Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rats euhydrated and dehydrated for two or four days were given intracerebroventricularly (i.c.v.) thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride.) A single dose of TRH administered to euhydrated animals was followed by a significant increase of the vasopressin content in the neurohypophysis and hypothalamus as well as of the hypothalamic oxytocin content. On the contrary, a single dose of TRH decreased the oxytocin content in the neurohypophysis. Under conditions of dehydration TRH distinctly restrained the decrease of vasopressin and oxytocin in the hypothalamus. In animals dehydrated for two or four days the decrease of oxytocin in the neurohypophysis, brought about by stimulation of osmoreceptors, was distinctly more marked under treatment with TRH. On the contrary, the depletion of neurohypophysial vasopressin was significantly less apparent under such conditions. 28 nmol/L TRH markedly increased vasopressin release but inhibited that of oxytocin from the neurointermediate lobes incubated in vitro both under basal conditions as well as during stimulation with excess (56 mmol) potassium.
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PMID:Thyrotropin-releasing hormone (TRH) and vasopressin and oxytocin release: in vitro as well as in vivo studies. 130 67

An inhibitory effect on water, sodium and potassium excretion occurs after both systemic and central injections of morphine, beta-endorphin and other opioid peptides. Some investigators claimed that antidiuretic hormone release could be a mechanism explaining opioid-induced oliguria. Injection into the subfornical organ of a synthetic Met-enkephalin analog (FK 33824) reduced urine outflow as well as renal Na+ and K+ excretion. Identical effects were observed in hypophysectomized or in median eminence-lesioned rats. In addition, no changes were seen in blood pressure after FK 33824 injection into the subfornical organ. These results suggest that opioid stimulation of this structure induces an inhibitory effect on renal water, Na+ and K+ excretion, and that antidiuretic hormone release is probably not important to these phenomena.
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PMID:Role of opioid peptides and subfornical organ in the renal function of intact and hypophysectomized rats. 131 88

The action of oxytocin on neurons located in the dorsal motor nucleus of the vagus nerve was studied in brain slices in vitro. It acted postsynaptically and caused a reversible, concentration-dependent excitation of vagal motoneurons in rats. This effect is specific, since it could be mimicked by a selective agonist and suppressed by an oxytocin antagonist. Single-electrode voltage-clamp recordings from rat vagal motoneurons indicated that oxytocin generates a noninactivating inward current, whose amplitude increased as the membrane was depolarized. This current was insensitive to TTX, to a reduction of membrane calcium currents, and to a reversal in the transmembrane chloride gradient; and it was unaffected by several potassium channel blockers. By contrast, it was reversibly reduced by partially substituting extracellular sodium with equimolar N-methyl-D-glucamine. These results suggest that oxytocin exerts its neuronal action in the rat brainstem by generating a sustained voltage-dependent sodium current. Vasopressin activates a similar current when acting on motoneurons located in the facial nucleus of newborn rats. These fast, neurotransmitter-like actions of oxytocin and of vasopressin may provide an explanation--though not necessarily the sole explanation--for their central effects on maternal, sexual, and social behaviors.
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PMID:Electrophysiology of oxytocin actions on central neurons. 132 Aug 38

The effect of papaverine, an inhibitor of the phosphodiesterase responsible for breakdown of cAMP, on the transepithelial sodium transport across the isolated frog skin was investigated. Serosal addition of papaverine caused initially an increase in the short-circuit current (SCC), a doubling of the cellular cAMP content and a depolarization of the intracellular potential under SCC conditions (Vscc). The initial increase in the SCC was followed by a pronounced decrease both in the SCC and in the natriferic action of antidiuretic hormone (ADH), but papaverine had no inhibitory effect on the ability of ADH to increase the cellular cAMP content. As SCC declines, no hyperpolarization was observed. The I/V relationship across the apical membrane during the inhibitory phase, revealed that papaverine reduces the sodium permeability of the apical membrane (PNaa) as well as intracellular sodium concentration. These observations and the previously noted effect of papaverine on Vscc indicates that papaverine must have an effect on the cellular Cl or K permeability. The basolateral Na,K,2Cl cotransporter was blocked with bumetanide, which should bring the cellular chloride in equilibrium. Bumetanide had no effect on basal SCC and Vscc. When papaverine was added to skins preincubated with bumetanide, the effect of papaverine on SCC and Vscc was unchanged. Therefore, the depolarization of Vscc, observed during the papaverine-induced inhibition of the SCC, must be due to a reduction in the cellular K permeability. In conclusion, it is suggested that papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane of the frog skin epithelium.
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PMID:Papaverine reduces the sodium permeability of the apical membrane and the potassium permeability of the basolateral membrane in isolated frog skin. 132 Dec 50

Hyponatraemia (HN) can result from a wide range of mechanisms, and therapy must be individualized. Two theories of the origin of HN in acute brain disease have prevailed. The first is the cerebral salt wasting syndrome (CSWS), where excessive natriuresis caused by some unknown cerebral natriuretic factor lowers the total sodium pool of the body and hence the plasma concentration. The second theory is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), where an increase in total body water is caused by unphysiological secretion of ADH, lowering the concentration of sodium in the plasma. A third possibility is 'sodium shift', i.e. a displacement of sodium from the extracellular to the intracellular space with a simultaneous movement of potassium in the opposite direction. The morbidity and mortality associated with HN only arise in cases where the rate of development of HN was 0.5 mmol h-1 or more. Symptoms respond promptly when the HN is quickly corrected with furosemide and 3% sodium chloride.
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PMID:Hyponatraemia in acute brain disease. 132 60

The cellular action of vasoconstrictive hormones, angiotensin II (AII) and Arg8-vasopressin (AVP), on vascular smooth muscle (VSM) in cultured VSM cells from rat mesenteric artery was studied. Both AII and AVP specifically induce a transient increases in cytosolic free calcium independent of extracellular calcium or calcium channels activated by high potassium depolarization in VSM cells loaded with Fura-2. Vasoconstrictive hormones induce a dose-dependency with formation of inositolphosphates. Analysis using high pressure liquid chromatography has shown that AVP stimulates rapid and transient increases in inositol 1,3,4-trisphosphate, inositol 1,4,5-trisphosphate and inositol 1,3,4,5-tetrakisphosphate within 1 minute. Moreover, a laser-excitation fluorescence system reveals high calcium concentration sites in subsarcolemmal region. These results indicate that, unlike voltage-dependent calcium influx across the cell membrane, AII and AVP induce receptor-mediated increases in cytosolic free calcium via phosphoinositide hydrolysis creating an intracellular messenger for calcium release from intracellular calcium stores.
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PMID:Phosphoinositide hydrolysis and calcium mobilization induced by vasopressin and angiotensin II in cultured vascular smooth muscle cells. 132 68

Experiments were carried out on 32 Nembutal anaesthetized mongrel dogs from both sexes. After 45 min control period unilateral renal ischemia was achieved by clamping the left renal artery for 90 min. In part of the experiments (n = 8) after clamp removal 3 consecutive 45 min periods were performed. The function of the intact right kidney was investigated. Mean arterial pressure (MAP), heart rate (HR), glomerular filtration rate (GFR), urine flow rate (V), fractional excretions of sodium (FENa), potassium (FEK) and chloride (FECl) and plasma levels of atrial natriuretic peptide, dopamine and antidiuretic hormone were evaluated. During ischemia MAP was elevated from 122.5 +/- 3.1 to 140.2 +/- 2.7 mmHg (p < 0.001), HR decreased from 119 +/- 4 to 102.5 +/- 3.9 beats/min (p < 0.01) as compared to the control period. GFR did not change significantly, while all excretory parameters increased: V from 8.7 +/- 1.2 to 14.5 +/- 1.7 microliters/min/gr kidney tissue (p < 0.05); FENa from 2.3 +/- 0.2 to 3.6 +/- 0.3% (p < 0.01); FEK from 40.0 < 3.5 to 51.2 < 2.8% (p < 0.05); FECl from 1.8 < 0.3 to 2.6 < 0.3% (p < 0.05). MAP remained elevated in the first and the second postischemic periods and was paralleled by the sustained increase in FENa and FECl, while FEK remained higher to the end of the experiment. ANP was significantly elevated during ischemia: on 75 min--p < 0.01 and on 105 min.--p < 0.05. AVP and dopamine showed no statistically significant changes during the investigated periods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intact kidney function during contralateral renal artery clamping in dogs. 134 85

The thermal dehydration test was performed in 12 patients with renal transplant and in 20 healthy subjects. The study was aimed at the evaluation of the effect of volume regulating hormones on electrolyte composition of thermal sweat in patients with renal transplant. Blood plasma renin activity (PRA) as well as plasma concentrations of aldosterone (ALD), vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined before and after thermal dehydration in all the subjects studied. In all the subjects sweat was also collected after 15 and 45 minutes of exposition to heat and the concentrations of sodium, potassium and chloride were determined in all sweat samples. Significantly elevated PRA and ANP concentrations and significantly lowered plasma AVP concentrations but normal ALD levels were found before thermal dehydration test in all the patients with renal transplant. After the exposition to heat lasting 1 hour the direction of changes was similar, their magnitude was, however, different in renal transplant patients than in healthy subjects. In addition, lower concentrations of sodium and chloride in thermal sweat and lower total concentration of sweat solids were found in renal transplant patients than in healthy controls. No significant correlation was found between the plasma concentrations of the hormones determined and the electrolyte concentrations of thermal sweat both in the renal transplant patients and in healthy subjects. The results suggest that the volume regulating hormones have no effect on the electrolyte composition of thermal sweat induced by short exposition to heat both in renal transplant patients and in healthy subjects.
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PMID:[Effect of thermal dehydration on blood levels of hormones regulating volume and electrolyte content of sweat in patients with kidney transplantation]. 134 26

Using dispersed cultures of fetal rat hypothalami, we studied the effects of forskolin and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), activators of protein kinase A and C, respectively, upon vasopressin (VP) secretion, VP mRNA expression and VP mRNA poly(A) tail length. Forskolin stimulated the VP mRNA content and peptide secretion 2.6-fold and induced an increase in the poly(A) tail length of approximately 90 nucleotides. TPA induced an increase in VP mRNA size and stimulated 1.9-fold the secretion of VP without an increase in VP mRNA content. Depolarization with potassium induced an increase in the VP peptide secreted of 2.2-fold, with no effect on the VP mRNA content or size. Increased osmolality had no effect on either VP peptide or VP mRNA. We conclude that VP expression in cultured fetal rat hypothalamic cells is regulated via both protein kinase A and protein kinase C pathways.
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PMID:Regulated expression of vasopressin gene by cAMP and phorbol ester in primary rat fetal hypothalamic cultures. 135 50

Rat neural lobes and isolated nerve terminals from the neurohypophysis were stimulated in the presence of different opioid agonists and antagonists. The secretion of arginine vasopressin and oxytocin and rise in cytoplasmic calcium induced by depolarization were analyzed by radioimmunoassay and the fluorescent probe fura-2, respectively. The kappa-agonists dynorphin A(1-13) and dynorphin A(1-8) did not affect electrically evoked release of vasopressin, although oxytocin release was slightly reduced. U-50 488, a relatively specific kappa-receptor agonist, had no effect on the amount of vasopressin or oxytocin secreted, although it significantly reduced K(+)-evoked changes in [Ca2+]i in isolated nerve endings. Two kappa-receptor antagonists, MR 2266 and diprenorphin, alone had no effect on vasopressin and oxytocin secretion from isolated nerve endings depolarized with potassium. Opioid agonists less selective for the kappa receptors, etorphin and ethylketocyclazocin, were found to inhibit the release of both vasopressin and oxytocin significantly. Naloxone, a nonselective opiate receptor antagonist, alone had no effect on vasopressin release but potentiated the electrically evoked release of oxytocin. Naloxone also could overcome the inhibitory effect of etorphin on oxytocin and vasopressin release observed after electrical stimulation of the neural lobe. A number of inconsistencies therefore exist between the effects of opioid agonists and antagonists on neuropeptide release and on the evoked changes in [Ca2+]i. In view of these inconsistencies and the high concentrations of opioid agonists and antagonists necessary to modify release, we conclude that it is doubtful that opioid molecules have a physiological role in controlling neurohypophysial secretion.
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PMID:Intracellular calcium and hormone release from nerve endings of the neurohypophysis in the presence of opioid agonists and antagonists. 135 68


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