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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acetylcholine (1 and 50 mug), carbamylcholine (1 and 10 mug), and oxotremorine (10 mug) were infused into the 3rd ventricle of rats with deafferented medial basal hypothalamus (MBH); infusions failed to stimulate ACTH release as shown by the plasma corticosterone level. Implants of an atropine-fluorescein mixture (200-250 mug) inhibited the stress-induced rise of plasma corticosterone only when dye from the implant stained large portions of the median eminence and the basal hypothalamus. Atropine implants near the electrodes inhibited the rise in plasma corticosterone usually produced by electrical stimulation in the anterior hypothalamus. Atropine crystals or a 2% atropine sulphate solution placed on the median eminence blocked conduction of action potential in the hypothalamo neurohypophyseal and tubero-infundibular pathways. The evidence will be discussed for and against the participation of a cholinergic synapse (in the MBH) that activates ACTH release after stressful neural stimuli.
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PMID:The effects of cholinomimetic drugs and atropine on ACTH release. 18 78

Acetylcholine and nicotine stimulated vasopressin (VP) release from the organ-cultured rat hypothalamo-neurohypophyseal system (HNS). Nicotinic antagonists, hexamethonium, tetraethylammonium chloride, and trimethaphan blocked VP release in response to acetylcholine and nicotine. A muscarinic agonist, methacholine, was ineffective in eliciting VP release from HNS explants at a molar concentration equal to the maximally effective concentration of acetylcholine (10(-5) M). Atropine, a muscarinic antagonist, was an ineffective blocking agent for acetylcholine. These data indicate that the cholinergic receptor in the HNS explant is nicotinic rather than muscarinic in character.
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PMID:Characterization of cholinergic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system. 43 24

A nicotinic-cholinergic receptor appears to mediate osmotic stimulation of vasopressin (VP) release by the hypothalamo-neurohypophyseal explant. Nicotinic blocking agents, hexamethonium, tetraethylammonium chloride, and trimethaphan, blocked VP release in response to the addition of sufficient NaCl to yield a 10 mosm/kg H2O increase in culture medium osmolality. Atropine at a similar molar concentration was ineffective in blocking VP release in response to the same osmotic stimulus. Tetraethylammonium chloride and trimethaphan also blocked acetylcholine-stimulated VP release. These findings support the hypothesis that the osmoreceptive element responsible for controlling VP release resides in a separate cell and communicates with the VP cell by way of a nicotiniccholinergic receptor.
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PMID:Cholinergic involvement in osmotic control of vasopressin release by the organ-cultured rat hypothalamo-neurohypophyseal system. 45 15

1. Unanaesthetized normal and water-loaded rats were tested for cardiovascular and antidiuretic responses to intracerebroventricular (I.V.T.) injections of prostaglandin E2 (PGE2). 2. I.V.T. injections of PGE2 produced tachycardia and a slow rise in blood pressure that reached a peak in 15 min and lasted up to 2 hr. 3. Intravenous pre-treatment with phenoxybenzamine, an alpha-adrenergic blocker, inhibited pressor but not heart rate responses to I.V.T. PGE2. Pre-treatment with propranalol, a beta-adrenergic blocker, inhibited tachycarcia but not pressor responses to I.V.T. PGE2. Atropine attenuated heart rate and blood pressure responses when higher doses of PGE2 were tested. 4. In water-loaded rats, I.V.T. PGE2 produced antidiuretic effects suggesting release of antidiuretic hormone in subpressor amounts. Antidiuretic but not cardiovascular responses to I.V.T. PGE2 were abolished by median eminence lesions. 5. Intravenous PGE2 infusions produced a decrease in blood pressure and no antidiuretic effects, indicating that both responses were centrally mediated. 6. The results indicate that I.V.T. PGE2 produces pressor and tachycardia responses in the unanaesthetized rat which are mediated primarily by centrally mediated sympathetic outflow.
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PMID:Cardiovascular and antidiuretic effects of central prostaglandin E2. 46 13

Dopamine (DA) and several blocking substances were administered into the 3rd ventricle of conscious goats to study the effects on water and electrolyte excretion. Intracerebroventricular infusion of DA in hydrated goats induced a significant dose-dependent inhibition of both the urine flow rate and the renal free water clearance. A biphasic response pattern of urinary electrolyte excretion, consisting of an initial fall, followed by an increase in the excretion rate was observed. The antidiuretic effects induced by DA could be prevented by prior administration of haloperidol, pimozide or phentolamine into the 3rd ventricle. Atropine, hexamethonium or propranolol were ineffective. It seems that excitatory responses of periventricular neurons resulting in vasopressin release in the goat may be mediated by both alpha-adrenoceptors and excitatory DA receptors. Furthermore, single injection of haloperidol or pimozide into the 3rd ventricle of goats with a normal water balance induced both a significant diuretic response and an increase in renal free water clearance. The data suggest that endogenous DA in the hypothalamus could be responsible for vasopressin release.
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PMID:Effect of intracerebroventricular administration of dopamine on urinary function in goats. 52 66

The vasopressin release rate from incubated in situ rats posterior pituitary lobe as observed following intracarotid infusions of hypertonic solutions (3 x 0.1 ml/100 g b.w. contained 1.0 mmol NaCl and 0.1 mmol CaCl2 per 1 ml) was studied when influenced by intraventricular injections of 0.6 microgram carbachol or 240 microgram atropine sulphate, respectively. The increase in the release of vasopressin following intracarotid infusions of hypertonic solution augmented by intraventricular injection of carbachol was found. Atropine was shown to be effective in preventing the vasopressin release caused by hypertonic solution. The effects of carbachol and atropine indicate that mediation at synapses in the nucleus supraopticus involved in the release of vasopressin induced by osmotic stimulation is cholinergic.
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PMID:Vasopressin release from incubated in situ posterior pituitary lobe after intraventricular injection of carbachol or atropine. 73 15

Central angiotensin effects may include baroreceptor alterations and/or ventilated, were given angiotensin intravertebrally (10 ng/kg/min), into a lateral cerebroventricle (0.4 microgram/min) or intravenously (10 ng/kg/min). Surgery was completed under methoxyflurane anesthesia; wounds were periodically infiltrated with viscous tetracaine and the methoxyflurane discontinued. The experiments were performed with the brain unanesthetized to optimize detection of an angiotensin effect on the cardioinhibitory component of the baroreceptor reflex. Bradycardia was evoked by norepinephrine injections (2 microgram/kg i.v.). Intraventricular and intravertebral angiotensin increased basal mean blood pressure 16 mm Hg (p less than 0.05); norepinephrine-induced pressor responses and bradycardia were unaffected by the peptide. Intravenous angiotensin did not affect basal blood pressure; a 16 mm Hg increase (p less than 0.05) in the norepinephrine pressor response with no change in bradycardia was observed. Atropine reversed the norepinephrine bradycardia and increased the pressor response in all cats, thus demonstrating the integrity of the reflex. We conclude that centrally administered angiotensin produces no change in the cardioinhibitory reflex to an acute pressor stimulus. The possibility of a peripheral effect of the peptide exists. The hypertensive response observed in the conscious spinal cats after central angiotensin infusions could be due to vasopressin release and/or action of the peptide at cardiovascular sites at high spinal levels.
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PMID:Norepinephrine-induced reflex bradycardia after central administration of angiotensin II. 91 46

Duriing water diuresis in conscious goats, noradrenaline (NA), its antagonists phentolamine, phenoxybenzamine and propranolol and also atropine were administered into the 3rd ventricle. The subsequent effects on water diuresis and on the excretion rates of Na+, K+ and Cl- were investigated. Infusion of NA into the 3rd ventricle induced a strong and significant antidiuretic response and a decrease in the Na+ : K+ excretion ratio; these effects were dose-dependent. High doses of NA produced a significant increase in urinary K+ excretion. Similar results were observed after i.v. administration of arginine-vasopressin. Pretreatment with phentolamine injected into the 3rd ventricle produced a dose-dependent inhibition of the NA-induced antidiuretic effects. Phenoxybenzamine also blocked the response to NA but a dose-response relationship was not apparent. Atropine and propranolol did not block the response to NA.
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PMID:Effect of intraventricular administration of noradrenaline on water diuresis in goats. 119 13

Abdominal cramps and urgent defecation are common side effects of clinical doses of arginine vasopressin, indicating that the drug may have stimulating effects on colonic motor activity. Four strain-gauge transducers were implanted on the colon in six monkeys. A blood flow probe was fixed on the inferior mesenteric artery. After a 1-hour control recording, vasopressin, 0.13, 1.3, or 13.0 ng.kg-1.min-1, was infused intravenously for 90 minutes. The frequency of basal colonic contractions was reduced with increasing doses of vasopressin, but their mean amplitude and duration were not altered. Giant migrating contractions associated with defecation were initiated by the highest dose of vasopressin. Atropine had no effect on these giant migrating contractions but completely inhibited normal phasic contractions. Hexamethonium completely inhibited both giant migrating contractions and phasic contractions. Parasympathetic denervation of the colon did not inhibit giant migrating contractions initiated by vasopressin. Our findings suggest that the physiological concentrations of serum vasopressin present perioperatively may transiently inhibit spontaneous colon contractions but are unlikely to be the major cause of postoperative ileus. The giant migrating contractions initiated by vasopressin may account for the defecation associated with pharmacological doses of vasopressin. The initiation of giant migrating contractions by vasopressin may be mediated through a neural pathway.
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PMID:Arginine vasopressin inhibits phasic contractions and stimulates giant contractions in monkey colon. 134 30

A portion of medial basal hypothalamus containing the supraoptic nuclei with the neurohypophysis attached was organ cultured. Hypothalamus and neurohypophysis were maintained in separate compartments, and the intact infundibular stalk passed through a hole in a fluid-tight barrier which separated the two compartments. After 24, 48 and 72 h in culture, vasopressin (VP) release from the neurohypophysis was measured during a control hour and again during an immediately subsequent test hour. Test hour VP release was expressed as a percentage of control hour release. Test substances were added to either the pituitary or the hypothalamus compartment. Acetylcholine stimulated pituitary VP release both when added to hypothalamus (10(-5) M) and when added directly to neural lobe (10(-6) M and above). Acetylcholine 10(-5) M had no effect when isolated neural lobes (severed from hypothalamus to culture) were similarly tested. Hexamethonium blocked the stimulation of pituitary VP release evoked by addition of acetylcholine to hypothalamus. However, in pituitary, atropine prevented the stimulatory effect of acetylcholine. Atropine had no effect on VP release from severed neural lobes. These data show that high concentrations of acetylcholine can stimulate VP release from pituitary both by a hypothalamic action and also by a direct effect in neural lobe. Further, a nicotinic cholinergic receptor mediates the action of acetylcholine in hypothalamus whereas a muscarinic cholinergic receptor is involved in the direct pituitary response to acetylcholine. Intact axonal connections between hypothalamus and pituitary are required in order for acetylcholine to stimulate VP release in neurohypophysis.
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PMID:The compartmentalized hypothalamo-neurohypophysial system: evidence for a neurohypophysial action of acetylcholine on vasopressin release. 286 80


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