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)

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

Principles of management of bleeding esophageal varices are 1. fluid therapy of bleeding shock, 2. prevention of hepatic coma, 3. emergency endoscopy, 4. balloon tubes (Senkstaken-Blakemore, Linton-Nachlas), and 5. with some restriction, selective infusion of vasopressin into the a. mesenterica superior. If these procedures fail, sclerosing of esophageal varices stops bleeding in more than 90% of the cases. Bleeding from varices of the gastric fundus may be stopped by gastro-esophageal disconnection (Pettinari-Hassab). Both procedures have with 15% and 25% respectively, the lowest mortality. Patients for surgical shunt are carefully selected within the interval after bleeding. Shunts are the distal splenal-renal and the mesenteric-caval anastomosis with dacron prothesis (H-shunt). The shunt is the favorable therapy for prehepatic block in patients older than 14 to 16 years. The endoscopic sclerosing of esophageal varices and the gastro-esophageal disconnection are chosen in younger patients or when shunt procedures are not possible. The posthepatic block is treated successfully by conservative means. In most cases, surgical therapy is contraindicated because of poor prognosis. When conservative measures fail, in few cases emergency endoscopic sclerosing of esophageal varices or latero-lateral porto-caval anastomosis can be tried.
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PMID:[Diagnostic and therapeutic measures in acute catastrophic bleeding esophageal varices]. 108 18

Conscious rats were given i. p. polyethylene glycol (PEG) or dextran injections to compare their efficacy in inducing moderate hypovolaemia. Dextran was found unsuitable, producing large variability in the plasma vasopressin (AVP) concentrations. Putative neurotransmitters involved in the AVP response to hypovolaemia and in basal release were examined using opioid, and beta-adrenoceptor and dopamine receptor-blocking agents. A dose of PEG was chosen to produce a decrease in blood volume of approx 14.5% giving plasma AVP concentrations of 19.0 +/- 4.6 pmol/l. Naloxone and phenoxybenzamine failed to influence AVP release under both hypovolaemic and basal conditions. Prazosin also failed to influence the AVP response. In contrast propranolol elevated the plasma AVP concentrations in both conditions. Haloperidol enhanced basal AVP release but did not influence release during hypovolaemia. Guanethidine pretreatment partially blocked the response to hypovolaemia, but did not affect basal plasma AVP. Thus it appears that aminergic pathways have an inhibitory influence on AVP release under hypovolaemic and basal conditions. However, endogenous opioids do not appear to contribute significantly to the hypovolaemic response.
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PMID:Vasopressin release in response to hypovolaemia in the conscious rat and the effect of opioid and aminergic receptor antagonists. 168 65

Vasopressin infusion and esophageal tamponade are still widely used to arrest variceal bleeding, but no objective evidence exists on the superiority of either of the two procedures. In this study, 108 cirrhotic patients bleeding from varices were included in a prospective, randomized trial to investigate the comparative effectiveness and safety of balloon tamponade (using the Sengstaken-Blakemore tube for esophageal varices and the Linton-Nachlas tube for gastric varices) (n = 52) and intravenous vasopressin infusion (0.4 to 0.8 mu/min) plus intravenous nitroglycerin infusion (40 to 400 micrograms/min) (n = 56). Both treatments were maintained for 24-hr. The hemostatic efficacy according to the intention to treat was 86.5% for tamponade and 66% for pharmacological therapy (p less than 0.01). No significant differences were found with respect to rebleeding during the first 72 hr after treatment, mortality rate or side effects. These results suggest that esophageal tamponade is more effective than vasopressin/nitroglycerin infusion in the treatment of variceal bleeding in cirrhotic patients.
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PMID:Vasopressin/nitroglycerin infusion vs. esophageal tamponade in the treatment of acute variceal bleeding: a randomized controlled trial. 211 50

The management of both acute and recurrent variceal bleeding continues to be a significant challenge to the clinician. The cause and pathogenesis of portal hypertension has been described. Alcoholic cirrhosis is the most common cause of intrahepatic sinusoidal and postsinusoidal obstruction in the United States. Long term survival depends on rapid institution of an established protocol of surgical management for variceal hemorrhage. A patient who presents with variceal bleeding must be rapidly stabilized with fluid resuscitation, and specific measures, such as the use of vasopressin and balloon tamponade, must be instituted to control hemorrhage so that endoscopy can be used to establish the diagnosis. Sclerotherapy achieves a high rate of success in the acute situation, but if hemorrhage cannot be controlled, percutaneous transhepatic embolization or emergent shunting must be performed, depending on the condition of the patient. Angiography, prior to surgical treatment, is necessary to define venous anatomy and determine portal hemodynamics, both of which provide information vital in choosing the type of shunt. If bleeding is massive and the patient is unstable, H-grafts are most appropriate, for they are technically easier and give excellent short term results. In a stable Child's A or B patient with minor ascites as well as suitable anatomy and hepatopedal flow, DSRS is the procedure of choice because it produces the smallest degree of HE postoperatively and increases the survival rate for nonalcoholics. If this is not feasible or if the surgeon lacks the technical expertise to perform DSRS, PCS is the logical alternative. In view of the data from the series observed in the United States, ablative procedures cannot be recommended at the present for the treatment of variceal bleeding. In the Child's C poor-risk patient, the operative mortality rate is prohibitive, and only nonsurgical means should be used to establish control of bleeding. In the elective situation, the surgical options change. The efficacy of ES as a definitive procedure to control recurrent variceal bleeding is unproved, and rebleeding can be significant; therefore, it cannot be recommended. H-grafts have a prohibitively high rate of long term thrombosis and are also not recommended, and the Linton or proximal splenorenal shunt offers no advantages over conventional portacaval shunting. Moreover, arterialization of the hepatic stumps of the portal vein does not prevent hepatic encephalopathy or alter the survival rate. Both PCS and DSRS prevent rebleeding, yet neither alters the survival rate for alcoholic patients.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Portal hypertension. 240 26

The separate role of mineralocorticoid and glucocorticoid hormone action in maintaining arterial pressure was studied in normotensive rats. Four groups were prepared: adrenalectomized (ADX) rats given 6 micrograms aldosterone/24 h (ALDO; n = 9) or 10 micrograms dexamethasone/24 h (DEX; n = 9) by intraperitoneal Alzet pumps, shamoperated controls (control; n = 10) and ADX rats with no hormone replacement (ADX; n = 9). All groups were given 1% NaCl + 2.5% glucose drinking solution. Measurements of plasma corticosterone and aldosterone and urinary aldosterone excretion confirmed the adequacy of the experimental groups. Forty-eight hours after ADX or sham, base-line intra-arterial mean arterial pressure (MAP) in conscious undisturbed rats was similar in the four groups. Captopril (1 mg/kg iv) produced a similar reduction in MAP in ALDO (-11 +/- 2 mmHg) and DEX (-12 +/- 1 mmHg) groups, despite a lower plasma renin activity (PRA) in ALDO (2.0 +/- 0.7 and 6.0 +/- 1.5 ng X ml-1 X h-1, respectively; P less than 0.05). dP (Me)TyrAVP (50 micrograms/kg iv) caused a greater decrease in MAP in ALDO (-15 +/- 3 mmHg) than in DEX (-8 +/- 1 mmHg; P less than 0.05). Combined blockade with both antagonists resulted in a greater MAP reduction in ALDO (-29 +/- 4 mmHg) than in DEX (-15 +/- 4 mmHg; P less than 0.05). These results indicate that glucocorticoid hormone action maintains arterial pressure in ADX rats by mechanisms similar to normal rats and largely independent of the renin-angiotensin system and vasopressin. In contrast, mineralocorticoid replacement alone in ADX rats requires increased participation of both peptide systems for maintenance of arterial pressure.
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PMID:Role of mineralocorticoids and glucocorticoids in blood pressure regulation in normotensive rats. 353 7

The intracerebroventricular (i.c.v.) injection of oxytocin, in doses ranging from 5 to 90 ng (5-90 pmol) induced penile erection and yawning in male rats. Such response was not induced by doses of the peptide higher than 100 ng, nor by equimolar doses of i.c.v. [Arg8]vasopressin, ACTH-(1-24), alpha-MSH, rat corticotropin-releasing factor (rCRF), delta sleep-inducing peptide, neurotensin or substance P. Oxytocin-induced penile erection and yawning were prevented by atropine and morphine, but not by methylatropine or the opiate antagonist naloxone. Haloperidol, a dopamine receptor antagonist, was ineffective at low doses; it partially prevented penile erection but not yawning at high doses. Since oxytocin is present not only in the neurohypophysis but also in other brain areas, our results suggest that oxytocin is implicated in the regulation of penile erection and yawning, and provide further evidence that oxytocin acts as a neuropeptide in the central nervous system.
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PMID:Oxytocin: an extremely potent inducer of penile erection and yawning in male rats. 379 49

To assess the efficacy of endoscopic paravariceal sclerotherapy (EPS) compared to balloon tamponade, 25 patients with massive hemorrhage from esophageal varices not responding to Sengstaken or Linton tube tamponade were treated by emergency EPS. None of the patients had received vasopressin. Immediate control of hemorrhage was achieved in 92%. Recurrent bleeding occurred in 17.4% of patients during their primary admission. Minor complications resulting from EPS were observed in three patients (12%): esophageal ulcer, esophageal stenosis, and pleural effusion. Ten patients (40%) died in the hospital, seven of them despite arrested hemorrhage. Fifteen patients were discharged and followed at 3-month intervals for a mean of 21.3 months (range, 8.8 to 29.7). During this period one death due to liver failure without recurrent hemorrhage and three rebleeding events in two patients were observed (rebleeding risk per patient month, 9.4 x 10(-3). We conclude that EPS is very effective in controlling acute bleeding from esophageal varices, even in poor risk patients with ineffective balloon tamponade.
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PMID:Emergency endoscopic sclerotherapy for bleeding esophageal varices: a prospective study in patients not responding to balloon tamponade. 660 Jun 99

Previous reports from this hospital in 1958 and 1967 have revealed that esophageal tamponade is a relatively dangerous type of treatment. Other investigators have been able to avoid many of the hazards of this technique. We have again assessed our results in 50 episodes of esophageal tamponade in bleeding esophageal varices in 39 patinets. Thirty-seven had alcoholic cirrhosis, one Wilson's disease, and one portal vein thrombosis. The diagnosis of variceal hemorrhage was established by endoscopy or angiography in virtually all. The great majority (86%) had had unsuccessful infusions of vasopressin previously. The Sengstaken-Blakemore tube (SBT) was used in 41 and the Linton tube (LT) in nine. Hemorrhage was controlled for at least 24 consecutive hours in 20 episodes (40%). Ninety percent of the patients died. Rupture of the esophagus following inflation of the gastric balloon in the esophagus caused three deaths (8%). Major nonfatal complications such as aspiration pneumonia occurred on five other occasions. Although the complications of esophageal tamponade were greatly reduced from our previous series, the efficacy of esophageal tamponade also decreased. There were no significant differences in the efficacy or complications of the SBT and LT. The high mortality and complication rates are still discouraging. We believe that the role of esophageal tamponade in the treatment of hemorrhage from varices is a secondary one.
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PMID:Esophageal tamponade in the treatment of bleeding varices. A decadel progress report. 696 5

The involvement of dopamine in the release of oxytocin and vasopressin was investigated in lactating rats during suckling or after changes in plasma osmolality. The effects of intraventricular injections of dopamine, agonists and antagonists, were tested on electrical unit activity of oxytocinergic or vasopressinergic cells in the paraventricular nucleus, on intramammary pressure (index of oxytocin release) and diuresis (index of vasopressin release). In urethane-anaesthetized lactating suckled rats, dopamine (1 microgram), apomorphine (2.5 and 5 micrograms) facilitated the established milk-ejection reflex, increasing the frequency and the amplitude of neurosecretory bursts of oxytocinergic cells. They also triggered the reflex in lactating rats without milk-ejections during suckling. The small doses injected were in no way such as to induce an acceleration in firing rate of oxytocinergic cells or an increase in mammary pressure. In alcohol-loaded rats, during water diuresis, dopamine (2 micrograms) and apomorphine (5 micrograms) activated the depressed vasopressinergic cells and inhibited diuresis. These facilitatory effects were progressive, reaching a maximum 10-15 min after injection. Haloperidol (5 micrograms) and alpha-flupentixol (10 micrograms) had an inhibitory effect on both types of neurosecretory cells in urethane-anaesthetized rats. They prevented the reflex activation of oxytocinergic cells induced by suckling and of vasopressinergic cells after a hyperosmotic stimulus (1 ml i.p 9% NaCl solution). These inhibitory effects were not of the "all-or-none' type. So, we can postulate that dopamine regulates the reflex release of oxytocin and vasopressin in the hypothalamus. On the one hand, dopamine permits and controls the periodic activation of oxytocinergic cells as long as the mothers are being suckled. On the other hand, it modulates the activity of vasopressinergic cells whenever the plasma osmolality changes.
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PMID:Excitatory effect of dopamine on oxytocin and vasopressin reflex releases in the rat. 710 13


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