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 18 dogs, intracoronary infusion of vasopressin produced a 40% reduction in coronary flow without significantly affecting systemic hemodynamics. The blood flow reduction occurred in a uniform transmural pattern without evidence of a gradient. The reduction in coronary flow resulted in a decrease in regional contractility as determined by isometric strain gauge arches. The decrease in regional contractility was transiently reversed by bolus injection of adenosine into the perfusion line. This suggests that the reduction of blood flow due to vasopressin was causing ischemia. Evidence for ischemia was also supported by measurements of local vein and tissue lactate production. Despite the apparently ischemic conditions, the vascular bed demonstrated evidence for significant reserve and regulation. Pressure-flow relationships performed under control and during vasopressin infusion demonstrated that the coronary vasculature retained its ability to regulate or defend a given level of coronary flow over a range of coronary perfusion pressures. Vasopressin produced a mild decrease in the peak hyperemic flow after a 15-s coronary occlusion and shortened the duration of reactive hyperemia. These overall findings are compatible with a predominant vasoconstrictor effect on the distal coronary vasculature. A role for a myogenic factor in the control of the coronary circulation is suggested, which is amplified by vasopressin.
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PMID:Effects of vasopressin on the coronary circulation: reserve and regulation during ischemia. 398 75

A case of delayed onset of diabetes insipidus (DI), which developed 27 days after a closed head injury, is reported. The patient sustained only a minor neurological deficit and, except for antidiuretic hormone (ADH) insufficiency, hypothalamic function was intact. This selective damage of posterior pituitary function was total and permanent. Ischemia due to vascular injury may be the most likely etiology. Once the diagnosis of delayed posttraumatic DI is confirmed, the treatment of choice is DDAVP (desmopressin acetate). In contradistinction to DI immediately following minor head injury, most patients with a delayed onset of DI after trauma have permanent ADH deficiency.
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PMID:Unusual delayed onset of diabetes insipidus following closed head trauma. Case report. 402 Apr 75

In a randomized controlled trial, the effect of continuous intravenous administration of vasopressin was compared with Sengstaken-Blakemore balloon tamponade in 37 episodes of bleeding esophageal varices in patients with cirrhosis. The majority were Group A and B of Child's classification. Bleeding was controlled in 11 of 17 (65%) patients on vasopressin and in 14 of 20 (70%) patients on tamponade. The patients who failed to respond initially (6 episodes on vasopressin and 5 on tamponade) were treated successfully with the alternative method. Overall mortality was similar in both groups: 3 patients in the vasopressin group and 4 in the tamponade group died. Only one patient died of uncontrolled bleeding; 4 patients probably died of complications of treatment, 2 of cardiac ischemia after vasopressin and 2 of pulmonary infection after tamponade. The vasopressin group required significantly fewer blood transfusions than did the tamponade group.
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PMID:Controlled trial of vasopressin and balloon tamponade in bleeding esophageal varices. 638 98

[(5Z,13E,9 alpha,11 alpha,15S)-2,3,4-Trinor - 1,5 - inter-m - phenylene - 6,9 - epoxy - 11,5 - dihydroxy - 15 - cyclohexyl - 16,17,18,19,20-pentanor]- prosta-5,13-dienoic acid (sodium salt) (CG 4203) is a new stable epoprostenol (prostacyclin) analogue with a relative platelet antiaggregatory potency of 0.46 (ADP aggregation in vitro) and a hypotensive potency of 0.14 (anaesthetized rat i.v.) as compared to epoprostenol. In isolated perfused rat hearts, CG 4203 (4.64 X 10(-9) mol/l) significantly attenuated arrhythmias and loss of left ventricular creatine kinase (CK) activity observed in control hearts after 30 min perfusion with hypoxic and 30 min reperfusion with oxygenated Krebs-Ringer solution. In anaesthetized rats, CG 4203 (1.0 microgram X kg-1 X min-1 i.v.) significantly reduced incidence of ventricular fibrillation and increase in plasma CK activity after ligation of the left coronary artery. Infusion of 1.0 and 2.15 micrograms X kg-1 X min-1 CG 4203 i.v. in anaesthetized rats dose-dependently inhibited electrocardiographic changes, i.e. ST depression observed after i.v. injection of 1.0 IU X kg-1 vasopressin. In rat models of sustained myocardial hypoxia, myocardial infarction, and transient cardiac ischemia, CG 4203 thus exerts cardioprotective effects which, depending on the model considered, may be ascribed to either its vasodilatory, coronary dilatory, antiaggregatory or epoprostenol-like cytoprotective activity.
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PMID:Cardioprotective action of the new stable epoprostenol analogue CG 4203 in rat models of cardiac hypoxia and ischemia. 644 79

An experimental model of amnesia induced by cerebral ischemia after one-trial passive avoidance learning was established to test the effects of a novel compound, 6-(10-hydroxydecyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (idebenone, CV-2619), and some commonly used drugs in rats. One day after the vertebral artery was electrocauterized bilaterally, the common carotid artery was transiently occluded bilaterally to produce cerebral ischemia. The amnesia was estimated by the response latency for a rat to step from a light safety compartment to a dark compartment in which a foot-shock was given. The results of the retention test given 24 hr after the ischemia indicated that amnesia was successfully produced when the 200-600 sec ischemia was provided within 20 min after the avoidance learning. The effects of drugs on the amnesia induced by a 200-sec ischemia immediately after the avoidance learning were as follows: CV-2619 (10, 30 mg/kg, i.p. or p.o.) given before the retention test significantly increased the response latency, indicating a reversal effect on the amnesia. Physostigmine (0.1, 0.2 mg/kg, i.p.) and arginine-vasopressin (10 micrograms/kg, s.c.) were also effective, and calcium hopantenate (500 mg/kg, p.o.) showed a slight reversal action. Furthermore, CV-2619 (10 mg/kg, i.p.), given before or after the ischemia, significantly inhibited the appearance of amnesia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effect of idebenone (CV-2619) on cerebral ischemia-induced amnesia in rats. 654 47

Renal cortical prostaglandin synthesis, particularly by arterioles and glomeruli, is important to preserve renal blood flow (RBF) and glomerular filtration rate (GFR). Glomeruli and arterioles synthesize not only the vasodilatory prostaglandins PGE2 and PGI2, but also the vasoconstrictor, thromboxane A2. The primary renal cortical actions of these prostaglandins are renal vasodilatation and maintenance of GFR (PGE2 and PGI2) or renal vasoconstriction and reduction of GFR (thromboxane A2). Vasodilatory renal prostaglandins are relatively unimportant under normal circumstances but play a modulatory role after ischemia or in the presence of increased concentrations of vasoconstrictor substances such as angiotensin II (ANG II), vasopressin or norepinephrine. ANG II and vasopressin stimulate the synthesis of PGE2 in rat glomerular epithelial and mesangial cells maintained in cell culture. These stimulatory actions of constrictor peptides are dependent upon calcium entry into the cells since removal of extracellular calcium or co-incubation with verapamil or nifedipine block the prostaglandin stimulatory capacity of ANG II or vasopressin. In vivo indomethacin potentiates the actions of ANG II on the kidney, particularly the reduction of RBF and GFR. Isolated rat glomeruli contract in response to ANG II and this contractile effect, which reflects reduction in glomerular filtration surface area, can be potentiated by cyclooxygenase blockade. Conversely, arachidonic acid reduces the glomerular contractile effect of ANG II. The importance of renal prostaglandins in support of RBF and GFR has been studied in dogs after chronic bile duct ligation (CBDL). CBDL dogs have significant increase in renal PGE2 and PGI2 which maintain RBF and GFR since cyclo-oxygenase inhibition resulted in a 50% decrease in both RBF and GFR. Indomethacin, ibuprofen, naproxen, and sulindac sulfide had comparable effects. The pro-drug, sulindac sulfoxide, was tested in normal volunteers and found to spare renal prostaglandin synthesis whereas indomethacin reduced renal synthesis of PGE2 and PGF2 alpha by more than 50%. In vitro, sulindac sulfide is a potent inhibitor of renal prostaglandin synthesis by kidney cells in culture. It is, therefore, concluded that renal prostaglandins play an important vasoregulatory role. Furthermore, sulindac sulfoxide may spare renal cyclo-oxygenase and thereby preserve renal function.
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PMID:Mechanisms of the nephrotoxicity of non-steroidal anti-inflammatory drugs. 659 99

Myoglobinuria and acute renal failure were observed in two patients with vasopressin-treated gastrointestinal hemorrhage. Because there were no other obvious causes of renal failure in either patient, we propose that skeletal muscle ischemia developed during vasopressin infusion, followed by release of myoglobin and renal damage. This association should be considered in the period after vasopressin-treated gastrointestinal hemorrhage.
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PMID:Myoglobinuria and acute renal failure associated with intravenous vasopressin infusion. 661 Sep 43

Glomerular visceral epithelial cells (podocytes) undergo flattening and spreading of major processes detectable by scanning electron microscopy in early postischemic acute renal failure in both animals and man. The authors examined the kinetics of development of these epithelial cell changes in the renal pedicle-clamping model of ischemic renal failure in the rabbit. They found that these changes develop progressively, increasing with increasing length of ischemia, and occur while the pedicle clamp is still in place. To assess the possible role of angiotensin II and vasopressin in producing the epithelial changes, the authors compared glomerular morphology before and during pedicle clamping in hydrated rabbits and in dehydrated rabbits. Dehydration alone produced changes in glomerular epithelial cells comparable to those seen in the postischemic kidney. The angiotensin-converting enzyme inhibitor captopril did not prevent the podocyte changes in either group. In vitro incubation studies confirmed that both angiotensin II and vasopressin produce glomerular epithelial cell changes with a threshold between 10(-7) M and 10(-8) M, a concentration that may be physiologically significant for angiotensin II, which is synthesized at the glomerulus and may have local paracrine effects. Such local synthesis may not be inhibited by systemic administration of captopril. Angiotensin II may play a role in producing podocyte alterations during renal ischemia, as well as in the dehydrated state.
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PMID:Glomerular epithelial cell changes after ischemia or dehydration. Possible role of angiotensin II. 669 12

In order to investigate effects of hydration state, different techniques of collecting blood samples, and of acute, stepwise hemorrhage, we studied plasma vasopressin (AVP) concentration, and plasma renin activity (PRA) in 80 female Wistar rats. Plasma AVP was decreased following hydration with 10 ml of water (1.0 +/- 0.3 pg/ml, mean +/- S.E.M.) as compared to controls (6.1 +/- 2.0 pg/ml), while withdrawal of water for 48 hours stimulated AVP release (29 +/- 8 pg/ml). AVP values in jugular venous blood during light ether anesthesia (9.6 +/- 4 pg/ml) were slightly higher than in trunk blood following decapitation (2.7 +/- 0.7 pg/ml). There was no effect of sham gastric lavage on AVP. PRA was slightly increased in trunk blood and in jugular venous blood following ether anesthesia, and 5-fold increased following 48 h of water withdrawal. In aortic blood obtained during ether anesthesia, AVP-levels were 12- to 560-fold those in control trunk blood. Rapid hemorrhage, 2.0 ml stepwise, resulted in corresponding increases of AVP blood concentration, presumably due to hypothalamohypophyseal ischemia. PRA values showed a similar, albeit less pronounced increase. These results show the importance of controlling conditions of blood sample collection for AVP and PRA analysis, and demonstrate massive release of AVP in response to acute hemorrhage. The amount of AVP released is well about the threshold for pressor activity, and may be of importance in vasoconstrictive adaptation to acute hypovolemic hypotension.
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PMID:Plasma vasopressin concentration and renin in the rat: effect of hydration and hemorrhage. 675 86

The administration of intraaterial mesenteric vasopressin to induce small intestinal ischemia was evaluated in the cat. Small intestinal blood flow was measured by carbonized microsphere distribution and electromagnetic flowmetry. Injection of 99mTc labeled isotope into the superior mesenteric artery was monitored by gamma camera, and isotope kinetics were evaluated as indicators of small intestinal blood flow. Superior mesenteric arterial and small intestinal mucosal blood flow could maximally be reduced to 15%-20% of control by vasopressin administration. 99mTcO4 mesenteric-cardiac transit time was doubled in all animals when small intestinal mucosal blood flow was reduced to less than one-third of control. However, significant blood flow reductions were induced in other abdominal organs, most importantly in retroperitoneal lymph nodes and adipose tissue. Intraarterial mesenteric vasopressin administration does not induce sufficiently severe and specific intestinal ischemia to provide optimal conditions for selective small intestinal hypoxic radioprotection.
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PMID:Mesenteric arterial vasopressin in cats: local and systemic effects. 678 37


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