed1990

[Regulation of vasopressin release in primary hypothyroidism and Addison's disease as well as in central diabetes insipidus].

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism, in 6 with Addison's disease, and in 21 with central diabetes insipidus (CDI). In the latter disease the effect of histamine stimulus was also evaluated. Plasma AVP was measured by radioimmunoassay (RIA). Patients with primary hypothyroidism were classified into subgroups with elevated or normal basal levels of plasma AVP. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels. Patients with Addison's disease exhibited an increased basal level of plasma AVP and a decreased osmotic threshold. CDI patients according to their AVP responses on osmotic stimulus fell into two groups: CDI I gave no response at all, while CDI II responded subnormally. CDI II exhibited blunted AVP release to histamine. The AVP reactions of the CDI I patients fell into two subgroups: CDI I/A had undetectable plasma AVP, whereas histamine evoked AVP release in CDI I/B. Patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease and CDI I/B presumably have an osmoreceptor failure.

Addison Disease↗
PubMed1989

The effects of beta-endorphin on arginine-8-vasopressin and oxytocin levels in rat brain areas.

Measurements were made of the effects of intracerebroventricular treatment with beta-endorphin (BE; 100 ng) on the arginine-8-vasopressin (AVP) and oxytocin contents of rat hypothalamic and limbic brain areas (hippocampus, amygdala and septum). The hormone concentrations were determined by radioimmunoassay. The administration of BE resulted in a significant reduction of the AVP level in the amygdala in a naloxone-reversible manner. Naloxone (Nal) administered subcutaneously significantly increased the AVP content in the septum. The results revealed that BE and Nal had regionally specific effects on the activity of the vasopressinergic system but not on that of the oxytocinergic system in the brain.

Animals↗
PubMed1989

Humoral changes in shock induced by cardiac tamponade.

Cardiac tamponade was induced in dogs by the infusion of saline into the pericardial cavity. The mean arterial pressure dropped to approximately one-third and the cardiac output to one-fourth of the control level. This was accompanied by the release of vasoactive humoral mediators. Among the vasoconstrictor mediators measured in the plasma, the greatest rise during early tamponade occurred in vasopressin concentrations. Considerable elevations of epinephrine and nonrepinephrine concentrations and plasma renin activity were also demonstrated, these mediators reaching their maximum levels in late tamponade. This study for the first time demonstrates significant rises in plasma thromboxane B2 and histamine levels in cardiac tamponade. The histamine level elevation was greater in the portal venous blood than in the arterial blood. It is suggested that histamine may play a counterregulatory role in cardiac tamponade by attenuating excessive vasoconstriction caused by the activation of various vasoconstrictor systems.

Animals↗
PubMed1989

Acute effects of peripheral histamine administration on arginine-8-vasopressin and oxytocin levels in rat spinal cord.

The effects of a single injection of 20 mg/kg histamine on the immunoreactive arginine-8-vasopressin (AVP) and oxytocin (OXT) levels in the rat spinal cord were studied after peripheral (intraperitoneal) administration. Histamine induced a 60% elevation in the AVP content of the spinal cord, whereas the spinal level of OXT decreased by 36%. The findings suggest that peripheral histamine differentially affects the AVP and OXT levels in the spinal cord.

Animals↗
PubMed1988

The effect of atrial natriuretic factor on arginine-8-vasopressin and oxytocin levels in various brain regions and plasma.

The effect of intracerebroventricular (i.c.v.) treatment of rat atrial natriuretic factor III (ANF III; 0.5 microgram) was measured on the arginine-8-vasopressin (AVP) and oxytocin (OXT) contents of rat hypothalamic and limbic brain areas as well as those in the plasma. The hormone concentrations were determined by radioimmunoassay (RIA). The administration of ANF III in conscious euhydrated rats resulted in a significant reduction of both AVP and OXT contents in the hippocampus. Ether anesthesia interfered with the effect of ANF III, since in anesthetized rats ANF III reduced the levels of AVP and OXT in the septal regions, too. ANF III had no effect on the basal plasma AVP and OXT concentrations, however, the peptide inhibited the plasma AVP and OXT elevation induced by hyperosmosis (intraperitoneal injection of 2.5% NaCl). The results suggest that ANF III may be important in the control of the activity of both the peripheral (hypothalamo-neurohypophyseal) and the central (brain) AVP-ergic and OXT-ergic systems.

Animals↗
PubMed1987

Presence of chromatographically identified oxytocin in human sensory ganglia.

Oxytocin-like immunoreactivity (IR-OXT) was detected in extracts of human spinal L5 and Gasserian ganglia by a radioimmunoassay (RIA) specific to oxytocin (OXT) and was identified by high-performance liquid chromatography (HPLC). One of the two immunoreactive peaks obtained on HPLC was found to elute at the same position as the OXT standard. The results reveal the presence of chromatographically identified OXT immunoreactivity in human sensory ganglia.

Aged↗
PubMed1987

Effects of beta-endorphin2-9 on arginine-8-vasopressin and oxytocin levels in hypothalamic and limbic brain regions.

Immunoreactive arginine-8-vasopressin (AVP) and oxytocin (OXT) were measured in rat hypothalamic and limbic brain regions after the intracerebroventricular administration of beta-endorphin fragment 2-9 (beta E2-9). The peptide decreased the AVP content of the hippocampus and the OXT levels in the septum and amygdala. The present data favor the view that beta E2-9 interacts with limbic AVP- and OXT-systems.

Amygdala↗
PubMed1987

Limbic oxytocin and arginine 8-vasopressin in morphine tolerance and dependence.

Immunoreactive oxytocin (OXT) and arginine8-vasopressin (AVP) levels were measured in limbic areas of the mouse brain (hippocampus, amygdala and basal forebrain). Peptides were measured by radioimmunoassay (RIA). Acute morphine treatment caused a naloxone-reversible increase in OXT content in all three brain regions. The AVP contents of the same brain areas, on the other hand, were not affected by acute morphine treatment. In mice rendered tolerant to/dependent on morphine with subcutaneous morphine pellets, the OXT levels in the limbic brain structures were in the control range (basal forebrain and amygdala) or even decreased (hippocampus). In the latter brain structure of the tolerant animals, the AVP content was also decreased. Naloxone-precipitated withdrawal syndrome in the tolerant/dependent animals resulted in abrupt increases in the OXT and AVP levels of the hippocampus and in the OXT content of the basal forebrain structures.

Amygdala↗
PubMed1987

Hyponatremia and increased secretion of vasopressin induced by vincristine administration in rat.

Administration of vincristine resulted in a hyponatremic state and concurrent elevation of the plasma immunoreactive arginine8-vasopressin (IR-AVP) level in rats. Development of the vincristine-induced hyponatremia and hypoosmolality was accompanied by a loss in weight, a decreased water intake and a large reduction in the daily urine sodium excretion. The cause of the sodium loss is thought to be the diarrhea observed during vincristine treatment. Hematocrit and serum urea nitrogen levels were increased. It is concluded that the condition differs from the syndrome of inappropriate secretion of antidiuretic hormone (SIADH): the increase in plasma IR-AVP concentration may be associated with dehydration due to vincristine toxicity.

Animals↗
PubMed1987

Osmoregulation of arginine-8-vasopressin secretion in primary hypothyroidism and in Addison's disease.

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism and in 6 with Addison's disease. Plasma AVP was measured by radioimmunoassay. Patients with primary hypothyroidism were classified into subgroups with elevated (6.81 +/- 1.12 pmol/l) or normal (3.92 +/- 0.96 pmol/l) basal levels of plasma AVP. Following the infusion of 2.5% saline, a positive correlation was established between plasma AVP and plasma osmolality. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels (pAVP = 0.37 (pOs-265), r = 0.71, P less than 0.01) as compared with that in hypothyroid patients with a normal AVP level (pAVP = 0.42 (pOs-280), r = 0.93, P less than 0.001). A relationship was demonstrated between the alteration in the AVP osmoregulation and the severity of the thyroid insufficiency. Patients with Addison's disease exhibited an increased basal level of plasma AVP (9.59 +/- 1.25 pmol/l) and a decreased osmotic threshold (pAVP = 0.42 (pOs-261), r = 0.63, P less than 0.01) contrasted to that of healthy volunteers (pAVP = 0.41 (pOs-280), r = 0.83, P less than 0.001). The osmoregulation disturbance of the AVP secretion may play a major role in the impaired water metabolism in primary hypothyroidism and in Addison's disease.

Addison Disease↗
PubMed1987

Differential effect of desglycinamide9-(Arg8)-vasopressin on cognitive functions of diabetes insipidus and alcoholic patients.

Intranasal treatment with desglycinamide9-(Arg8)-vasopressin (DGAVP) improved certain aspects of cognitive functions of patients with acquired and congenital diabetes insipidus and of alcoholic patients with mild cognitive impairments. Patients with Korsakoff's syndrome, presenting with severe cognitive impairments, were resistent to DGVP treatment. DGAVP treatment did not affect blood pressure and water metabolism. The action of DGAVP on cognitive functions is probably mediated by centrally located target sites and may be expressed only in patients in whom these target sites are unimpaired.

Administration, Intranasal↗
PubMed1986

Stimulatory effect of intracerebroventricularly administered dopamine on vasopressin release in rats.

Experiments were designed to investigate the effects of the intracerebroventricular administration of dopamine (DA) and a DA antagonist (pimozide) on the immunoreactive-vasopressin (IR-VP) contents of the rat magnocellular nuclei (MCN), neurohypophysis (NH) and plasma. The IR-VP levels in the MCN and NH were decreased 5 min after administration of DA in a dose of 20 nmol, but that in the plasma was increased. This effect was not observed after pretreatment with pimozide. Administration of pimozide alone did not affect the IR-VP contents of the MCN, NH or plasma. The results suggest that DA given icv. has a stimulatory effect on VP release from the neurohypophysial system.

Animals↗
PubMed1986

Plasma arginine-8-vasopressin responses to osmotic or histamine stimulation contribute to the differential diagnosis of central diabetes insipidus.

The arginine-8-vasopressin (AVP) responses to osmotic and histamine stimuli were evaluated in 21 patients with central diabetes insipidus (CDI) and compared to those of 10 healthy controls. Plasma AVP was measured by radioimmunoassay. Following the infusion of 2.5% saline, the AVP responses of CDI patients fell into two distinct groups: CDI I gave no response at all, while CDI II responded subnormally. Histamine increased the plasma AVP level significantly in healthy volunteers. Patients with CDI II gave subnormal AVP responses to histamine. The AVP reactions of the patients with CDI I fell into two subgroups: CDI I/A had undetectable plasma AVP, while histamine evoked AVP release in CDI I/B. Histamine trial did not lead to any change in plasma osmolality. The authors conclude that patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease. The remainder (CDI I/B) presumably have an osmoreceptor failure. Osmotic and non-osmotic stimulation may provide a useful tool in the differential diagnosis of CDI.

Adolescent↗
PubMed1985

Acute morphine treatment and morphine tolerance/dependence alter immunoreactive oxytocin levels in the mouse hippocampus.

Immunoreactive oxytocin levels were measured in the mouse hippocampal tissue (h-OXT). Acute morphine treatment increased h-OXT, which effect was reversed by naloxone. In mice rendered tolerant to and dependent on morphine h-OXT was lower than in placebo pellet-implanted control mice. In the tolerant/dependent animals naloxone resulted in precipitated withdrawal syndrome which was associated with a slight increase in h-OXT. The data indicate that h-OXT is affected by acute morphine treatment and by morphine tolerance/dependence and raises the possibility that h-OXT participates in the adaptive response of the organism towards narcotic drugs.

Animals↗
PubMed1984

Levels of arginine-vasopressin in cerebrospinal fluid during passive avoidance behavior in rats.

The concentration of immunoreactive arginine-vasopressin (IR-AVP) was measured in the cerebrospinal fluid (CSF) during acquisition and retention of passive avoidance behavior. IR-AVP level in CSF of male Wistar rats immediately after the learning trial was increased; the rate of which was related to the intensity of the electric footshock during the learning trial and the avoidance latency as measured 1 day after the learning trial. Immediately after the 24 h retention test IR-AVP levels were significantly increased in rats subjected to the low (0.25 mA) shock intensity during the learning trial, but IR-AVP levels of rats exposed to the high shock (1.0 mA) were under the limit of detection. If the retention test was postponed till 5 days after the learning trial, the increase of IR-AVP level in the CSF was related to avoidance latencies which reflect the intensity of aversive stimulation (electric footshock). The results suggest an association between central AVP release and passive avoidance behavior and may be indicative of the role of this peptide in neuronal mechanisms underlying learning and memory processes.

Animals↗
PubMed1984

The stimulatory effect of a non-opiate beta-endorphin fragment on arginine-vasopressin release in rats.

The effect of the non-opiate beta-endorphin (beta E) fragment 2-9 and related peptides on immunoreactive (IR) arginine8 -vasopressin (AVP) levels was studied in the rat eye plexus plasma. Additionally, the effect of beta E 2-9 on AVP release from pituitary neurointermediate lobes ( NILs ), in vitro was studied. IR AVP levels in the eye plexus plasma increased after subcutaneous (s.c.) injection of beta E 2-9. In female rats peak values were observed 2 min after the administration of beta E 2-9 (10 micrograms/rat). Male rats were 100 times more sensitive than female rats. A dose-response study revealed a U-shaped relationship for this effect of beta E 2-9 in animals of both sexes. From structure-activity studies it appeared that beta E 2-9 was the most effective fragment. Intracerebroventricular (i.c.v.) administration of beta E 2-9 did not affect the IR-AVP levels in eye plexus plasma. Moreover, AVP release from the rat NILs cells in vitro was stimulated by perfusion with beta E 2-9, indicating a direct effect of the peptide on the pituitary. Therefore we suggest that beta E 2-9 increases AVP release by a direct action on the posterior pituitary.

Animals↗
PubMed1983

Arginine-vasopressin content of hippocampus and amygdala during passive avoidance behavior in rats.

Arginine-vasopressin (AVP) is involved in memory processes. The memory effects of AVP are mediated by neuronal mechanisms taking place in limbic-midbrain structures. Therefore, immunoreactive AVP (IR-AVP) was measured in hippocampus and amygdala of male Wistar rats during acquisition and retention of passive avoidance behavior. IR-AVP concentration was decreased in the hippocampus immediately after the learning trial while IR-AVP content of the amygdala was not affected. Animals that showed the passive avoidance response (good avoiders) at the 24 h or 120 h retention test had a reduced IR-AVP concentration in the hippocampus immediately after the test. However, IR-AVP content of the hippocampus was not different from that of non-shocked control animals when measured immediately before the 120 h retention test. Poor avoiders that showed only minor avoidance behavior did not differ in hippocampal IR-AVP content from non-shocked control animals. IR-AVP content of the amygdala was also not altered after the retention session. These effects on IR-AVP content could only be shown in animals that were trained and habituated to the passive avoidance procedure. Such trained and habituated animals had an IR-AVP level in the hippocampus which did not differ from that of animals that were left undisturbed until sacrifice. When the animals were not trained, but placed for the first time in the passive avoidance apparatus without being exposed to the learning trial, the hippocampal IR-AVP content was reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Amygdala↗