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)

Thirty-nine patients admitted during a 16-month period for acute bleeding from varices confirmed by emergency endoscopy were randomized to receive either continuous intravenous infusions of vasopressin alone (0.66 units per min) (Group I: 19 patients) or vasopressin plus sublingual nitroglycerin (0.6 mg every 30 min for 6 hr) (Group II: 20 patients). The two groups of patients were similar in the type and severity of their cirrhosis. Bleeding was controlled initially in 47% (9/19) of the patients in Group I and 55% (11/20) of the patients in Group II after 6 hr of infusion (not statistically significant). Complete control of bleeding during 24 hr of infusion was achieved in only 4 of 19 patients in Group I (21%) but in 9 of 20 in Group II (45%). This difference is not statistically significant. The total number of patients with complications during infusions were significantly different statistically in the vasopressin and vasopressin-nitroglycerin groups, respectively (17/19 vs. 7/20, p less than 0.001). Major complications requiring immediate cessation of infusions were observed in 6 of 19 of the patients in Group I (32%) and in 2 of 20 in Group II (10%) (p less than 0.05). Mortality (58% in Group I, 55% in Group II) and transfusion requirements were similar in the two groups. This study shows that the addition of sublingual nitroglycerin to intravenous vasopressin does not alter the efficacy of vasopressin alone in controlling hemorrhage from esophageal varices, but it does significantly reduce the complications.
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PMID:Controlled trial of vasopressin plus nitroglycerin vs. vasopressin alone in the treatment of bleeding esophageal varices. 308 3

A randomized trial was undertaken to determine efficacy of nitroglycerin when added to a vasopressin infusion in both reducing the complication rate and giving improved control of acute variceal hemorrhage. Seventy-two bleeding episodes in 57 patients were included, with vasopressin being used on 34 occasions and vasopressin plus nitroglycerin on 38 occasions, for an infusion period of 12 hr. At the end of the 12-hr period, hemorrhage had been controlled significantly more frequently in those receiving combined therapy (26 of 38; 68%) than in those given vasopressin alone (15 of 34; 44%, p less than 0.05), although this difference was not statistically significant if those patients in whom therapy was discontinued due to drug complications were excluded from the analysis [hemorrhage controlled in the combined group (68%) and vasopressin alone (48%); chi 2 = 2.4, p greater than 0.05]. Major complications requiring cessation of therapy were significantly less common in those given nitroglycerin--one occasion compared to seven in those given vasopressin alone (p less than 0.02). Thus, the addition of nitroglycerin to a vasopressin infusion results in a lower rate of complications and is more effective in controlling variceal hemorrhage.
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PMID:A randomized trial of vasopressin and vasopressin plus nitroglycerin in the control of acute variceal hemorrhage. 308 4

The steady-state pharmacokinetics of nitroglycerin (NTG) were investigated in 11 rats after sequential infusions of either NTG alone (10 micrograms/kg/min) or NTG plus vasopressin (the latter at 5.5 mU/kg/min). Arterial and venous plasma concentrations of NTG in the femoral bed were obtained at 41 and 45 min during each infusion phase. Cardiac output was estimated twice in each animal using 85Sr and 141Ce microspheres. NTG systemic clearance in arterial plasma was found to be strongly correlated with cardiac output (r = 0.784, n = 22, P less than .001). Because NTG distribution between red blood cells and plasma was independent of concentration (up to 150 ng/ml in plasma) and hematocrit (25-48%), the systemic clearance of NTG in arterial blood could be estimated as about 3/4 of cardiac output. Vasopressin co-infusion decreased both the cardiac output and the arterial NTG plasma clearance, but it also increased the arteriovenous extraction of NTG. Thus, vasopressin had not net effect on the venous plasma clearance, of NTG. In animals with NTG infusions alone, cardiac output also significantly correlated with NTG venous plasma clearance (P less than .01) and arteriovenous extraction (P less than .05). These data indicate that, in the absence of vasopressin, NTG pharmacokinetics are dependent on the cardiac output, thus providing an example wherein the systemic clearance of a drug was shown to be related to systemic blood flow. These results support the concept that the vasculature acts as a clearing organ for organic nitrates, and they also provide a hemodynamic explanation for the high variability in NTG plasma concentrations observed under presumed steady-state conditions.
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PMID:Cardiac output is an apparent determinant of nitroglycerin pharmacokinetics in rats. 309 60

Nitroglycerin is a potent venous dilator and a mild arterial vasodilator that has been shown to improve the hemodynamic response to vasopressin in portal hypertensive patients and to decrease portal pressure in experimental animals. In order to determine the effect of nitroglycerin on portal venous hemodynamics, we studied 11 patients with alcoholic cirrhosis before and during the administration of sublingual nitroglycerin (0.4 and 0.6 mg). The hepatic venous pressure gradient (which was obtained by subtracting the free hepatic venous pressure from the wedged hepatic venous pressure) decreased from 17.9 +/- 6.5 mm Hg (mean +/- S.D.) to 15.1 +/- 5.1 mm Hg (p less than 0.02) at the peak of the effect, which occurred from 2 to 12 min after nitroglycerin administration. The mean arterial pressure was reduced from 96 +/- 10 mm Hg to a peak decrease of 76 +/- 18 mmHg (p less than 0.001). The peak change in the hepatic venous pressure gradient induced by nitroglycerin correlated directly with the peak change in mean arterial pressure (r = 0.79, p less than 0.01). There was a moderate increase in heart rate in response to the decrease in blood pressure (73 +/- 15 to 83 +/- 15 beats per min, p less than 0.001). Two of the 11 patients did not reduce their hepatic venous pressure gradient after 0.6 mg nitroglycerin. Reductions in portal pressure were observed with both increases and moderate decreases in azygos blood flow, suggesting that, as observed in experimental animals, the portal-pressure-reducing effect of nitroglycerin could be due to two different and independent mechanisms, a reduction in portal blood flow or portal-collateral vasodilatation.
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PMID:Portal hemodynamics during nitroglycerin administration in cirrhotic patients. 311 81

We have evaluated the haemodynamic effects of intravenous (iv) nitroglycerin (NG) and vasopressin (VP) alone and in combination, in 12 patients with cirrhosis and recent variceal haemorrhage (two to seven days). Nitroglycerin infusion alone (200 micrograms/min) produced a significant fall in portal pressure (WHVP-FHVP) (from 16.4 (0.6) to 13.3 (1.2) mmHg; p less than .001) associated with hypotension (mean arterial pressure from 95 (7) to 78 (9) mmHg; p less than 0.005). Vasopressin alone (0.4 IU/min) reduced portal pressure (20.7 (1.3) to 14.0 (1.3) mmHg; p less than 0.001), but there was considerable variation in the systemic haemodynamic changes with increased cardiac output in four of six patients. The combination of vasopressin and nitroglycerin corrected all systemic haemodynamic disturbances produced by either agent alone. This combination led, however, to a further reduction in portal pressure (from 13.7 (0.9) to 11.7 (0.7) mmHg p less than 0.01). These results show that: (1) intravenous nitroglycerin reduces portal pressure, and (2) the combination of nitroglycerin and vasopressin reverses systemic haemodynamic disturbances produced by either agent alone and leads to a further decrease in portal pressure.
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PMID:Haemodynamic response to intravenous vasopressin and nitroglycerin in portal hypertension. 312 65

We tested the hypothesis that the pharmacokinetics of nitroglycerin might be governed by haemodynamics, viz: cardiac output. The steady state pharmacokinetics of nitroglycerin, both in arterial and in venous plasma, were investigated in 11 rats after sequential infusions either of nitroglycerin alone (10 micrograms kg-1 min-1) or of nitroglycerin plus vasopressin (the latter at 5.5 mU kg-1 min-1). Cardiac output was estimated twice in each animal using 85Sr and 141Ce microspheres. Nitroglycerin systemic clearance in arterial plasma was found to be correlated strongly with cardiac output (r = 0.784, N = 22, P less than 0.001). Using the distribution ratio of nitroglycerin between red blood cells and plasma, we determined the systemic clearance of nitroglycerin in arterial blood to be about 3/4 of cardiac output. Vasopressin co-infusion decreased both the cardiac output and the arterial nitroglycerin clearance, but it also increased the arteriovenous extraction of nitroglycerin. Thus, vasopressin had no net effect on the venous plasma clearance of nitroglycerin. In animals infused with nitroglycerin alone, cardiac output also significantly correlated with nitroglycerin venous plasma clearance (P less than 0.01) and arteriovenous extraction (P less than 0.05). These data indicate that haemodynamic alterations may have profound effects on the observed plasma concentrations of nitroglycerin. These parameters need to be standardized and controlled if meaningful plasma concentrations of organic nitrates are to be obtained and interpreted.
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PMID:Interpretation of nitrate plasma concentrations. Effect of cardiac output on nitroglycerin pharmacokinetics in experimental animals. 313 71

Addition of nitroglycerin (NTG) improves the hemodynamic response to vasopressin and may thus be useful in the treatment of gastrointestinal hemorrhage. We studied in the rat the influence of vasopressin on the disposition of a constant intravenous infusion of NTG and the cutaneous absorption of NTG ointment. The effect of NTG on the pharmacokinetics of vasopressin was also determined. Animals were divided into four groups: control, NTG, vasopressin and vasopressin + NTG. Infusions (or ointments) were maintained for 70 min; cardiac output and regional blood flows were determined with the microsphere technique. Both intravenous and cutaneous NTG resulted in similar hemodynamic responses. Vasopressin caused generalized vasoconstriction, while the addition of NTG reversed the deleterious systemic hemodynamic effects of vasopressin. Addition of vasopressin to NTG did not alter NTG systemic clearance nor did NTG affect vasopressin clearance. Of note, the systemic clearance of NTG was directly correlated with the cardiac output (r = 0.804), supporting a model of NTG distribution where blood vessels and/or extrahepatic tissues are the site of elimination of the drug. The marked reduction in skin blood flow by vasopressin did not decrease the steady-state plasma concentration of NTG nor the estimated cutaneous absorption rate of NTG ointment, indicating that cutaneous blood flow is not an important determinant in the absorption of NTG ointment. The skin is an appropriate route of delivery for NTG when combined with vasopressin.
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PMID:Pharmacokinetic-hemodynamic interactions between vasopressin and nitroglycerin: comparison between intravenous and cutaneous routes of nitrate delivery. 392 Jan 34

In urethane-anesthetized rats, injections of 50 pmol of arginine-vasopressin (AVP) or thyrotropin-releasing hormone (TRH) into a lateral cerebral ventricle (i.c.v.) elicit short-latency increases in blood pressure. i.c.v. injection of 50 pmol of the AVP antagonist, d(CH2)5Tyr(Me)AVP, but not of the vehicle (artificial cerebrospinal fluid; a CSF), abolished the pressor action of i.c.v. AVP. The AVP antagonist did not antagonize the TRH-induced pressor responses. In another group of rats, a monopolar stainless-steel electrode was positioned stereotaxically in the paraventricular nucleus (PVN) and pressor responses were elicited by electrical stimulation of the PVN. Micro-injection of 1 nmol of the AVP antagonist, but not of aCSF alone, into the nucleus tractus solitarius/vagal area (NTS/VA), reduced PVN-stimulated pressor responses to 26 +/- 6% of control and stimulation-induced tachycardia to 37.3 +/- 9.0% of control. These studies indicate that the pressor and heart-rate responses to PVN stimulation may be mediated, in part, via AVP receptors in the NTS/VA.
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PMID:Vasopressin antagonist in nucleus tractus solitarius/vagal area reduces pressor and tachycardia responses to paraventricular nucleus stimulation in rats. 392 90

The administration of dopamine (5--100 microgram) in rat kidneys perfused with physiological solution containing vasopressin and pretreated with an alpha-adrenoreceptor antagonist produced dose-dependent vasodilatation. The dopamine receptor antagonist haloperidol produced marked dilatation in the preparation at high doses (10--50 microgram), while a low dose of haloperidol (5 microgram) had no significant effect on the response to dopamine. The response to dopamine, however, was significantly reduced by the dopamine receptor antagonist, ergometrine (50 microgram). This dose of ergometrine had no significant effect on the vasodilator response to acetylcholine (0.01--0.2 microgram) or glyceryl trinitrate (GTN, 0.05--1 microgram). Administration of the beta-adrenoreceptor antagonist propranolol (0.5 mg) had no significant effect on the response to dopamine.
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PMID:Dopamine-induced vasodilatation in the isolated perfused rat kidney. 610 92

Somatostatin (SRIF) and vasopressin (AVP) were measured in hypothalamic and extrahypothalamic areas in normotensive Wistar-Kyoto (WK) and in spontaneously hypertensive, adult rats (SRH) under control conditions and after acute immobilization stress. Hypothalamic areas included the median eminence (ME) and the periventricular, suprachiasmatic, paraventricular, supraoptic, ventromedial and dorsomedial nuclei. Extra-hypothalamic areas included the striae medullaris, striae terminalis (N. Interst.), locus coeruleus, central gray, Areas 1 and 2 (NTS), and circumventricular organs. Under basal conditions, SHR and WK rats did not differ in their content of SRIF and AVP for most areas examined. After acute stress, however, striking differences were found in peptide content. Somatostatin content was not changed in SHR, but was significantly decreased in most areas in WK rats. On the contrary, generalized increases in AVP content were found in SHR after stress, with no changes in WK animals. An exception was the ME, which showed a decrease in peptide levels in both groups of rats. These results suggest that both hypothalamic and extra-hypothalamic AVP and SRIF are involved in the central stress response. The different changes in peptide levels observed for SHR and normotensive rats after acute stress further support the hypothesis of a role of both AVP and SRIF in central regulation of cardiovascular function.
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PMID:Changes in brain somatostatin and vasopressin levels after stress in spontaneously hypertensive and Wistar-Kyoto rats. 610 6


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