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PubMed1975

Activation of rat kidney adenylate cyclase by vasopressin analogues: lack of correlation with antidiuretic activity.

Vasopressin analogues with enhanced antidiuretic activity in vivo (deamino-[D-arg8]-vasopressin, deamino-6-carba-[Orn8]-vasopressin, deamino-6-carba-[Arg8]-vasopressin, and deamino-6-carba-[D-Arg8]-vasopressin) were tested for their ability to activate rat renal medullary adenylate cyclase and compared to the natural antidiuretic hormones [Arg8]- and [Lys8]-vasopressin. The enzyme preparation used did not inactivate the vasopressins or the analogues tested. The analogues activated adenylate cyclase. However, several of them were far less effective than expected on the basis of their very high in vivo antidiuretic activity. It was concluded that the enhanced in vivo activity reflects greater metabolic stability in vivo rather than enhanced affinity for the renal antidiuretic hormone receptor.

Adenylyl Cyclases↗
PubMed1996

A benzodiazepine, chlordiazepoxide, blocks vasopressin and oxytocin release after footshocks but not osmotic stimulus in the rat.

Noxious as well as hypertonic stimuli potentiate vasopressin and oxytocin secretion in rats. Neurohypophysial vasopressin- and oxytocin-secreting neurons receive inhibitory synaptic inputs mediated by gamma-aminobutyric acid (GABA). Benzodiazepines modulate GABA-A receptor activity in a facilitatory fashion. It is thus possible that benzodiazepines suppress vasopressin and oxytocin release after noxious stimuli. To test this hypothesis, we investigated whether chlordiazepoxide impairs the enhanced release of vasopressin and oxytocin after noxious or hypertonic stimuli in male rats. Chlordiazepoxide (5-20 mg/kg, i.p.) blocked dose-dependently the vasopressin and oxytocin responses to footshocks. Chlordiazepoxide, however, did not impair the hormonal responses to hypertonic stimulus. The results demonstrate that chlordiazepoxide selectively prevents vasopressin and oxytocin release after noxious stimuli and therefore suggest that the sites of chlordiazepoxide actions are not on the vasopressin or oxytocin neurons in rats.

Animals↗
PubMed1975

Metabolic actions of vasopressin, glucagon and adrenalin in the intact rat.

Metabolic effects of vasopressin, glucagan and adrenalin were compared, in intact rats, especially in regard to time courses of effects. Hyperglycaemia was transient in response to vasopressin, prolonged following adrenalin, and, suprisingly, was not discernible after glucagon, except in response to a very large dose. Vasopressin decreased and adrenalin increased, the plasma free fatty acid concentration; both hormones decreased the triacylglycerol level. Muscle glycogen concentrations, measured in heart, diaphragm and skeletal muscle, exhibited small changes, with complex time courses, following hormone administration. Vasopressin brought about a rapid but transient activation of heaptic glycogen phosphorylase which resembled that due to adrenalin. The activation by glucagon of phosphorylase was greater and more prolonged, despite the absence of hyperglycaemia. In response to vasopressin, there was in increase in plasma insulin. Incorporation of 14C from [14C]glucose into glycogen or fatty acids was not influenced by vasopressin. Taken together, these results may be explained by rapid metabolic action of vasopressin on hepatic glycogenolysis, whereas adrenalin has multiple prolonged actions.

Adipose Tissue↗
PubMed1991

Opioid synapses on vasopressin neurons in the paraventricular and supraoptic nuclei of juvenile monkeys.

Opioid peptide- as well as vasopressin-containing neurons synapse on gonadotropin releasing hormone neurons in juvenile macaques. In this study we performed double-label immunostaining for opioid and vasopressin neurons in the paraventricular and supraoptic nuclei in order to assess their interrelationships. Neuroendocrine neurons in the hypothalamus were prelabeled by microinjection of electron-dense retrograde tracer into the median eminence, and were easily identified in frontal Vibratome sections. Sections through the paraventricular and supraoptic nuclei were immunostained for vasopressin with the peroxidase-antiperoxidase technique, and for opioids using the indirect immunogold method. By light microscopy, opioid-immunoreactive inputs appeared to innervate an average of 39% of the vasopressin neurons in the paraventricular nucleus and 33% in the supraoptic nucleus, and were more prevalent anteriorly. Clusters of opioid afferents formed cup-like calices around major processes of many vasopressin neurons, especially in the paraventricular nucleus. Electron microscopy revealed that these groups of opioid axon terminals made frequent symmetrical and fewer asymmetrical synapses on both neuroendocrine and non-neuroendocrine vasopressinergic cell bodies and dendrites. Our study did not reveal vasopressin-opioid synapses in these hypothalamic nuclei, but this does not preclude the possibility of their existence elsewhere. These results indicate that opioid afferents modulate vasopressin neuronal activity in the monkey paraventricular and supraoptic nuclei. Previous results have suggested that corticotropin releasing hormone acts via vasopressinergic neurons to stimulate opioid neuronal activity and to inhibit gonadotropin releasing hormone release. Taken together, the data suggest that stressful stimuli could initiate a series of neuropeptidergic interactions which ultimately alter pulsatile gonadotropin releasing hormone secretion and thus gonadotropin secretion in primates.

Afferent Pathways↗
PubMed1993

Annual variations in the vasopressin neuron population of the human suprachiasmatic nucleus.

The mammalian suprachiasmatic nucleus is considered to be the major component of the biological clock, involved in the temporal organization of a wide variety of physiological and behavioral processes. The present study was conducted to investigate whether there are diurnal or annual variations in the morphology of the vasopressin-containing neuron population of the suprachiasmatic nucleus in human beings. To that end, the brains of 48 human subjects were investigated. A marked annual variation was observed in the volume and vasopressin cell number of the human suprachiasmatic nucleus: the volume of the vasopressin cell population was, on average, 2.5 times larger in October-November than in May-June and contained 2.7 times as many vasopressin-immunoreactive neurons. In general, the annual cycle of the human suprachiasmatic nucleus showed a non-sinusoidal pattern with a maximum in early autumn, a lower plateau in winter and a deep trough in late spring and early summer. In contrast, no such seasonal variations could be detected in suprachiasmatic nucleus vasopressin numerical cell density or cell-nuclear diameter. The number of vasopressin-immunoreactive neurons in the paraventricular nucleus of the hypothalamus, on the other hand, did not show any significant periodic changes over the year, indicating the specificity of the suprachiasmatic nucleus rhythm. In contrast with the annual cycle of the suprachiasmatic nucleus, no significant diurnal variations were observed in any of these parameters. In conclusion, the findings indicate that photoperiod may be considered a potential environmental factor controlling the activity of the vasopressin system of the human suprachiasmatic nucleus.

Adolescent↗
PubMed1996

Oxytocin and vasopressin mRNA expression in rat hypothalamus following kainic acid-induced seizures.

In this study, the regulation of hypothalamic oxytocin and vasopressin messenger RNA expression following the induction of seizures was investigated by in situ hybridization. Following kainic acid-induced seizures, a significant increase in oxytocin messenger RNA in the paraventricular nucleus was demonstrated at 1.5 h, one and two weeks; its level decreased at three weeks and was significantly increased again at four weeks; at eight weeks the messenger RNA level still remained higher than that of controls. Vasopressin messenger RNA in the paraventricular nucleus was increased significantly only at 1.5 h following induction of seizures. The oxytocin messenger RNA level in the supraoptic nucleus was also increased early at 1.5 h and later at four weeks following seizures; however, these increases did not last as long as those in the paraventricular nucleus. Vasopressin messenger RNA in the supraoptic nucleus was also increased after the initial seizures; however, its messenger RNA level vacillated up and down throughout the post-seizure times studied. The earliest significant increase of vasopressin messenger RNA was at one week after seizures, and there was a late significant increase of vasopressin messenger RNA at three weeks after seizures. The present study demonstrates that following kainic acid-induced seizures both, the oxytocin and vasopressin messenger RNA expressions, were up-regulated and these up-regulations were long-term events. The increase of oxytocin messenger RNA in the paraventricular nucleus was more persistent than the others. The pattern of messenger RNA up-regulation was different for oxytocin and vasopressin, and different in the paraventricular nucleus and supraoptic nucleus. These different patterns of messenger RNA elevations suggest that the different components of the rat hypothalamus were regulated differentially by kainic acid-induced seizures.

Animals↗
PubMed1996

Immunocytochemical evidence for the presence of vasopressin in intermediate sized neurosecretory granules of solitary neurohypophyseal terminals in the homozygous Brattleboro rat.

A single base deletion (delta G) in the vasopressin gene is the cause of diabetes insipidus in the homozygous Brattleboro rat (di/di). The resulting frameshift leads to the expression of an aberrant vasopressin precursor which is unable to enter the secretory pathway, thereby preventing vasopressin biosynthesis. In a small number of solitary magnocellular hypothalamic neurons within the supraoptic and paraventricular nuclei, the reading frame is restored by a dinucleotide (delta GA) frameshift mutation, at two separate GAGAG motifs downstream of the original G-deletion. This results in two + 1 di-vasopressin precursors that are still partially mutated within the neurophysin region. The present study provides immunocytochemical evidence which demonstrates that, within magnocellular solitary neurons of the supraoptic and paraventricular nuclei of the di/di rat, the + 1 di-vasopressin precursors can enter the secretory pathway followed by their enzymatic processing into vasopressin during axonal transport to the neural lobe. However, the cellular characteristics of biosynthesis are different from those of wild-type rats. Immunoelectron microscopical localization of vasopressin gene products in the neural lobe of did/di rats revealed their presence in neurosecretory granules, the diameter of which is intermediate (116 nm) between those of the neurosecretory granules in the di/di (80-100 nm) and wild-type (160 nm) rats.

Animals↗
PubMed1991

Solid-phase extraction of plasma vasopressin: evaluation, validation and application.

A new solid-phase extraction method using octyl-silica columns to extract vasopressin-like immunoreactivity from plasma has been developed. The extraction was followed by a radioimmunoassay on the vacuum-dried extracts, which were reconstituted in assay buffer. The total recovery of synthetic vasopressin was ca. 100%. Based on co-elution with synthetic vasopressin after separation by reversed-phase high-performance liquid chromatography of plasma extracts from normal Wistar and Brattleboro rats, and the cross-reactivity of the antiserum used in the radioimmunoassay system, the extracted material was found to be indistinguishable from authentic vasopressin. Unknown experimental samples were interpolated on a standard curve established in "zero" plasma (plasma derived from rats subjected to waterload) spiked with known amounts of synthetic vasopressin, and not on a standard curve established in assay buffer. The limit of detection was 1 fmol of vasopressin equivalent per millilitre. The intra- and inter-assay coefficients of variance were 10-16% and 16%, respectively. The procedure reliably showed that osmotic challenge and 24-h dehydration increased, whereas ethanol ingestion decreased vasopressin-like immunoreactivity plasma levels in the rat, compared with normally hydrated controls.

Animals↗
PubMed1992

Baroreflex loading maneuvers do not suppress increased plasma arginine vasopressin in patients with congestive heart failure.

Nonspecific baroreflex loading maneuvers such as head-down tilt readily suppress stimulated arginine vasopressin levels in normal humans. To test the hypothesis that the increased arginine vasopressin levels in patients with congestive heart failure would not respond normally to baroreflex loading, 12 patients with congestive heart failure had arginine vasopressin levels and osmolality determined in the supine position and after 15 min of 30 degrees head-down tilt. Arginine vasopressin was increased to 6.5 +/- 2.0 pg/ml at control measurement and did not decrease. Eight patients underwent further study after osmotic stimulation with mannitol. Mannitol increased osmolality from 287 +/- 9.2 to 294 +/- 7.8 mOsm/kg (p less than 0.001) and from 288 +/- 9 to 299 +/- 8.2 mOsm/kg (p less than 0.01) on two occasions. No significant suppression of arginine vasopressin was seen during head-down tilt after mannitol infusion compared with values in a time control period. These results are consistent with an abnormality in baroreflex suppression of arginine vasopressin secretion in chronic congestive heart failure and suggest that such a defect may contribute to long-term high levels of arginine vasopressin in this condition.

Adult↗
PubMed2005

Angiotensin-induced vasopressin release and activation of hypothalamic neuron in pre-term fetuses.

Our previous studies have shown that central administration of angiotensin II (ANG II) causes vasopressin release in the near-term fetus in utero as evidence that the hypothalamic-neurohypophysial system has relatively matured before birth. However, it is still unknown whether the vasopressin controlling centers have been functionally developed in younger fetuses. This study determined fetal plasma vasopressin levels and hypothalamic vasopressin neuron activity in the chronically instrumented pre-term ovine fetuses. Introcerebroventricular (i.c.v.) administration of ANG II did not affect fetal plasma osmolality and sodium concentrations. However, fetal plasma vasopressin levels were significantly increased ( approximately 3-fold) in response to central injection of ANG II. Central ANG II also induced vasopressin-neuron activity marked with c-fos expression in the fetal hypothalamus at pre-term. In addition, the fetal organum vasculosum of the lamina terminalis and the subfornical organ were activated. The results suggest that hypothalamic-neurohypophysial system has been relatively intact and functional at 70% gestational age, and that central angiotensin is important in inducing fetal vasopressin release in utero.

Angiotensin II↗
PubMed2004

Vasopressin excitatory action on smooth muscle from human renal calyx and pelvis.

The motor response to vasopressin, a neuropeptide promoting the reabsorption of water, was isometrically investigated in vitro in human renal calyces and pelvis in relation to possible modulation of urinary flow by these tubular structures. Kidneys were obtained from nine male patients who underwent nephrectomy for either renal or ureteral cancer. Minor calyces and pelvis were carefully removed. Strips (10 mm x 3 mm) were cut from infundibular region of minor calyces and from renal pelvis and placed in 10 ml organ bath for isometric tension recordings. Calyceal and pelvic smooth muscle strips exhibited spontaneous phasic contractions which occurred with regular frequency and amplitude. Vasopressin induced a dose-dependent [10(-10) to 10(-6) M] enhancement of basal tone (P <0.01) and a decrease of spontaneous contractions on isolated strips from minor calyces and pelvis. The effect of vasopressin was inhibited by prior administration of D(CH2)5Tyr(Me)2-Arg8-Vasopressin antagonist [10(-7) M]. The excitatory response to vasopressin was Tetrodotoxin [TTX]-resistant and was not affected by pre-treatment with phentolamine [10(-5) M], atropine [10(-5) M], and hexamethonium [10(-5) M]. After incubation of the specimens in Ca2+-free medium containing EGTA [0.5 mM] or after treatment with nifedipine [10(-5) M], both spontaneous and vasopressin-induced contractions [10(-10) to 10(-6) M] were completely inhibited in all specimens. Our results can be interpreted to imply that the tonic contractions induced by vasopressin facilitate the reabsorption of water by increasing the hydraulic resistance of the tubular structures below collecting ducts.

Dose-Response Relationship, Drug↗
PubMed2004

Vasopressin versus continuous adrenaline during experimental cardiopulmonary resuscitation.

OBJECTIVE: To evaluate the effects of a bolus dose of vasopressin compared to continuous adrenaline (epinephrine) infusion on vital organ blood flow during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation was induced in 24 anaesthetised pigs. After a 5-min non-intervention interval, CPR was started. After 2 min of CPR the animals were randomly assigned to receive either vasopressin (0.4 U/kg) or adrenaline (bolus of 20 microg/kg followed by continuous infusion of 10 microg/(kg min)). Defibrillation was attempted after 9 min of CPR. RESULTS: Vasopressin generated higher cortical cerebral blood flow (P < 0.001) and lower cerebral oxygen extraction (P < 0.001) during CPR compared to continuous adrenaline. Coronary perfusion pressure during CPR was higher in vasopressin-treated pigs (P < 0.001) and successful resuscitation was achieved in 12/12 in the vasopressin group versus 5/12 in the adrenaline group (P = 0.005). CONCLUSIONS: In this experimental model, vasopressin caused a greater increase in cortical cerebral blood flow and lower cerebral oxygen extraction during CPR compared to continuous adrenaline. Furthermore, vasopressin generated higher coronary perfusion pressure and increased the likelihood of restoring spontaneous circulation.

Animals↗
PubMed2003

Comparison of the in vivo coronary action of endothelin-1 and vasopressin role of nitric oxide and prostanoids.

To compare the coronary effects of endothelin-1 and vasopressin, as well as the role of nitric oxide (NO) and prostanoids in these effects, blood flow in the left circumflex (73 animals) or left anterior descending (19 animals) coronary artery (coronary flow) was electromagnetically measured, and both peptides were intracoronarily injected in anesthetized goats under control conditions and after intravenous administration of the inhibitor of NO synthesis NW-nitro-L-arginine methyl ester (L-NAME, 47 mg/kg, nine animals) or the inhibitor of cyclooxygenase meclofenamate (6-8 mg/kg, seven animals). In every animal, both endothelin-1 and vasopressin reduced coronary flow in a dose-dependent way, but these reductions by 0.03, 0.1 and 0.3 nmol of endothelin-1 (16%, 33% and 66%, respectively) were significantly higher than those by the equimolar doses of vasopressin (11%, 22% and 35%, respectively). After L-NAME treatment, the reductions of coronary flow by both peptides were augmented, and this augmentation was about two times higher for endothelin-1 than for vasopressin. Meclofenamate treatment did not affect the reductions of coronary flow caused by both peptides. Therefore, we suggest that endothelin-1 is more effective than vasopressin for producing coronary vasoconstriction, but vasopressin also produces remarkable coronary vasoconstriction. Also, it is suggested that NO may play a more relevant role for modulating the coronary vasoconstriction by endothelin-1 than by vasopressin, and that cyclooxygenase products may not be involved in the coronary effects of these two peptides.

Animals↗
PubMed2003

A double-blind randomized trial: prophylactic vasopressin reduces hypotension after cardiopulmonary bypass.

BACKGROUND: Inhibition of angiotensin-converting enzyme (ACE) predisposes patients to vasodilatory hypotension after cardiopulmonary bypass (CPB). This hypotension has been correlated with arginine vasopressin deficiency and can be corrected by its replacement. In patients receiving ACE inhibition, we investigated whether initiation of vasopressin before CPB would diminish post-CPB hypotension and catecholamine use by avoiding vasopressin deficiency. METHODS: Cardiac surgical patients on ACE inhibitor therapy were randomized to receive vasopressin (0.03 U/min) (n = 13) or an equal volume of normal saline (n = 14) starting 20 minutes before CPB. RESULTS: Vasopressin did not change pre-CPB mean arterial pressure or pulmonary artery pressure. After CPB, the vasopressin group had a lower peak norepinephrine dose than the placebo group (4.6 +/- 2.5 versus 7.3 +/- 3.5 microg/min, p = 0.03), a shorter period on catecholamines (5 +/- 6 versus 11 +/- 7 hours, p = 0.03), fewer hypotensive episodes (1 +/- 1 versus 4 +/- 2, p < 0.01), and a shorter intensive care unit length of stay (1.2 +/- 0.4 versus 2.1 +/- 1.4 days, p = 0.03). CONCLUSIONS: In this cohort, prophylactic administration of vasopressin, at a dose without a vasopressor effect pre-CPB, reduced post-CPB hypotension and vasoconstrictor requirements, and was associated with a shorter intensive care unit stay.

Adult↗
PubMed2000

Arginine vasopressin in the treatment of 50 patients with postcardiotomy vasodilatory shock.

BACKGROUND: The barroreflex-mediated secretion of arginine vasopressin has been found to be defective in a variety of vasodilatory shock states, such as postcardiotomy shock, and administration of the hormone markedly improves vasomotor tone and blood pressure. The high incidence of vasodilatory shock in patients undergoing left ventricular assist device (LVAD) implantation makes this population an ideal model in which to assess the risks and benefits of vasopressin. METHODS: The medical records of the 102 patients receiving LVADs at Columbia-Presbyterian Medical Center from January 1995 to August 1998 were reviewed. Fifty patients were eligible for study based on a history of arginine vasopressin administration in the operating room or intensive care unit within 24 hours of implantation. RESULTS: Despite LVAD implantation and the administration of vasopressors, patients were hypotensive with a mean arterial pressure less than 60 mm Hg. The administration of vasopressin (0.09+/-0.05 U/min) increased mean arterial pressure (58+/-13 to 75+/-14 mm Hg; p<0.001) while reducing norepinephrine administration (11.7+/-13 to 7.9+/-6.0 mcg/min; p = 0.023). There was no significant change in LVAD flow. The incidence of compromised regional perfusion was not different between LVAD patients who received vasopressin as compared to hemodynamically stable LVAD patients who did not receive vasopressin. CONCLUSIONS: We have demonstrated vasopressin at low doses to be a safe and an effective vasopressor in 50 patients with postcardiotomy vasodilatory shock.

Arginine Vasopressin↗
PubMed1986

Inhibitory roles of the hypothalamic atrial natriuretic polypeptide on the vasopressin release in the sodium-loaded rats.

Implication of the brain atrial natriuretic polypeptide on the vasopressin release was investigated using rats fed with a high-sodium containing diet. Sodium loading increased not only the blood pressure but also the urinary output of vasopressin significantly. The plasma vasopressin concentration increased about 10 times after the intracerebroventricular injections of angiotensin II. Thereby, magnitude of the response was significantly smaller in the rat fed with a high sodium diet than in rats with the regular-diet. The hypothalamic content of both vasopressin and atrial natriuretic polypeptide was significantly larger in the high-salt group than the regular-salt. The intraventricular injections of atrial natriuretic polypeptide abolished the vasopressin release induced by the intraventricular injections of angiotensin II. These results indicate that the vasopressin production in the hypothalamus is increased, but the release is relatively suppressed in the sodium-loaded rats, and that increased hypothalamic atrial natriuretic polypeptide is involved in the suppression of the vasopressin release and in decreasing their sodium appetite to avoid the high sodium environment.

Angiotensin II↗
PubMed1988

Rapid development of vasopressin-induced hydroosmosis in kidney collecting tubules measured by a new fluorescence technique.

The pre-steady-state kinetics of the vasopressin-induced increase in collecting tubule osmotic water permeability (Pf) has been measured by a new fluorescence technique. Isolated cortical collecting tubules (CCT) from rabbit kidney were perfused with physiological buffers containing the impermeant fluorophores fluorescein sulfonate (FS) and pyrenetetrasulfonic acid (PTSA). Tubules were subject to a 120 mOsm bath-to-lumen osmotic gradient in the presence and absence of 250 microU/ml vasopressin. The magnitude of transepithelial volume flow was determined from the self-quenching of FS, or from the ratio of PTSA/FS fluorescence, measured at 380 nm excitation and 420 +/- 10 nm (PTSA) and greater than 530 nm (FS) emission wavelengths. Pf was calculated from the magnitude of transepithelial volume flow, lumen and bath osmolarities, lumen perfusion rate, and tubule geometry. The instrument response time for a change in bath osmolality was less than 3 s. At 37 degrees C, CCT Pf was (in units of cm/s x 10(4] 13 +/- 2 (mean +/- SE, 16 tubules) before, and 227 +/- 10 after addition of vasopressin to the bath. CCT Pf began to increase in 23 +/- 3 s after vasopressin addition and was half-maximal after 186 +/- 20 s. At 23 degrees C, Pf was 9 +/- 1 (seven tubules) before, and 189 +/- 12 after vasopressin addition. Pf began to increase in 40 +/- 4 s and was half-maximal after 195 +/- 35 s. After vasopressin removal from the bath, Pf decreased to its baseline value with a half-time of 14 min. These results establish a direct fluorescence method to monitor instantaneous transepithelial Pf in perfused tubules and show a very fast stimulation of CCT Pf in response to vasopressin.

Animals↗
PubMed1999

The neurotensinergic synaptic innervation of vasopressin containing neurons in the rat hypothalamic paraventricular nucleus.

A recent physiological report suggested that neurotensin could inhibit the vasopressin releasing from vasopressin-producing neurons in the hypothalamic paraventricular nucleus but not in the supraoptic nucleus. In the present study, the synaptic relationship between the neurotensin-like immunoreactive and vasopressin-like immunoreactive neurons has been examined using a pre-embedding double immunostaining technique in the rat hypothalamic paraventricular nucleus. At the light microscopic level, many neurotensin-like immunoreactive fibers were found near the vasopressin-like immunoreactive neurons. At the electron microscopic level, the neurotensin-like immunoreactive fibers were identified as axon terminals that made many synapses on the vasopressin-like immunoreactive perikarya and dendrites. The synapses were both asymmetrical and symmetrical. These findings of the present study suggest that the inhibitory effect of neurotensin on the vasopressin neurons in the hypothalamic paraventricular nucleus may be due to the direct synapses made by neurotensin-like immunoreactive axon terminals on the vasopressin-like immunoreactive neurons.

Animals↗