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)

The facilitation of peptide secretion from the neurohypophysis induced by increasing stimulation frequency is accompanied by action potential (AP) prolongation. One hypothesis argues that inactivation of potassium channels in the neural lobe terminal membranes, under these conditions, is the underlying mechanism which leads to AP prolongation, and, therefore, increased calcium entry and secretion per AP. Therefore, factors which are known to cause AP prolongation, such as stimulus frequency and potassium channel blocking agents, were studied and compared with regard to their ability to augment electrically evoked release of oxytocin (OT) and vasopressin (VP) from isolated rat neurointermediate lobes (NILs). OT release (to a constant applied stimulus of 600 spikes) was maximally facilitated by increasing frequency up to a rate of 30 Hz, whereas VP release in the same stimulus paradigm was maximal between 12 and 20 Hz. Tetraethylammonium (TEA), 4-aminopyridine (4AP) and barium each caused a significant augmentation of AP-dependent, electrically stimulated hormone release, without affecting basal levels. The magnitude of the effect of the K channel blocking agents was inversely related to the frequency of the applied stimulus. Application of either 4AP or TEA caused a shift in the range of frequency dependence for OT such that maximal release was seen at a stimulus frequency of 12 Hz, but there was no comparable change in the pattern of VP release. The maximal effects of TEA and 4AP were additive indicating that the NIL terminals have two types of K channels which appear to be involved in the regulation of secretion. Addition of the three agents together produced maximal release at a stimulus frequency of 4 Hz, which was not facilitated further by the increase of stimulus frequency to 20 Hz. These data demonstrate the importance of potassium channels in the regulation of VP and OT secretion, and provide indirect support for the spike prolongation hypothesis of frequency facilitated secretion in the neural lobe.
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PMID:Effects of stimulus frequency and potassium channel blockade on the secretion of vasopressin and oxytocin from the neurohypophysis. 244 64

Continuous membrane voltage (V) recordings were obtained in A10 vascular smooth muscle cells (rat aorta) using glass microelectrodes. Resting membrane voltage in 262 impalements averaged 54.0 +/- 0.4 (SE) mV. Relative K+ conductance was characterized, and the contribution of electrogenic Na+-K+-ATPase to membrane voltage was investigated. Action potentials could be induced by application of 1 mM barium or 10(-4) M acetylcholine. In a few recordings, spontaneous spike activity occurred, and this could be abolished by 5 mM MgCl2 or by removal of extracellular Ca2+. Barium-induced action potentials were not dependent on the presence of extracellular Na+ and not inhibitable by 10(-6) M tetrodotoxin. Application of 10(-6) M [Arg8] vasopressin (AVP) for 30 s caused a typical biphasic membrane voltage response with an initial transient hyperpolarization of -9.5 +/- 1.1 mV and a more sustained subsequent depolarizing response averaging 28.2 +/- 1.3 mV (mean +/- SE, n = 58). The effect of AVP on membrane voltage was blocked by the V1-antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,O-Me- Tyr2,Arg8]vasopressin. The initial hyperpolarizing component of the membrane voltage response to AVP became more prominent when V was predepolarized, for example, by a preceding AVP application. However, when AVP was applied during high K+ depolarization or in the presence of quinidine (1 mM), the initial hyperpolarizing response was practically abolished. The time course of the initial hyperpolarization was shown to be similar to the calcium transient observed in fura-2-loaded A10 cell suspensions after the application of AVP. We conclude that the initial AVP-induced hyperpolarization in A10 cells corresponds to an activation of Ca2+-activated K+ channels.
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PMID:Continuous membrane voltage recordings in A10 vascular smooth muscle cells: effect of AVP. 254 89

Methods of diagnosis and treatment of lower gastrointestinal bleeding depend on the rate of bleeding and the amount of blood lost. If bleeding is occult, colonoscopy is the single best way to determine the source, if bleeding is gross but mild, causing melena or small amounts of hematochezia, colonoscopy or a combination of flexible sigmoidoscopy and double-contrast barium enema should be used to evaluate the colon. In most patients with melena, the upper tract must be examined endoscopically. Acute lower gastrointestinal bleeding stops spontaneously in 75 to 90 per cent of patients, permitting preparation of the colon before colonoscopy. If bleeding is continuing, diagnostic options include colonoscopy with no preparation of the colon, relying on the cathartic effect of blood, or a red cell radionuclide scan followed by angiography if the scan is positive. A bleeding lesion seen on angiography is usually treated by infusion of vasopressin. Colonoscopic treatment of a bleeding site uses the BICAP probe, heater probe, or argon laser. Patients who bleed severely and those who do not respond to treatment or rebleed after treatment are candidates for operation. Segmental resection is preferred if the bleeding site is known. If not, total colectomy with ileorectal anastomosis may be necessary. A mortality rate of 10 to 15 per cent in patients with severe bleeding reflects the advanced age of many of these patients and the difficulty of managing gastrointestinal bleeding in the presence of associated medical conditions.
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PMID:Colonoscopic diagnosis and treatment of lower gastrointestinal bleeding. 259 25

For the patient and the clinician, it is well that small-bowel diseases are unusual, as our ability to access this area remains limited. Frequently, all of the diagnostic and therapeutic modalities of radiology, endoscopy, and surgery are required for successful resolution of a given problem. Because management of bleeding from a small-bowel source usually will involve the surgeon at some point, it is mandatory that the best "road map" be obtained prior to exploration. If a small-bowel source is suspected after a negative endoscopic evaluation of the esophagus, stomach, duodenum, and colon, then the clinician must decide which radiographic and endoscopic examination is most appropriate. If bleeding is slow or intermittent, push-type enteroscopy to evaluate the proximal jejunum will have an expected diagnostic discovery rate of about 30 per cent. A stiffening over-tube or internal cable should result in deeper passage of the instrument and a potentially greater yield. Retrograde ileoscopy should be a part of every colonoscopy done for occult bleeding. If endoscopy does not identify a bleeding source, then a detailed barium study of the small bowel using an enteroclysis double-contrast technique will discover more pathology than a standard small-bowel-follow-through. Because sonde-type enteroscopes are not readily available, the clinician must decide at this point whether to refer the patient to an enteroscopist or consider surgery and intraoperative endoscopy. If a bleeding source has been found, then intraoperative endoscopy can localize lesions for specific resection. If the pathology remains obscure, intraoperative endoscopy will have a discovery rate of about 70 per cent. For more active hemorrhage, a bleeding scan with 99mTc-labeled red blood cells can confirm that blood loss is continuing and also will guide the angiographer toward a more directed study, thus decreasing the contrast material load for the patient. If a bleeding source can be identified angiographically, a short course of vasopressin infusion to convert the need for surgical intervention to a more elective situation would be beneficial to the patient. Intraoperative endoscopy under urgent conditions is more difficult, because luminal blood must be lavaged or cleared for a proper examination. Many times, however, intraoperative endoscopy can "surround" a segment of intestine by identifying areas that are clearly normal.
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PMID:Endoscopy of the small intestine. 268 52

The present study was conducted to measure norepinephrine release during sympathetic nerve stimulation and to evaluate vascular reactivity in the isolated perfused mesenteric vasculature of normotensive and Doca-salt hypertensive rats. Significantly greater vasoconstrictor responses to periarterial nerve stimulation, norepinephrine, and vasopressin, but not to barium chloride, were observed in the mesenteric vasculature of the hypertensive rats in comparison with the control normotensive group. Norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation at 4 Hz for 2 min, was identical in both normotensive and hypertensive animals. Phentolamine (5.3 micro M) significantly increased tritium overflow, but to the same extent in the normotensive and the hypertensive mesenteric vasculature, suggesting that the negative feedback presynaptic alpha-adrenoceptor mechanism, which has been proposed to modulate transmitter release, was unaltered in this form of hypertension. These results indicate that hyperresponsiveness of the mesenteric vasculature to periarterial nerve stimulation in the hypertensive rats is due to increased sensitivity of the vascular alpha-adrenoceptor and not facilitation of the transmitter release. The increased vascular reactivity to norepinephrine and vasopressin may be involved in the maintenance of Doca-salt hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in Doca-salt hypertensive rats. 625 76

We recently investigated the effect of chronic sympathetic denervation on the intact ear vasculature of normotensive rabbits and found an important long-term or trophic influence of sympathetic nerves on vascular structural properties. To determine the effect of coarctation hypertension on this relationship, we studied 12 wk old rabbits 8 wk after a unilateral superior cervical ganglionectomy and induction of coarctation hypertension. Successful denervation was demonstrated by a shift of the norepinephrine dose-response curve to the left in the denervated ears as well as a decreased threshold (p less than 0.05), an increased slope (p less than 0.02) and a decreased M50 (p less than 0.01) (the concentration of norepinephrine that produced 50% of the maximal vasoconstrictor response to norepinephrine). The flow-pressure curves of the denervated compared to the innervated ears at maximal dilation (used as a functional assessment of structural alterations) did not differ. The maximal pressor responses to vasopressin and barium chloride (used as an indication of smooth muscle mass) also did not differ. These results suggest that sympathetic innervation does not importantly influence blood vessel structure during coarctation hypertension in contrast to the changes we previously found in normotensive rabbits.
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PMID:The trophic influence of sympathetic nerves on rabbit ear vasculature is absent in coarctation hypertension. 666 Oct 40

The contraction of the potassium depolarized pulmonary artery of the guinea pig was diminished by the calcium antagonists nifedipine, gallopamil, diltiazem, verapamil and prenylamine. The drugs are listed here in order of activity. The uptake of 45Ca of the depolarized pulmonary artery was reduced by nifedipine, verapamil and prenylamine in this order of activity. The depression of the coronary flow of the isolated guinea pig heart, which was brought about by barium chloride, antigenic rabbit serum or vasopressin plus oxytocin was reduced by infusion of prenylamine. The positive inotropic effect of K-strophanthin on the isolated, electrically stimulated left atrium of the guinea pig heart was reduced by gallopamil, verapamil, prenylamine, diltiazem and nifedipine in this order of activity.
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PMID:Effects of calcium antagonists on coronary spasm and pulmonary artery contraction in comparison to their antagonistic action against K-strophanthin in isolated guinea pig atria. 710 Feb 59

Increased neurotransmitter release during sympathetic nerve stimulation may contribute importantly to the maintenance of spontaneous hypertension. Therefore, transmitter release and vascular reactivity were measured in perfused mesenteric vasculature of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Increase in norepinephrine release, measured as total tritium overflow, during periarterial nerve stimulation was significantly greater in SHR than in WKY, as was the vasoconstrictor response. Even after blockade of neuronal uptake with cocaine (10 microM), or of neuronal as well as extraneuronal uptake with cocaine plus metanephrine (20 microM), norepinephrine overflow was still greater in SHR than in WKY. The greater vasoconstrictor response in SHR still persisted following uptake blockade. Phentolamine (5.3 microM) increased transmitter overflow markedly but equally in both SHR and WKY thereby suggesting that increased transmitter release in SHR was not due to alterations in presynaptic alpha-adrenoceptor mechanism. Vascular reactivity not only to periarterial nerve stimulation but also to norepinephrine, vasopressin, and barium chloride was increased in SHR. These results suggest that, in SHR, increases in norepinephrine release as well as vasoconstrictor reactivity contribute to the maintenance of hypertension.
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PMID:Sympathetic nerve function and vascular reactivity in spontaneously hypertensive rats. 730 83

Acute renal failure was produced in vasopression-pretreated rabbits by clamping the left renal pedicle for one hour and removing the opposite kidney. Treatment with clonidine, as antihypertensive drug that blunts the kidney's response to vasopressin, resulted in significantly higher creatinine clearance and urine flow rate in the first 6 hours after unclamping. Clonidine (30 microgram/kg given intravenously 30 minutes before unclamping) also significantly lessened the number of hyaline casts in outer medullary tubules and inner medullary loops of Henle 6 hours after unclamping and reduced the number of abnormal tubular contours in microadiograms produced by infusing barium sulfate into the renal artery at sufficient pressure to rupture glomerular capillaries, causing an escape of contrast material into the tubules. The spaces consistently observed between the ends of barium columns and hyaline casts in microdissection studies and the great lengths of the hyaline casts suggest that hyaline casts obstruct the flow of tubular fluid. Clonidine treatment resulted in fewer, shorter, and thinner hyaline casts. These results indicate that tubular obstruction by hyaline casts plays an important role in early postischemic acute renal failure, and that clonidine's beneficial effect is due in part to a reduction in cast formation.
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PMID:The effect of clonidine on tubular obstruction in postischemic acute renal failure in the rabbit demonstrated by microradiography and microdissection. 735 Aug 13

Vascular reactivity to vasoconstrictors in relation to altered thyroid function was studied in two preparations: aortic strips and the isolated perfused kidney. To assess whether the possible alterations in vascular reactivity were restricted to a specific agonist or whether they involved the contractile system, receptor-mediated and nonspecific smooth muscle stimulants were used. Male Wistar rats were divided into three groups: control, hyperthyroid and hypothyroid rats. Aortic strips from hypothyroid rats were less sensitive to phenylephrine and KCl when the data were expressed in absolute values or as percentages of the maximum responses. Sensitivity and reactivity in strips from hyperthyroid rats were similar to those observed in control strips. Renal vasculature obtained from hypothyroid rats also showed a markedly reduced sensitivity to phenylephrine, with normal maximal responses. The response to vasopressin at 3-10(-11) mol/l was also decreased, as was the reactivity to barium chloride. In contrast, renal vasculature of hyperthyroid rats showed markedly enhanced reactivity to all agonists: the concentration-response curves were characterized by a similar threshold and a greater maximal response. These results demonstrate that hypothyroidism is accompanied by a marked decrease in sensitivity to vasoconstrictors in large arteries as well as in resistance vessels. This decrease may be secondary to a generalized alteration in the contractile system of vascular smooth muscle cells and may play a role in the decreased blood pressure in these animals. In contrast, isolated perfused kidneys of hyperthyroid rats showed increased vascular reactivity to vasoconstrictors, which may play a role in the maintenance of elevated blood pressure in these animals.
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PMID:Vascular reactivity to vasoconstrictors in aorta and renal vasculature of hyperthyroid and hypothyroid rats. 783 89


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