Changes In Vasopressin Levels Research Articles

Oxytocin delivered nasally or intraperitoneally reaches the brain and plasma of normal and oxytocin knockout mice

Intranasal delivery of oxytocin (Oxt) has been identified as a potential therapeutic to target human conditions characterized by social deficits, yet the ability of this administrative route to deliver to the brain is unconfirmed. Oxt knockout (Oxt KO) and wildtype C57BL/6 J male mice received Oxt (12 μg total amount) either by nasal or intraperitoneal administration. Oxt concentrations were monitored for 2 h after administration in circulation via a jugular vein catheter and in the brain by two intracerebral microdialysis probes. Group sizes varied from 4 to 7 mice (n = 22 total). We document for the first time that Oxt applied to the nasal mucosa after nasal administration is delivered to the extracellular fluid in the brain. After nasal application, Oxt concentrations in circulation and in the extracellular fluid of the amygdala and, to an extent, the dorsal hippocampus, rose within the first 30 min and remained elevated for the subsequent hour. These findings were confirmed in an Oxt KO mouse line, establishing that the circulating and brain Oxt elevations derive from the administered dose. Interestingly, the pharmacokinetics of Oxt were slightly biased to the brain after nasal administration and to the periphery following intraperitoneal injection. No change in vasopressin levels was detected. These findings have stimulating implications for the interpretation of various behavioral and physiological effects described in animal and human studies after nasal administration of Oxt and provide the pharmacokinetics necessary to develop this drug delivery route for therapeutic purposes.

Attenuating the hormonal response to rigid bronchoscopy; comparison between iv fentanyl, dexmedetomidine or lidocaine

Hormonal stress response due to manipulation of the upper and lower respiratory tracts occurring during rigid bronchoscopy represents a potentially great hazard to safeanesthesia.There were many attempts to attenuate these adverse effects.Dexmedetomidine is highly selective, short-acting central alpha 2 agonist. It has increasingly gained popularity among anesthesiologists as adjuvant to general and regional anesthesia techniques. This study was conducted to compare the efficacy of administrating fentanyl, dexmedetomidine or lidocaine on control of hormonal changes in response to rigid bronchoscopy in pediatric patients. Ninety ASA I-II children aged 2-12 year were randomly assigned to 3 groups: fentanyl (F), dexmedetomidine (D) and lidocaine (Z). cortisol, ACTH and vasopressinlevels were measured and recorded. Results revealed that patients in the D group showed less elevation of ACTH levels in in response to the insertion of the rigid bronchoscope compared with the other groups, cortisol levels increased significantly after bronchoscopy in the lidocaine group, meanwhile, changes in vasopressin levels were not significant between the groups We concluded that dexmedetomidine can be used safely and effectively to attenuate the hormonal responses to rigid bronchoscopy in pediatric patients.

Presence of Oxytocin, Vasopressin and Atrial Natriuretic Peptide and Their Modification in Rat Hypothalamic Paraventricular Nucleus During Resistance Training

Many studies have demonstrated the physiological effects of oxytocin (OT), atrial natriuretic peptide (ANP) and vasopressin (VP) in the homoeostasis of body fluids during physical exercise. However, a little information is available about the related immunohistochemical changes in hypothalamic magnocellular neurosecretory system during and after the training. The aim of the present work was to study the immunohistochemical changes in OT, ANP and VP levels in the hypothalamic paraventricular nucleus during and after resistance exercise protocol. Three groups of Wistar rats were trained by a rung ladder protocol for 15, 30 and 45 days, respectively; a fourth group was left to rest for 15 days after the training. Finally, four sedentary groups were used as controls. The results show that resistance training induces a significant reduction in the percentage of OT-positive neurons, compared with sedentary controls. In contrast, this protocol did not induce any change in VP levels, and ANP levels did not change significantly. However, VP increased after the resting period of 15 days. Our work shows that neurons of the paraventricular nucleus are involved in body fluid homoeostasis during and after resistance exercise. The functional significance of these changes in OT and VP levels, during and after the protocol, needs to be further investigated.

Renal hemodynamics during carbon dioxide pneumoperitoneum: an experimental study in pigs.

Laparoscopic living donor nephrectomy is increasingly being performed, although the effects of carbon dioxide pneumoperitoneum (CO2 PP) on renal function and hemodynamics and the levels of vasopressin are not well studied. Renal blood flow, renal venous pressure, urine output, and vasopressin concentrations in renal venous blood were measured in pigs subjected to 12 mmHg of CO2 PP for 150 min. Renal blood flow was decreased at induction of PP and increased during the first 30 min after exsufflation. Renal venous pressure was increased during PP. There was indirect evidence of a decrease in urine output during PP. No changes in renal venous vasopressin concentrations were seen. A CO2 PP of 12 mmHg causes changes in renal hemodynamics and urine output. No changes in vasopressin levels were seen in this pig model, suggesting that other explanations for the observed changes must be sought.

Stress increases oxytocin release within the hypothalamic paraventricular nucleus

Evidence indicates that the hypothalamic paraventricular nucleus (PVN) and oxytocin (OT) neurons in particular play a role in the physiological response to stress. Microdialysis (MD) experiments were performed to determine whether OT is released into the PVN during shaker stress. Male rats were prepared with venous catheters and PVN guide cannulae. OT and vasopressin (VP) release into PVN and peripheral blood were measured under basal conditions and during and after shaker stress (10 min at 110 cycles/min). Stress produced a specific increase in PVN and plasma OT. Dialysate OT levels were 0.3±0.1, 2.8±1.2 and 1.3±0.6 pg/sample (control, stress and recovery, respectively). Plasma OT was significantly increased during stress (3.7±1.2 vs. 11.7±2.3 pg/ml, basal vs. stress, respectively). When MD probes were located outside the PVN, there was no increase in OT release, demonstrating site specificity. Stress produced no change in VP levels, either in dialysate or plasma. These results show that OT, but not VP, is released into the PVN and peripheral blood in response to shaker stress. The data raise the possibility that local release of OT into the PVN plays a role in the neuroendocrine stress cascade.

Clonidine stimulates atrial natriuretic factor (ANF) release in water-deprived rats.

To determine the effect of clonidine, an alpha 2-adrenergic agonist, on atrial natriuretic factor (ANF) release during water deprivation, plasma immunoreactive ANF (IR-ANF) arginine vasopressin, diuresis and natriuresis were measured in rats which had been deprived of water for 24 and 48 hr after intravenous (IV) administration of 50 micrograms clonidine. In normally-hydrated rats clonidine produced a marked elevation of plasma IR-ANF from 40.5 +/- 4.6 pg/ml to 1064 +/- 22 pg/ml (mean +/- SEM) and sodium excretion from 73.3 +/- 6.8 microEq to 723.4 +/- 62.3 microEq. Clonidine evoked an increase in plasma IR-ANF from 16.6 +/- 5.9 pg/ml to 229.5 +/- 60 pg/ml (mean +/- SEM) after 24 hr water deprivation and from 13.6 +/- 7.4 pg/ml to 104.8 +/- 21 pg/ml (mean +/- SEM) after 48 hr water deprivation. Clonidine did not induce any significant changes in vasopressin levels. During 24 hr and 48 hr water deprivation vasopressin rose from 3.1 +/- 0.3 pg/ml to 7.3 +/- 1.3 pg/ml and 8.4 +/- 0.6 pg/ml (mean +/- SEM), respectively. In normally-hydrated rats clonidine produced a marked diuresis and natriuresis. These effects and urinary cGMP excretion were significantly inhibited by anti-ANF antibodies. Clonidine caused a significant increase in urine output in 24 hr water-deprived rats but the response was markedly lower than that seen in normally-hydrated rats. In conclusion, clonidine stimulates ANF release both in normally-hydrated and water-deprived rats. The diuretic effect of clonidine appears to be related to ANF release but not to inhibition of vasopressin.

Cold water stimulation of oropharyngeal receptors in man inhibits release of vasopressin.

The act of drinking ameliorates thirst and inhibits the secretion of vasopressin before changes in extracellular fluid volume or osmolality in both animals and man. We evaluated whether this reflex inhibition of vasopressin secretion might be due to the presence of oropharyngeal receptors in humans. After dehydration, normal subjects (n = 4) were allowed to suck on ice chips for 30 min. Despite the absence of changes in plasma sodium (Na+) or osmolality, the mean plasma vasopressin level decreased promptly within 10 min from 2.8 to 1.8 pg/mL, and it remained low for 30 min after ice ingestion. When the dehydration protocol was repeated with the subjects receiving 100 mL water (25 C) for 30 min rather than ice chips, plasma vasopressin levels did not change. These data demonstrate that activation of cold-sensitive oropharyngeal receptors results in inhibition of vasopressin secretion independently of osmotic or gastric factors. In a second study 0.2 mL/kg X min 3% NaCl was administered for 90 min as a second stimulus to vasopressin secretion, and ice chips were given during the last 30 min of infusion. Plasma vasopressin levels increased steadily to 3.3 +/- 0.5 (+/- SEM) pg/mL by 45 min, and despite ice ingestion increased further to 4.6 +/- 0.8 pg/mL by 90 min. Consequently, hypertonicity appears to be a stronger stimulus to vasopressin release, since the suppressive effect of stimulation of oropharyngeal receptors with ice was not evident during the NaCl infusion. Finally, no changes in vasopressin levels were found in subjects holding concentrated NaCl solutions in their mouths for 30 min, indicating that the oropharyngeal receptors are not responsive to local changes in osmolality. The presence of such cold-sensitive oropharyngeal receptors may explain the desire of severely dehydrated patients, e.g. patients with diabetes insipidus, for cold liquids.

Pseudotumor cerebri associated with obstructive nephropathy

We report two infants with pseudotumor cerebri associated with renal disease. The pathogenesis of increased intracranial pressure in this clinical setting is unclear, but may be mediated by one or more of the conditions commonly associated with pseudotumor cerebri, including sinus thrombosis, increased intravascular fluid volume, anemia, and endocrine disturbances resulting in abnormal calcium and phosphorus metabolism. The onset of pseudotumor cerebri also may be related to changes in vasopressin levels that affect brain water permeability.

Changes in the vasopressin content of discrete brain regions in response to stimuli for vasopressin secretion.

In order to better understand the function of vasopressin-containing axons which project to areas outside the hypothalamus, we measured vasopressin content in hypothalamic and extrahypothalamic brain regions following various periods of oral hypertonic saline or 1 week after pituitary stalk section. The supraoptic and paraventricular nuclei and nearly all of the brain regions examined which are known to receive vasopressin-containing axons from these nuclei showed parallel changes in vasopressin levels in response to both stimuli. In response to hypertonic saline there was an initial rise followed by a fall in vasopressin content. The suprachiasmatic and lateral septal nuclei, as well as the nucleus of the solitary tract, were unaffected by either stimulus. These results indicate that there are at least two functionally different vasopressin systems within the central nervous system, one of which is responsive to osmotic stimulation.