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)

To evaluate techniques for retrograde pancreatic venography similar to epinephrine renal venography, 35 dogs had transjugular portography before and after the infusion of various doses of vasopressin systemically or selectively into the superior mesenteric and celiac arteries, or after occlusion of the distal thoracic aorta. Increased filling of the peripheral portal branches resulted, but none of the techniques provided diagnostically useful enhanced pancreatic visualization.
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PMID:Retrograde pancreatic venography after reduction of the arterial visceral flow: an experimental study. 52 66

Electromagnetic flow measurement study was performed in 20 anesthetized dogs to evaluate the effect of selective celiac infusion of vasopressin on the hepatic arterial vasculature. Teh hepatic arterial flow showed a biphasic response with an initial decrease followed by a substantial increase in spite of a continued infusion. The left gastric, splenic, and superior mesentric arteries showed a monophasic response with persistent decrease of flow during the whole infusion. The biphasic response of the hepatic arterial flow is thought to be due to autoregulatory dilative action of the liver to a decrease of the portal flow. The results and previous clinical experience suggest that the selective infusions of vasopressin into arteries supplying the liver can be used for short-term vasoconstrictive therapy of acute gastrointestinal bleeding in patients without liver damage. Further experience is necessary to evaluate the safety of prolonged hepatic infusions in patients with liver damage.
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PMID:Vasopressin and hepatic artery. Effect of selective celiac infusion of vasopressin on the hepatic artery flow. 107 20

The authors review the role of the gastroduodenal blood flow as a factor ensuring the secretory activity and protective properties of the gastric mucosa. The possibilities of its pharmacoregulation are also reviewed. It has been shown that the decrease of the gastric blood flow in experimental hemorrhagic shock, extravasal celiac artery stenosis, effects of indomethacin, vasopressin, etc. leads to ischemic injuries to the gastric mucosa accompanied by serious morphological and functional disturbances. The pathogenetic aspects of ischemic injuries to the stomach and duodenum are confirmed by the results of clinical examinations of patients with compression celiac artery stenosis and peptic ulcer. It has been noted that in these patients, the tissue blood flow in the mucosa in considerably decreased in the area of ulcerous defect. The lowering of the content of total phospholipids and changes in their composition were also observed both in relapse and after healing. Out of agents that improve peripheral circulation, propranolol, tavegil combined with cimetidine, trimin appeared most potent. These drugs regulate metabolic processes in gastric tissue, normalizing blood flow, reducing the content of histamine, serotonin, lipid peroxidation products, raising the level of total phospholipids and pepsin.
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PMID:[Physiological significance of gastroduodenal blood flow and possibilities of its regulation by drugs]. 128 20

Duplex ultrasound scanning has been used to assess mesenteric blood flow in normal and disease states. To investigate this technique we studied nine normal volunteers at rest and under conditions known to modify intestinal blood flow. After a baseline mesenteric duplex scan, each subject was given one of three treatments in random order: (1) test meal (710 kcal), (2) intravenous glucagon (40 micrograms/min), or (3) intravenous vasopressin (0.2 units/min). Peak systolic and diastolic velocities and vessel diameters were measured at intervals after treatment in the celiac and the superior mesenteric arteries (SMAs) and the right common carotid artery. Resting velocities did not differ among the groups. Peak systolic velocity increased significantly in both celiac and SMAs after the meal, with maximal changes in the celiac artery preceding those in the SMA in most subjects. Early diastolic flow reversal in the SMA was consistently lost after the meal (eight of nine subjects). Velocity changes after glucagon closely paralleled those after the meal. Vasopressin produced significant decreases in peak systolic velocity in both visceral vessels. No changes in vessel diameter were noted after any treatment. Coefficient of variation for repeated measures of peak velocities was 19% in the celiac and 12% to 16% in the SMA and the common carotid. The coefficient of variation for repeated measurements of arterial diameter was 6% to 8% in the SMA and 11% in the celiac artery. Clinically relevant changes in mesenteric hemodynamics can be reproducibly detected and quantitated by means of current duplex ultrasound technology. The similarities between the visceral arterial responses to a meal and glucagon are of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Duplex ultrasound measurement of changes in mesenteric flow velocity with pharmacologic and physiologic alteration of intestinal blood flow in man. 264 79

Initial stabilization of blood volume and immediate resuscitative measures should be used for lower gastrointestinal tract bleeding. Upper gastrointestinal tract lesions should be excluded with nasogastric intubation and upper endoscopy if the history or nasogastric aspirate suggests an upper gastrointestinal tract source. Proctosigmoidoscopy should be done to exclude mucosal disease, hemorrhoidal bleeding or local carcinoma. If all of these are negative and the patient is bleeding massively, we recommend arteriography with catheterization of the superior mesenteric, inferior mesenteric and celiac arteries. These procedures should be carried out within less than four hours. If a bleeding site is demonstrated, the use of local infusion of vasopressin for permanent control should be considered only in the poor risk patient in whom the operative risk is prohibitive. Massive hemorrhage from the lower gastrointestinal tract in an elderly population is usually due to diverticular bleeding and not to angiodysplasia. The bleeding site was more common in the right than in the left colon. Angiography has been proved to be an important diagnostic procedure to localize the site of the bleeding and has been invaluable in the surgical management of these patients.
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PMID:Angiography in the management of massive lower gastrointestinal tract hemorrhage. 696 32

Our earlier autoradiographic work had documented a wide distribution of vasopressin receptors in the hippocampus [R.E. Brinton, K.W. Gee, J.K. Wamsley, T.P. Davis, H.I. Yamamura, Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography, in: Proc. Natl. Acad. Sci. USA, 81 (1984) pp. 7248-7252; C. Chen, R.D. Brinton, T.J. Shors, R.F. Thompson, [Arg 8]-Vasopressin-induction of long lasting potentiation of synaptic transmission in the dentate gyrus, Hippocampus 3 (1993) 193-203.] which suggested the possibility that receptors for vasopressin were present in both neurons and glia. In the periphery, vasopressin is a potent mitogen in select proliferative cell types [E. Rozengurt, A. Legg, P. Pettican, Vasopressin stimulation of mouse 3T3 cell growth, Proc. Natl. Acad. Sci. USA, 76 (1979) pp. 1284-1287.] which also suggested a possible association between vasopressin receptor activation and the proliferative capacity of astrocytes. We therefore investigated whether vasopressin would induce the expression of the immediate early response gene, NGFI-A (also known as zif/268, ZENK, egr-1, krox 24), which is associated with initiation of mitogenesis [M. Sheng, M.E. Greenberg, The regulation and function of c-fos and other immediate early genes in the nervous system, Neuron, 4 (1990) pp. 477-485.]. Cultured hippocampal glial cells were exposed to vasopressin or a selective V1 vasopressin receptor agonist and in situ hybridization for NGFI-A mRNA was conducted. Results of these experiments demonstrated that vasopressin induced a highly significant dose-dependent increase in the number of cells expressing NGFI-A. Studies to determine the receptor subtype mediating vasopressin induction of NGFI-A were conducted utilizing the specific V1 agonist, [Phe2, Ile3, Orn8]-vasopressin. The V1 receptor agonist induced a highly significant dose dependent increase in the number of grains per NGFI-A positive cell. Time course analysis demonstrated that V1 agonist induction of NGFI-A occurred within 5 min, was maximally induced at 15 min of exposure and exhibited a gradual decline within 30 min of exposure which continued to decline over the 60 min time course. Glial cell responsivity was selective in that vasopressin and V1 agonist induction of NGFI-A occurred in a subpopulation of glial cells. Within a sea of glial cells, vasopressin and V1 agonist would induce islands of NGFI-A positive cells. Results of combined immunocytochemical labeling for the astrocyte specific marker, GFAP, and in situ hybridization for NGFI-A demonstrated that V1 agonist-induced NGFI-A expression occurred in GFAP positive cells. We observed no evidence for V1 agonist induction of NGFI-A in neurons. Collectively, these data document that vasopressin, acting via V1 vasopressin receptors, induces a highly significant increase in NGFI-A expression in select GFAP positive hippocampal astrocytes. To our knowledge, these data are the first report of a vasopressin mediated response in hippocampal glial cells. The potential functional significance of these findings is discussed.
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PMID:Vasopressin-induction of the immediate early gene, NGFI-A, in cultured hippocampal glial cells. 963 May 27

Earlier autoradiographic studies from our laboratory detected vasopressin recognition sites in the mammalian cerebral cortex [R.E. Brinton, K.W. Gee, J.K. Wamsley, T.P. Davis, H.I. Yamamura, Regional distribution of putative vasopressin receptors in rat brain and pituitary by quantitative autoradiography, Proc. Natl. Acad. Sci. U. S.A., 81 (1984) 7248-7252; C. Chen, R.D. Brinton, T.J. Shors, R.F. Thompson, Vasopressin induction of long-lasting potentiation of synaptic transmission in the dentate gyrus, Hippocampus, 3 (1993) 193-204]. More recently, we have detected mRNA for the V1a vasopressin receptors (V1aRs) in cultured cortical neurons [R.S. Yamazaki, Q. Chen, S.S. Schreiber, R.D. Brinton, V1a Vasopressin receptor mRNA expression in cultured neurons, astroglia, and oligodendroglia of rat cerebral cortex, Mol. Brain Res., 45 (1996) 138-140]. To determine whether these recognition sites are functional receptors, we have pursued the signal transduction mechanism associated with the V1a vasopressin receptor in enriched cultures of cortical neurons. Results of these studies demonstrate that exposure of cortical neurons to the selective V1 vasopressin receptor agonist, [Phe2,Orn8]-vasotocin, (V1 agonist) induced a significant accumulation of [3H]inositol-1-phosphate ([3H]IP1). V1 agonist-induced accumulation of [3H]IP1 was concentration dependent and exhibited a linear dose response curve. Time course analysis of V1 agonist-induced accumulation of [3H]IP1 revealed a significant increase by 20 min which then decreased gradually over the remaining 60 min observation period. V1 agonist-induced accumulation of [3H]IP1 was blocked by a selective V1a vasopressin receptor antagonist, (Phenylac1, D-Tyr(Me)2, Arg6,8, Lys-NH29)-vasopressin. Results of calcium fluorometry studies indicated that V1 agonist exposure induced a marked and sustained rise in intracellular calcium which was abolished in the absence of extracellular calcium. The loss of the rise in intracellular calcium was not due to a failure to induce PIP2 hydrolysis since activation of the phosphatidylinositol pathway occurred in the absence of extracellular calcium. V1 agonist activation of calcium influx was then investigated. V1 agonist-induced 45Ca2+ uptake was concentration dependent with a biphasic time course at 250 nM. Preincubation with the L-type calcium channel blocker, nifedipine, blocked V1 agonist-induced calcium influx suggesting V1 agonist-induced L-type calcium channel activation in cortical neurons. Furthermore, V1 agonist-induced calcium influx was blocked by both bisindolyleimide I (PKC inhibitor) and U-73122 (PLC inhibitor) suggesting a modulation of V1 agonist-induced L-type calcium channel activation by downstream components of the phosphatidylinositol signaling pathway such as protein kinase C. These results indicate that in cultured cortical neurons, V1a vasopressin receptor activation leads to induction of the phosphatidylinositol signaling pathway, influx of extracellular calcium via L-type calcium channel activation, and a rise in intracellular calcium which is dependent on V1a receptor activated influx of extracellular calcium. These data are the first to demonstrate an effector mechanism for the V1 vasopressin receptor in the cerebral cortex and provide a potential biochemical mechanism that may underlie vasopressin enhancement of memory function.
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PMID:Vasopressin-induced calcium signaling in cultured cortical neurons. 963 Jun 55

The vasoactive hormones vasopressin, angiotensin II, adrenaline, and noradrenaline may all be released after central neural stimulation, but our knowledge of their relative actions on regional vascular resistances is incomplete. A comprehensive account of these patterns will help our understanding of their contributions to centrally generated patterns of blood flow. In the present study, regional blood flows and resistances of five major arteries were measured during sequential intravenous infusions of a range of doses of each substance in conscious rats. Vasopressin strongly increased superior mesenteric, hindquarters, carotid, and renal resistance but did not affect celiac artery resistance until the highest infusion rate. Both angiotensin II and noradrenaline increased resistance, although to different extents, in all vascular beds except the hindquarters, which was unaffected. Adrenaline infused at pressor rates markedly increased superior mesenteric resistance while moderately increasing renal, carotid and celiac arterial resistances. At subpressor rates, however, adrenaline increased celiac resistance but decreased hindquarters vascular resistance without significantly affecting the other beds. It is concluded that each vasoactive substance released into the systemic circulation causes its own characteristic pattern of vascular responses. This information should be useful for understanding the humoral basis of hemodynamic responses to central stimuli.
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PMID:Regional hemodynamic responses to exogenous catecholamines and vasoactive peptides in conscious rats. 1039 53

The effects of paraventricular nucleus (PVN) stimulation and vasopressin on gastric ischemia-reperfusion injury (GI-RI) were investigated in male SD rats of which the celiac artery was clamped for 30 min and reperfused for 1 h by removal of the clamp. The results were as follows. Both electrical and chemical stimulation of the PVN obviously attenuated the GI-RI. Bilateral electrolytic lesion of the nucleus tractus solitarius (NTS) or microinjection of AVP-V(1) receptor antagonist into the NTS could eliminate the protective effect of electrical stimulation of the PVN on GI-RI. Hypophysectomy did not influence the effect of electrical stimulation of the PVN. Both vagotomy and sympathectomy could increase the effect of stimulating PVN on GI-RI. Microinjection of arginine-vasopressin (AVP) into the PVN also attenuated the effect on GI-RI. These results suggest that the PVN and AVP participate in the regulation of GI-RI and play an important role in protection against GI-RI. This protective effect of PVN on GI-RI might be mediated by activation of AVP-ergic neurons in the PVN, which release AVP from the descending projection fibers and activate the AVP-V(1) receptors on the NTS neurons. The vagus and sympathetic nerves are involved in the efferent pathway exerting their effects on GI-RI. Hypophysis does not seem to be involved in the protective effect of PVN stimulation.
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PMID:[Protective effects of paraventricular nucleus stimulation and vasopressin on gastric ischemia-reperfusion injury in rats]. 1197 93

The adrenal glands and sympathetic celiac ganglia are innervated mainly by the greater splanchnic nerves, which contain preganglionic sympathetic nerves that originated from the thoracic spinal cord. The adrenal medulla has two separate populations of chromaffin cells, adrenaline-containing cells (A-cells) and noradrenaline-containing cells (NA-cells), which have been shown to be differentially innervated by separate groups of the preganglionic sympathetic neurons. The present study was designed to characterize the centrally activating mechanisms of the adrenal A-cells, NA-cells and celiac sympathetic ganglia with expression of cFos (a marker for neural excitation), in regard to the brain prostanoids, in anesthetized rats. Intracerebroventricularly (i.c.v.) administered corticotropin-releasing factor (CRF) induced cFos expression in the adrenal A-cells, but not NA-cells, and celiac ganglia. On the other hand, i.c.v. administered arginine-vasopressin (AVP) resulted in cFos induction in both A-cells and NA-cells in the adrenal medulla, but not in the celiac ganglia. Intracerebroventricular pretreatment with indomethacin (an inhibitor of cyclooxygenase) abolished the CRF- and AVP-induced cFos expression in all regions described above. On the other hand, intracerebroventricular pretreatment with furegrelate (an inhibitor of thromboxane A2 synthase) abolished the CRF-induced cFos expression in the adrenal A-cells, but not in the celiac ganglia, and also abolished the AVP-induced cFos expression in both A-cells and NA-cells in the adrenal medulla. These results suggest that centrally administered CRF activates adrenal A-cells and celiac sympathetic ganglia by brain thromboxane A2-mediated and other prostanoid than thromboxane A2 (probably prostaglandin E2)-mediated mechanisms, respectively. On the other hand, centrally administered AVP activates adrenal A-cells and NA-cells by brain thromboxane A2-mediated mechanisms in rats.
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PMID:Adrenal adrenaline- and noradrenaline-containing cells and celiac sympathetic ganglia are differentially controlled by centrally administered corticotropin-releasing factor and arginine-vasopressin in rats. 1735 Jun 15


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