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)

In acute gastrointestinal bleeding visceral angiography has been showing its importance for years. It contributes to diagnosis especially in cases with persistent acute hemorrhage. In chronic gastrointestinal bleeding conventional radiographic procedures such as upper gastrointestinal series and barium enema will be preferred to angiography. The function of the radiologist goes beyond mere diagnosis of gastrointestinal bleeding. Treatment with vasopressin via the angiographic catheter has proven its clinical value. This method will be indicated especially in cases with high risk anesthesia and surgery. It will help to postpone necessary surgery to a more favorable moment following hemostasis. Side effects such as hypertension and antidiuresis are relatively rare and easy to manage. Numerous substances are used for embolization showing that ideal material has not been found yet and further development seems necessary. In contrast to vasopressin treatment, vascular occlusion is often irreversible, complications (unwanted reflux of embolization material, necrosis and plugging of the catheter) are more difficult to manage. Superselective visualization of a bleeding artery is always needed. Embolization is justified in cases when a possibility for anesthesia and surgery cannot be foreseen. The electrical vascular occlusion using direct current is still in the phase of animal experiments; its clinical value has not sufficiently been assessed as yet.
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PMID:[Angiographic diagnosis and therapy of acute and chronic gastrointestinal hemorrhages]. 30 84

The emergency evaluation of a patient with acute life-threatening gastrointestinal hemorrhage requires the coordinated efforts of medical, surgical, and radiologic personnel. In most patients with an acute upper gastrointestinal hemorrhage, endoscopy represents the primary diagnostic procedure. Arteriography may follow, depending on the identification of the lesion at endoscopy or the need for therapy through the vascular catheter. Arteriography should precede endoscopy when bleeding is massive or the clinical situation suggests that therapy by a catheter must be instituted on a more urgent basis. When personnel are available to perform endoscopy and arteriography, the barium examination of the upper gastrointestinal tract is best postponed for a few days until the patient can be stabilized completely. In the patient with massive red rectal bleeding and a negative nasogastric aspirate, the arteriogram is clearly the procedure of choice for the emergency diagnostic evaluation. Bleeding diverticular and vascular ectatic lesions can be diagnosed only by arteriography and treatment can usually begin immediately by a catheter infusion of vasopressin. Colonoscopic and barium enema examinations of the acutely bleeding patient are not reliable. In addition, the presence of barium in the colon interferes with arteriography for a number of hours. The barium examination of the colon should be performed at some time during the hospitalization to exclude other possible bleeding lesions and to provide a better overall anatomic assessment of the colon. Both the retrograde and antegrade small bowel enemas are useful in detecting obscure small bowel bleeding lesions that occasionally present as a massive lower gastrointestinal hemorrhage.
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PMID:Acute gastrointestinal hemorrhage: the changing role of barium examinations. 30 36

Lower gastrointestinal bleeding from intestinal varices cannot readily be detected at operation; hence, preoperative identification is important. Our experience with six patients having sudden, massive bleeding per rectum from intestinal varices suggests a group of common findings. These patients had cirrhosis, no blood in the stomach or duodenum, characteristic mucosal imprints on barium enema, or direct visualization of varices on sigmoidscopy or colonoscopy. Only two had demonstrable esophageal varices. The diagnosis was confirmed and the site of the varices localized on the venous phase of selective mesenteric angiography in five patients. Varices were located in the duodenojejunum in two, in the cecum and ascending colon in two, and in the rectum and sigmoid colon in two patients. Three patients were treated nonoperatively with transfusion and intraarterial infusion of vasopressin into the superior mesenteric artery; one died. One patient with cecal varices had a right hemicolectomy that controlled the bleeding, but progressive hepatic failure resulted in postoperative death. The remaining two patients had successful decompression of left colonic varices by portasystemic shunt.
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PMID:Massive lower gastrointestinal bleeding from intestinal varices. 31 92

Angiography has added a new dimension to the management of hemorrhage from the large bowel. In patients with diverticular hemorrhage, mesenteric angiography not only localizes the bleeding site but, in addition, the bleeding can be acutely controlled with intraarterial infusion of vasopressin, making an emergency colectomy unnecessary. Similarly in patients bleeding from inflammatory bowel disease or in patients with post-operative hemorrhage, angiography provides information about the nature of the lesion and selective arterial infusions of vasopressin can control the bleeding. At times intestinal varices have angiographically been demonstrated as a potential source of rectal hemorrhage while in patients with unexplained lower gastrointestinal bleeding and repeatedly negative barium and endoscopic examinations, angiography has been valuable for the diagnosis of angiodysplasia of the colon.
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PMID:Angiography in the diagnosis and therapy of hemorrhage from the large bowel. 108 2

Emergency fiberoptic panendoscopy and visceral angiography both had comparable diagnostic accuracy in our series of 55 patients with actively bleeding upper gastrointestinal lesions. The diagnostic accuracy of the barium meal was found inferior to both fiberoptic panendoscopy and visceral angiography. Panendoscopy proved capable of quickly and safely diagnosing site and source of the active bleeding lesion. Visceral angiography requiring additional time, expense and personnel commitment proved an effective back-up procedure when panendoscopy was unsuccessful or contradictions existed. Emergency angiography was well tolerated by gravely ill patients. The therapeutic advantage of angiography with infusion of vasopressin upon completion of the diagnostic study remains to be shown as an advantage over panendoscopy.
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PMID:Diagnostic accuracy of fiberoptic panendoscopy and visceral angiography in acute upper gastrointestinal bleeding. 108 65

During the period of life that precedes weaning, the facial nucleus of the newborn rat is rich in 3H-vasopressin binding sites, and exogenous arginine vasopressin (AVP) can excite facial motoneurons by interacting with V1 (vasopressor-type) receptors. We have investigated the mode of action of this peptide by carrying out single-electrode voltage-clamp recordings in coronal brainstem slices from the neonate. Facial motoneurons were identified by antidromic invasion following electrical stimulation of the genu of the facial nerve. When the membrane potential was held at or near its resting level, vasopressin generated an inward current whose magnitude was concentration related; the lowest peptide concentration still effective in eliciting this effect was 10 nM. The vasopressin-induced current, IAVP, was resistant to tetrodotoxin (TTX) and was insensitive to a reduction in extracellular calcium concentration. It was sustained, was inward at all potentials tested (-120 to -25 mV), and increased in magnitude during depolarization. IAVP was not generated by the blockade of a potassium current, because it did not reverse at hyperpolarized potentials, was not affected by a two-fold increase in the transmembrane potassium gradient, and was not modified by the potassium channel blockers tetraethylammonium bromide (TEA), 4-aminopyridin (4-AP), barium, cesium, quinine, glibenclamide, and apamin. Also, IAVP was not affected by changes in the transmembrane chloride gradient. In contrast, it could be reduced by partially substituting extracellular sodium with equimolar N-methyl-D-glucamine or Tris. Our results suggest that vasopressin increases the excitability of facial motoneurons by generating a persistent sodium-dependent membrane current that is voltage gated and TTX resistant.
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PMID:Vasopressin generates a persistent voltage-dependent sodium current in a mammalian motoneuron. 164 97

The potent vasoconstrictor endothelin leads to smooth muscle cell depolarization and increases in intracellular Ca2+. Although effects of endothelin on calcium channels have been described, it also has been speculated that endothelim may activate additional ion channels. The purpose of the present study was to identify an alternative ion current that could play a role in depolarizing cells in response to vasoconstrictors like endothelin and vasopressin. The effects of endothelin, vasopressin, sarafotoxin S6b, and phenylephrine were assessed using whole-cell patch-clamp recordings from primary dissociated rat aortic or mesenteric arterial smooth muscle cells cultured for 24-72 hours. From the usual resting potentials of these cells of -50 to -60 mV, endothelin (1-100 nM) induced a depolarization via an increase in membrane conductance. This depolarization was phasic, oscillating repeatedly from the resting potential to a relatively depolarized level and back to the resting potential. From a holding potential of -60 mV, endothelin-1, endothelin-3, vasopressin, or sarafotoxin S6b (but not phenylephrine) induced transient inward currents that also could be phasic. In external sodium, lithium, or cesium (but not Tris) and in internal potassium or cesium, these currents reversed near 0 mV. Although nifedipine-insensitive, the inward currents were absent in zero calcium, barium, or strontium, or in the presence of cobalt or nickel. These results represent the first report of a nonselective cation current in primary vascular smooth muscle cells that is calcium dependent and that could be responsible for the depolarizations induced from the resting potential by vasoconstrictors such as endothelin.
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PMID:Endothelin induces a nonselective cation current in vascular smooth muscle cells. 171 35

The A7r5 smooth muscle cell line, which originally was derived from fetal rat aorta, shows spontaneous calcium oscillations associated with electrical activity (frequency of 0.2-0.5 Hz). Organic calcium antagonists such as isradipine (10(-8) M) stopped the calcium oscillations whereas calcium agonists (e.g., Bay K 8644, 10(-8) M) increased the frequency and amplitude of calcium oscillations without changing the shape of the electrical spikes. The enantiomers of the dihydropyridine SDZ 202-791 known to have opposite activity with respect to L-type Ca2+ channels antagonized each other when tested for their effects on the calcium oscillations. The modulation of the activity of these cells by inorganic ions that affect Ca2+ and K+ channels was also investigated. The addition of barium chloride (10(-4) M) to the bathing solution increased the spiking rate whereas cadmium chloride (10(-6) M) abolished the spikes. The vasoconstrictor peptide vasopressin first induced a hyperpolarization associated with the cessation of spiking activity followed by a slow depolarization. The intracellular Ca2+ concentration ([Ca2+]i), measured with the calcium indicator fura-2, was increased transiently to a level about 10-fold above basal and then gained a new steady state at about twice the basal level. Vasopressin stimulated Ca2+ release from intracellular stores (via InsP3), resulting in membrane hyperpolarization through activation of Ca(2+)-activated K+ channels. The late and long-lasting [Ca2+]i elevation was due to Ca2+ influx through dihydropyridine-insensitive channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Modulation of electrical activity and of intracellular calcium oscillations of smooth muscle cells by calcium antagonists, agonists, and vasopressin. 172 8

The efflux of GSH has been shown previously to be a saturable process in both isolated rat hepatocytes and perfused liver, suggesting a carrier-mediated transport mechanism. The possibility in hormonal regulation of this process has been raised by recent reports. Our present work examined the role of hormones known to affect intracellular signal transduction mechanisms on GSH efflux in cultured rat hepatocytes and perfused rat livers. We found that cAMP-dependent factors, such as cholera toxin (CT), dibutyryl cAMP, forskolin, and glucagon all stimulated GSH efflux in cultured rat hepatocytes. The efflux kinetics were compared in cultured cells incubated with or without CT; the stimulation of GSH efflux was related to a near doubling of the Vmax while exhibiting no significant alteration of the Km. The increase in intracellular cAMP level associated with the threshold for this stimulatory effect was 25% above control. The stimulatory effect of CT could not be blocked by cyclohexamide pretreatment or reversed by colchicine treatment. The stimulatory effect of glucagon was abolished in the presence of ouabain but not in the presence of barium. On the other hand, hormones which act through Ca2+ and protein kinase C, such as phenylephrine and vasopressin, had no effect on GSH efflux in the cultured cells. In the perfused liver model, glucagon (10 nM) and dibutyryl cAMP (8 microM) stimulated sinusoidal GSH efflux to 130 and 144% of control values, respectively, and increased bile flow while not affecting biliary GSH efflux. Finally, the physiological significance of glucagon-mediated stimulation of sinusoidal GSH efflux was assessed by both plasma GSH and glucose levels in response to in vivo glucagon infusion. The threshold dose of glucagon for significant increase in plasma GSH (5.21 pmol/min) was lower than for glucose (15.61 pmol/min). At the highest glucagon infusion rate (261 pmol/min), plasma GSH level doubled while glucose level increased 80%. In conclusion, increased cAMP stimulates GSH efflux in cultured rat hepatocytes and perfused livers. The stimulatory effect of cAMP is exerted at the sinusoidal pole and appears to be mediated by hyperpolarization of hepatocytes by stimulation of Na(+)-K(+)-ATPase. In vivo studies confirmed the importance of cAMP-mediated stimulation of sinusoidal GSH efflux as it resulted in significant elevation of the plasma GSH level.
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PMID:Hormonal regulation of glutathione efflux. 216 79

The mechanism of ion transport across principal cells of rat cortical collecting tubules (CCT) and its regulation by vasopressin (ADH) has been studied in the isolated perfused tubule. To amplify the response to ADH rats were treated with 5 mg I. M. desoxycorticosterone 4-9 days prior to the experiments. Addition of 2 X 10(-10) mol X l-1 ADH increased the transepithelial voltage from -5.1 +/- 0.7 mV to -16.1 +/- 1.4 mV (n = 37) and decreased the transepithelial resistance from 51 +/- 4 omega cm2 to 39 +/- 2 omega cm2 (n = 33). Optical and functional differentiation of impalements of principal and intercalated cells was made and only data of principal cells are presented. ADH depolarized the apical membrane from 79 +/- 1 mV to 66 +/- 2 mV (n = 26) and decreased the fractional resistance of the apical membrane from 0.76 +/- 0.04 to 0.70 +/- 0.04 (n = 13). These ADH effects were prevented by 10(-5) or 10(-4) mol X l-1 luminal amiloride which hyperpolarized the apical membrane when added in the presence or absence of ADH. Apical and basolateral membranes were dominated by large K+ conductances and addition of 3 mmol X l-1 barium to bath or lumen perfusates increased transepithelial resistance almost two-fold, whereas luminal amiloride increased the transepithelial resistance only by 26-35%. Ouabain (0.5 mmol X l-1, bath) depolarized the basolateral membrane and decreased its K+ conductance. These effects were prevented by the simultaneous presence of apical amiloride suggesting that the only route of Na+ entry into the principal cells occurred via the amiloride sensitive Na+ conductance. We conclude that ADH stimulates Na+ reabsorption and K+ secretion in the rat CCT primarily by increasing the Na+ conductance in the apical cell membrane.
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PMID:Electrophysiological studies in principal cells of rat cortical collecting tubules. ADH increases the apical membrane Na+-conductance. 244 57


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