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 effects of SQ 29,548 on vasoconstrictor responses were investigated in the feline mesenteric vascular bed. Injections of the thromboxane (TX) A2 mimics, U46619 and U44069, caused dose-related increases in mesenteric arterial perfusion pressure. After administration of SQ 29,548, 0.5 mg/kg i.v, vasoconstrictor responses to U46619 and U44069 were reduced markedly whereas responses to prostaglandin (PG) F2 alpha, angiotensin II, vasopressin and BAY K 8644, an agent which enhances calcium entry, were not altered. The duration of the TXA2 receptor blockade was greater than 2 h and SQ 29,548 had no significant effect on mesenteric vasodilator responses to PGE2, isoproterenol, nitroglycerin, acetylcholine or bradykinin. SQ 29,548, at a dose of 0.5 mg/kg i.v., significantly reduced the response to TXB2, which had modest vasoconstrictor activity in the mesenteric vascular bed. However, when the dose of SQ 29,548 was reduced to 0.05 mg/kg i.v., responses to TXB2 were not altered, whereas responses to U46619 were significantly decreased. SQ 29,548 had no significant effect on vasoconstrictor responses to norepinephrine or to sympathetic nerve stimulation. The TXA2 receptor antagonist blocked the vasoconstrictor component of the biphasic response to the PG precursor, arachidonic acid, and the endoperoxide, PGH2. The results of these studies suggest that SQ 29,548 is a specific TX receptor antagonist in the mesenteric vascular bed, that the vasoconstrictor component of the biphasic response to arachidonic acid and PGH2 is due to formation of TXA2, and that endogenously formed TXA2 does not modulate adrenergic responses in the mesenteric circulation of the cat.
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PMID:Influence of SQ 29,548 on vasoconstrictor responses in the mesenteric vascular bed of the cat. 236 76

Bleeding from esophageal varices is related to the size and pressure of varices, endoscopic danger signs, and severity of liver failure. Prevention of bleeding with propranolol has given conflicting results in controlled trials, but is a safe treatment. Prophylactic sclerotherapy has been shown to reduce bleeding in European studies, but this has not been confirmed by studies in the United States. Acute variceal bleeding can usually be controlled by sclerotherapy, which may be supplemented by pharmacotherapy with vasopressin, nitroglycerin, or somatostatin. Recurrent bleeding is prevented initially by sclerotherapy, with surgery reserved for patients who have not responded to this treatment. Once bleeding has been controlled, the suitability and timing of hepatic transplantation must be considered.
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PMID:Esophageal varices. 236 82

This study examined the ability of moderately well-developed coronary collateral vasculature to undergo vasoconstriction in response to alpha-adrenergic agonists, vasopressin and angiotensin, and vasodilation in response to nitroglycerin. Studies were performed in 20 dogs 4-16 wk after left anterior descending coronary artery occlusion had been produced by an Ameroid constrictor or hollow intravascular plug. Collateral flow was estimated from retrograde flow from the cannulated left anterior descending artery. Tissue flow was measured with microspheres. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left circumflex and septal arteries. Vasopressin and angiotensin II decreased retrograde flow from 22.7 +/- 5.5 to 15.5 +/- 2.7 and from 19.2 +/- 2.8 to 14.3 +/- 1.9 ml/min, respectively (each P less than 0.05). Both agents also significantly decreased tissue flow to normally perfused and collateral dependent myocardium. Neither the selective alpha 1-adrenergic agonist phenylephrine nor the alpha 2-agonist B-HT 933 decreased retrograde flow. Nitroglycerin increased retrograde flow by 63 +/- 27% (P less than 0.01). Thus, although the moderately well-developed coronary collateral circulation is capable of vasoconstriction in response to vasopressin and angiotensin II, these data fail to support a role for alpha-adrenergic mechanisms in modulating collateral flow.
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PMID:Vasomotor activity of moderately well-developed canine coronary collateral circulation. 246 13

In the present study, 52 patients with cirrhosis, portal hypertension, and variceal hemorrhage underwent either an elective or an emergency side-to-side portacaval shunt operation. Vasopressin was infused intravenously at 60 units/hour from just prior to abdominal incision until completion of the anastomosis. Eight of 35 patients who received vasopressin alone (23 percent) tolerated increased doses of 75 to 90 units/hour to obtain hemostasis. Four of 52 patients required simultaneous infusion of sodium nitroprusside to correct systemic hypertension. An additional 15 percent reduction in portal venous pressure occurred in these patients. Eleven of 13 patients with vasopressin-induced myocardial ischemia responded to simultaneous infusion of nitroglycerin. Further prospective studies are indicated to adequately delineate the dose and duration of therapy with either nitroprusside or nitroglycerin for simultaneous administration with intravenous vasopressin.
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PMID:Simultaneous infusion of nitroglycerin and nitroprusside to offset adverse effects of vasopressin during portosystemic shunting. 249 34

In a prospective, randomized clinical trial, immediate injection sclerotherapy was compared with treatment by a combined infusion of vasopressin (0.4 unit per min) and nitroglycerin (40 to 400 micrograms per min) in 50 consecutive patients with 64 episodes of endoscopy-proven variceal hemorrhage. Control of bleeding was assessed over a 12-hr period following entry into the trial. Patients in the vasopressin + nitroglycerin group were then treated by sclerotherapy, as were those in the sclerotherapy group who continued to bleed. At 12 hr, bleeding was controlled in 29 (88%) of the 33 episodes treated by sclerotherapy compared with 20 (65%) of 31 episodes treated by vasopressin + nitroglycerin (p less than 0.05). Recurrence of variceal bleeding occurred at the same frequency (31%). Although admission mortality was less in those initially treated by sclerotherapy compared to those managed by vasopressin + nitroglycerin, this did not reach statistical significance (27 and 39%, respectively, p greater than 0.20). Sclerotherapy carried out as the first treatment of the active variceal hemorrhage proved both safe and effective, even in the presence of major hemorrhage, and as compared to combined vasopressin and nitroglycerin it proved superior.
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PMID:Controlled clinical trial of injection sclerotherapy for active variceal bleeding. 249 52

We measured the coronary, systemic, and splanchnic effects of vasopressin and vasopressin plus nitroglycerin in 8 stable patients with alcoholic cirrhosis. Vasopressin (0.1-0.8 U/min) increased pressure in the hepatic vein, pulmonary artery and pulmonary capillaries. Wedged hepatic (portal) vein pressure was unchanged; the hepatic venous pressure gradient (wedged-free hepatic vein pressure) fell. Insignificant declines occurred in cardiac output, gastroesophageal collateral (azygous) blood flow, hepatic blood flow and coronary sinus (cardiac) blood flow. The addition of nitroglycerin (40-70 micrograms/min) reduced pressure in the hepatic vein, pulmonary artery and pulmonary capillaries, while increasing the hepatic venous pressure gradient. Wedged hepatic vein pressure did not change. Gastroesophageal collateral (azygous) flow increased markedly; cardiac output rose to a lesser degree. Coronary sinus and hepatic blood flow did not change. Nitroglycerin ameliorated the increases in systemic and pulmonary artery pressure produced by vasopressin but also tended to reverse the decline in the hepatic venous pressure gradient and markedly increased gastroesophageal flow. Neither drug significantly affected coronary blood flow.
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PMID:Vasopressin and vasopressin plus nitroglycerin for portal hypertension. Effects on systemic and splanchnic hemodynamics and coronary blood flow. 249 16

The aim of this study was to evaluate, using a double-blind technique, the efficacy of the association of transdermal nitroglycerin to vasopressin infusion for the treatment of variceal bleeding. Sixty-nine cirrhotic patients with active variceal bleeding were randomly allocated to receive vasopressin (0.4 to 0.8 unit per min until variceal bleeding has been controlled for 12 hr) associated with nitroglycerin administered transdermically in a slow-release preparation (10 mg in 24 hr) or placebo. An initial control of variceal hemorrhage was achieved in 83% of the patients receiving vasopressin-nitroglycerin and in 74% in the vasopressin-placebo group. Owing to a lower frequency of recurrent bleeding during therapy (18 vs. 42%, p = 0.11), vasopressin-nitroglycerin achieved a definitive control of bleeding in a higher proportion of patients than vasopressin-placebo (73 vs. 54%, p = 0.13). The group treated with the drug combination showed favorable results in relation to transfusion requirements (2.9 +/- 0.4 vs. 4.2 +/- 0.5 units, p = 0.05), total dose of vasopressin required (453 +/- 47 vs. 587 +/- 50 units, p less than 0.05), need of balloon tamponade (6 vs. 15, p less than 0.05) and requirement for emergency surgery (0 vs. 4, p = 0.07). There were no significant differences in the undesirable effects associated with treatment, observed in 37 and 49% of cases, respectively. Hospital mortality was similar (33 vs. 25%). This study demonstrates that transdermal nitroglycerin improves the effectiveness of vasopressin for controlling variceal hemorrhage.
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PMID:Association of transdermal nitroglycerin to vasopressin infusion in the treatment of variceal hemorrhage: a placebo-controlled clinical trial. 251 Nov 36

The cardiovascular effects of althesin (ALT) and urethan-chloralose (UC) anesthesia were compared in conscious, chronically instrumented rats. Althesin had no effect on arterial pressure or base-line resistance in the renal, superior mesenteric, and hindquarters vasculatures but increased heart rate. In contrast, UC decreased arterial pressure, heart rate, and mesenteric resistance. Although UC attenuated depressor responses to nitroglycerin, neither anesthetic significantly altered regional vascular reactivity to intravenous phenylephrine and nitroglycerin. The cardiac chronotropic baroreflex was examined by comparing the slope of the curves relating maximal changes (delta) in heart rate (pulse interval) that occurred at the point coinciding in time with the maximal changes in mean arterial pressure produced by phenylephrine and nitroglycerin. Neither anesthetic significantly altered the baroreflex slope (delta pulse interval/delta mean arterial pressure) for pressor and depressor stimuli. Both anesthetics attenuated the sympathoexcitatory response to cerebroventricular angiotensin II, although ALT had less of a depressive effect (pressor response during ALT and UC = 65 and 30%, respectively, of conscious). Plasma renin activity (PRA) and the hemodynamic response to peripheral angiotensin-receptor antagonism were significantly increased (PRA by almost 6-fold) during UC, whereas ALT was without effect. Similarly, UC but not ALT induced vasopressin-dependent vascular tone. Ganglionic blockade indicated that peripheral neurogenic tone was not altered by ALT anesthesia. These data suggest that althesin produces fewer hemodynamic disturbances than urethan-chloralose and largely maintains cardiovascular regulation intact.
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PMID:Effects of althesin and urethan-chloralose on neurohumoral cardiovascular regulation. 256 59

This paper describes the vasopressin (VP) and oxytocin (OXT) immunoreactive structures in the brain and upper spinal cord of the adult male and female Macaca fascicularis. Immunocytochemistry following intraventricular application of colchicine displayed VP neurons in the diagonal band of Broca (DBB), bed nucleus of the stria terminalis (BST), medial amygdaloid nucleus, dorsomedial hypothalamic nucleus, area of the locus coeruleus (LC), solitary tract nuclei (NTS), and the dorsal horn of the cervical spinal cord in addition to those known to exist in the paraventricular, supraoptic, and suprachiasmatic hypothalamic nuclei. Furthermore, a dense accumulation of VP fibers was observed in areas such as the DBB, medial septum, BST, amygdala, hippocampus, ventral tegmental area, periaquaductal gray, dorsal and ventral raphe, area of Forel, LC region, parabrachial nuclei, and NTS. The lateral septum and lateral habenula displayed no and very few VP fibers, respectively. No extrahypothalamic OXT neurons were found in the brain of this macaque monkey. Dense concentrations of OXT fibers were demonstrated in the amygdala, NTS, and marginal layer of the cervical spinal cord. No sexual dimorphism was found in this primate VP or OXT system. The results show a distribution of the central VP and OXT systems in this primate which is quite different from that in the rat. However, in various aspects it agrees with current data on the VP and OXT systems of the human brain. The present results suggest, therefore, that this monkey might serve as a better model for the human VP system than the rat.
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PMID:Vasopressin and oxytocin systems in the brain and upper spinal cord of Macaca fascicularis. 277 7

a) In the hypothalamus, NPY immunoreactive neurons are non catecholamine containing neurons whereas in the medulla oblongata NPY is present in the majority of the catecholamine neurons. NPY immunoreactive neurons in the MO are critically located at the site of the baroreceptor afferents termination. b) High densities of receptors, as indicated by 125I-pNPY binding studies are present in the various subnuclei of the NTS and area postrema. In slice preparations of this region NPY reduces forskolin and phorbolester-induced cAMP accumulation. c) Antagonistic interactions between NPY-and alpha 2-receptors exist in the NTS. d) Neuropeptide Y and adrenaline both lower the mean arterial blood pressure, heart and respiratory rates after central administration. When given together they antagonize the hypotensive but not the respiratory response of each other. e) Central NPY administration leads to alterations in serum levels of corticosterone, aldosterone, angiotensin II, vasopressin, PRL, LH, GH and TSH which are parallel to changes in discrete hypothalamic catecholamine neuronal systems. f) It is proposed that NPY is a transmitter involved in central cardiovascular and neuroendocrine regulation operating in close association with the CA systems. Before the precise role of NPY can be established, however, specific antagonists have to be developed.
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PMID:Brain neuropeptide Y mechanisms. Basic aspects and involvement in cardiovascular and neuroendocrine regulation. 282 7


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