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Biomedical subjects

F Laczi

Publications and source records attributed to F Laczi.

At least 19 recordsLinked to original sources

Oxytocin modulates behavioural adaptation to repeated treatment with cocaine in rats.

Behavioural adaptation to and the effects of the neurohypophyseal peptide, oxytocin, on repeated treatment with cocaine were investigated in rats. The content of immunoreactive oxytocin in the plasma, hypothalamus and different limbic structures in the brain were also studied after treatment with cocaine, identical to that used in the behavioural experiment. Repeated administration of cocaine (7.5 mg/kg, s.c.) produced a behavioural tolerance to the stereotyped sniffing-inducing effect of the challenge doses (1.875, 3.75 and 7.5 mg/kg, s.c.) of cocaine on the fifth day, which was demonstrated by parallel shifting of the dose-response and time-effect curves of the test doses of cocaine. The development of tolerance was inhibited by pretreatment with oxytocin (0.05 micrograms, (s.c.), administered before each daily injection of cocaine. A smaller dose of oxytocin (0.005 micrograms, s.c.) had no effect in this model. A decreased amount of immunoreactive oxytocin was detected in the plasma, in the hypothalamus and in the hippocampus, after repeated treatment with cocaine. Replacement of oxytocin by local injection (100 pg) into the ventral hippocampus, before each daily administration of cocaine, prevented the development of tolerance to cocaine. These results suggest that endogenous oxytocin, localized in limbic-forebrain areas, may have an important regulatory role in the development of behavioural changes induced by the repeated administration of cocaine.

Analysis of Variance

Effects of cocaine on the contents of neurohypophyseal hormones in the plasma and in different brain structures in rats.

The effects of acute and chronic cocaine treatments on the levels of the neurohypophyseal hormones oxytocin (OXT) and vasopressin (AVP) in the plasma and in different brain structures in rats were measured by radioimmunoassay (RIA). Acute cocaine treatment had no effect on the level of OXT in the plasma or in the amygdala, but increased OXT contents were measured in the hypothalamus and in the hippocampus. The OXT levels in the basal forebrain structures (including the septum and the nucleus accumbens) were decreased by a single dose of cocaine. The acute injection of cocaine increased the level of AVP in the plasma, and decreased contents of OXT were measured in the amygdala and in the basal forebrain. Repeated treatment with cocaine decreased the level of OXT in the plasma, hypothalamus and hippocampus. The AVP contents were decreased in all of the brain structures investigated, but no change was caused in the plasma level of AVP by repeated injections of cocaine. These results demonstrate complex, region-specific interactions between cocaine and the neurohypophyseal hormones in the brain and in the periphery underlying the alteration in behavioral and autonomic functions caused by acute and chronic cocaine exposure.

Amygdala

Chromatographically identified oxytocin in the human peripheral nervous system.

Immunoreactive oxytocin (OXT) detected in extracts of human coeliac ganglia and nn. vagi was characterized by high-performance liquid chromatography (HPLC). HPLC/RIA examinations demonstrated that a major part of the immunoreactive material in both investigated areas co-eluted with a reference synthetic OXT, but in the extracts of coeliac ganglia a second immunoreactive peak was also observed.

Aged

Two families with hereditary diabetes insipidus not due to osmoreceptor failure.

Two families with hereditary central diabetes insipidus (CDI) are reported. The pedigree in both families shows an autosomal dominant trait. The plasma arginine-8-vasopressin (AVP) determined by radioimmunoassay was markedly lower in these CDI patients than in healthy controls; the difference being even more pronounced after a hyperosmotic challenge. Since in the present study histamine also failed to increase the plasma AVP concentration, the authors consider it unlikely that an osmoreceptor failure would be implicated in the pathogenesis of CDI in these cases. The AVP concentration of the lumbar cerebrospinal fluid was also measured in two members of one of the families: the level found at the lower normal range indicates that some AVP secretion has been maintained in the extrahypothalamic vasopressinergic system of these patients.

Adolescent

Central effects of antiserum against human atrial natriuretic polypeptide on water and electrolyte metabolism and plasma arginine-8-vasopressin level in conscious rats.

Although synthetic atrial natriuretic polypeptide (ANP) is known to influence the water and electrolyte metabolism and arginine-8-vasopressin (AVP) secretion, the physiological role of endogenous ANP in the rat brain is still unclear. Accordingly, an investigation was made of the effects of intracerebroventricular (icv) administration of human h-ANP antiserum, which can neutralize endogenous ANP, on the water intake, urine output, urinary excretion of potassium and sodium, and plasma AVP level in normally hydrated rats. Apart from the water intake, all the parameters were also determined in 48-h water-deprived rats after h-ANP antiserum treatment. The icv administration of the h-ANP antiserum significantly increased the spontaneous water intake, urine output and urinary potassium excretion in rats given water ad libitum. These effects developed by 24 h after icv treatment. The h-ANP antiserum had no effect on the urine volume in 48-h water-deprived rats, suggesting a primary effect of endogenous ANP in the brain on the spontaneous water intake in rats given water ad libitum. These results suggest that ANP may have a physiologically important role in the central regulation of the water and electrolyte metabolism. The h-ANP antiserum did not alter the basal and dehydration-induced AVP release. This raises the possibility that the endogenous ANP in the brain may not participate in the control of AVP secretion.

Animals

Effect of vasopressin antagonist d(CH2)5Tyr(Et)VAVP on plasma arginine vasopressin level after osmotic stimulus.

The effect of the vasopressin antagonist d(CH2)5Tyr(Et)VAVP on the immunoreactive arginine vasopressin (AVP) level in plasma was studied in rats after osmotic stimulus. The blood samples were obtained from the eye plexus. An increased AVP level (193.2 +/- 70.0; control: 30.5 +/- 4.3 pmol/l) was detected after the administration of hypertonic NaCl solution. A much higher elevation of AVP level (1180.9 +/- 181.0 pmol/l) was observed when treatment with the antagonist was applied before the osmotic stimulus. The results indicate that this compound exerts a biological effect as a vasopressin receptor blocking agent through a mechanism of competitive antagonism.

Animals

Characterization of oxytocin immunoreactivity in human sympathetic paravertebral ganglia.

Immunoreactive oxytocin (IR-OXT) detected in extracts of human lumbar sympathetic paravertebral ganglia was characterized by high-performance liquid chromatography (HPLC). The immunoreactive substance was found to elute at the same position as the reference preparation of oxytocin (OXT). The results revealed the presence of chromatographically identified OXT in human sympathetic ganglia.

Adult

[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

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

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

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

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

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

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

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

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

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

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