PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 10419925-5 1999 In addition, VIP significantly increased bile pH, bicarbonate concentration, and output in the isolated perfused livers from both normal and 2 week bile duct-ligated rats, although bile flow increased only in the bile duct-ligated model. Bicarbonates 50-61 vasoactive intestinal peptide Rattus norvegicus 13-16 10419925-10 1999 CONCLUSIONS: VIP is a potent stimulant of fluid and bicarbonate secretion from cholangiocytes via cAMP-independent pathways, suggesting that this neuropeptide plays a major regulatory role in biliary transport and secretion. Bicarbonates 52-63 vasoactive intestinal peptide Rattus norvegicus 13-16 7590000-5 1995 RESULTS: C7-sorbin was the minimal peptide able to decrease duodenal VIP-stimulated fluxes of water, Na and bicarbonate. Bicarbonates 108-119 vasoactive intestinal peptide Rattus norvegicus 69-72 9714419-6 1998 These results suggest that PACAP-27 increases duodenal HCO3- secretion and this action may be important in maintaining the duodenal mucosal integrity against acid, and VIP affords duodenal protection by both increasing duodenal HCO3- secretion and decreasing acid secretion. Bicarbonates 228-232 vasoactive intestinal peptide Rattus norvegicus 168-171 9257115-9 1997 The putative VIP antagonist [Lys1,Pro25,Arg3,4,Tyr6]-VIP (abbreviated as VIPi) caused a selective and significant reduction in the HCO3- secretion evoked by VIP and blocked the vasodepressor response caused by VIP. Bicarbonates 131-135 vasoactive intestinal peptide Rattus norvegicus 13-16 9257115-9 1997 The putative VIP antagonist [Lys1,Pro25,Arg3,4,Tyr6]-VIP (abbreviated as VIPi) caused a selective and significant reduction in the HCO3- secretion evoked by VIP and blocked the vasodepressor response caused by VIP. Bicarbonates 131-135 vasoactive intestinal peptide Rattus norvegicus 53-56 9257115-9 1997 The putative VIP antagonist [Lys1,Pro25,Arg3,4,Tyr6]-VIP (abbreviated as VIPi) caused a selective and significant reduction in the HCO3- secretion evoked by VIP and blocked the vasodepressor response caused by VIP. Bicarbonates 131-135 vasoactive intestinal peptide Rattus norvegicus 53-56 9257115-9 1997 The putative VIP antagonist [Lys1,Pro25,Arg3,4,Tyr6]-VIP (abbreviated as VIPi) caused a selective and significant reduction in the HCO3- secretion evoked by VIP and blocked the vasodepressor response caused by VIP. Bicarbonates 131-135 vasoactive intestinal peptide Rattus norvegicus 53-56 9990657-9 1998 These peptide antagonists suppressed duodenal HCO3- secretory response to VIP but did not have any effect on either basal or PGE2-stimulated HCO3- secretion. Bicarbonates 46-50 vasoactive intestinal peptide Rattus norvegicus 74-77 9990657-11 1998 Duodenal damage induced by acid perfusion (100 mM HCl for 4 h) was significantly worsened by PACAP6-27, VIP antagonist as well as indomethacin at the doses that suppressed acid-induced HCO3- secretion. Bicarbonates 185-189 vasoactive intestinal peptide Rattus norvegicus 104-107 9655689-5 1998 Similarly, NKA partially inhibited the VIP-stimulated bicarbonate secretion. Bicarbonates 54-65 vasoactive intestinal peptide Rattus norvegicus 39-42 9403800-5 1997 The potency of duodenal HCO3- secretory action was in the following order; PACAP-27 > PACAP-38 = VIP, and that of PACAP-27 was about 100-fold greater than that of PGE2. Bicarbonates 24-28 vasoactive intestinal peptide Rattus norvegicus 100-103 9124587-4 1997 The duodenal HCO(3)- stimulatory action was similarly observed after intravenous administration of PACAP-38 and VIP, and the potency of action was in the following order: PACAP-27 > PACAP-38 = VIP. Bicarbonates 13-19 vasoactive intestinal peptide Rattus norvegicus 112-115 9124587-4 1997 The duodenal HCO(3)- stimulatory action was similarly observed after intravenous administration of PACAP-38 and VIP, and the potency of action was in the following order: PACAP-27 > PACAP-38 = VIP. Bicarbonates 13-19 vasoactive intestinal peptide Rattus norvegicus 196-199 9124587-5 1997 The duodenal HCO(3)- stimulatory action of PACAP-27 was potentiated by pretreatment with 3-isobutyl-1-methylxanthine, similar to that of prostaglandin E2, and was significantly attenuated by PACAP-(6--27) (PACAP antagonist) or Ac-Tyr1,D-Phe2-VIP (VIP antagonist) but was not affected by bilateral vagotomy or prior administration of atropine, verapamil, and indomethacin. Bicarbonates 13-19 vasoactive intestinal peptide Rattus norvegicus 242-245 9124587-5 1997 The duodenal HCO(3)- stimulatory action of PACAP-27 was potentiated by pretreatment with 3-isobutyl-1-methylxanthine, similar to that of prostaglandin E2, and was significantly attenuated by PACAP-(6--27) (PACAP antagonist) or Ac-Tyr1,D-Phe2-VIP (VIP antagonist) but was not affected by bilateral vagotomy or prior administration of atropine, verapamil, and indomethacin. Bicarbonates 13-19 vasoactive intestinal peptide Rattus norvegicus 247-250 8023967-0 1994 In vivo modulation of rat distal tubule net HCO3 flux by VIP, isoproterenol, angiotensin II, and ADH. Bicarbonates 44-48 vasoactive intestinal peptide Rattus norvegicus 57-60 7924732-2 1994 Using an isolated loop of the proximal duodenum of conscious rats, the role of vasoactive intestinal peptide (VIP) in the duodenal HCO3- response to HCl was examined, especially interactions with participating cholinoceptor mechanisms and prostaglandins. Bicarbonates 131-135 vasoactive intestinal peptide Rattus norvegicus 110-113 7924732-5 1994 The HCO3- secretion in response to graded doses of intravenous VIP (0.00625-6 nmol/kg/30 min) was dose-dependent to maximally 33.5 +/- 10.5 mumol/cm/hr. Bicarbonates 4-8 vasoactive intestinal peptide Rattus norvegicus 63-66 7924732-6 1994 The HCO3- secretion during a single intravenous infusion of VIP (12 nmol/kg/hr), 13.9 +/- 4.2 mumol/cm/hr, was unchanged by atropine, reduced to 10.0 +/- 3.5 mumol/cm/hr by hexamethonium, and augmented to 18.9 +/- 4.7 mumol/cm/hr by indomethacin. Bicarbonates 4-8 vasoactive intestinal peptide Rattus norvegicus 60-63 7924732-9 1994 In conclusion, in the duodenal HCO3- response to luminal HCl, VIP may have a stimulatory role, which partially depends on nicotinic, but not on muscarinic cholinoceptor mechanisms, and which is negatively modulated by prostaglandins. Bicarbonates 31-35 vasoactive intestinal peptide Rattus norvegicus 62-65 7875437-6 1994 RESULTS: Results show that C20-sorbin and C7-sorbin decreased the VIP-stimulated net flux of water (inhibition of 40 and 37%, respectively), Na (inhibition of 31 and 30%), C1 (inhibition of 80 and 63%) and HCO3 (inhibition of 15 and 25%). Bicarbonates 206-210 vasoactive intestinal peptide Rattus norvegicus 66-69 8271207-11 1993 The putative VIP (vasoactive intestinal polypeptide) antagonist [D-p-chloro-Phe6, Leu17]-VIP injected intravenously also increased the vagally evoked weight of juice, with total HCO3- and total protein unchanged. Bicarbonates 178-182 vasoactive intestinal peptide Rattus norvegicus 13-16 7904126-6 1993 Systemic infusion of VIP (2.5 micrograms.kg-1 x h-1) increased LA and fluid secretion; the HCO3- concentration in secreted fluid was 86 mM. Bicarbonates 91-95 vasoactive intestinal peptide Rattus norvegicus 21-24 7904126-14 1993 We conclude that NO may be an inhibitory regulator of LA and that both L-NNA and VIP increase LA via stimulation of active HCO3- transport. Bicarbonates 123-127 vasoactive intestinal peptide Rattus norvegicus 81-84 7904126-15 1993 VIP probably increases HCO3- and fluid secretion by two separate ion transport mechanisms. Bicarbonates 23-27 vasoactive intestinal peptide Rattus norvegicus 0-3 8271207-11 1993 The putative VIP (vasoactive intestinal polypeptide) antagonist [D-p-chloro-Phe6, Leu17]-VIP injected intravenously also increased the vagally evoked weight of juice, with total HCO3- and total protein unchanged. Bicarbonates 178-182 vasoactive intestinal peptide Rattus norvegicus 18-51 8271207-11 1993 The putative VIP (vasoactive intestinal polypeptide) antagonist [D-p-chloro-Phe6, Leu17]-VIP injected intravenously also increased the vagally evoked weight of juice, with total HCO3- and total protein unchanged. Bicarbonates 178-182 vasoactive intestinal peptide Rattus norvegicus 89-92 2531983-8 1989 Vagal stimulation induced by TRH increases duodenal bicarbonate secretion by the release of VIP and, in part, by activation of a muscarinic pathway but not by pituitary, adrenal, and noradrenergic pathways or endogenous opiates and prostaglandins. Bicarbonates 52-63 vasoactive intestinal peptide Rattus norvegicus 92-95 2531983-0 1989 TRH-induced vagal stimulation of duodenal HCO-3 mediated by VIP and muscarinic pathways. Bicarbonates 42-47 vasoactive intestinal peptide Rattus norvegicus 60-63 2531983-4 1989 The vasoactive intestinal peptide (VIP) receptor antagonist, (4Cl-D-Phe6, Leu17) VIP given intravenously completely prevented the stimulatory effect of central TRH on duodenal bicarbonate secretion. Bicarbonates 176-187 vasoactive intestinal peptide Rattus norvegicus 35-38 2531983-4 1989 The vasoactive intestinal peptide (VIP) receptor antagonist, (4Cl-D-Phe6, Leu17) VIP given intravenously completely prevented the stimulatory effect of central TRH on duodenal bicarbonate secretion. Bicarbonates 176-187 vasoactive intestinal peptide Rattus norvegicus 81-84 2531983-6 1989 Intravenous administration of VIP and carbachol significantly stimulated bicarbonate outputs, and these responses were blocked by the VIP antagonist and atropine, respectively. Bicarbonates 73-84 vasoactive intestinal peptide Rattus norvegicus 30-33 2531983-6 1989 Intravenous administration of VIP and carbachol significantly stimulated bicarbonate outputs, and these responses were blocked by the VIP antagonist and atropine, respectively. Bicarbonates 73-84 vasoactive intestinal peptide Rattus norvegicus 134-137 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 181-192 vasoactive intestinal peptide Rattus norvegicus 70-73 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 181-192 vasoactive intestinal peptide Rattus norvegicus 167-170 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 310-321 vasoactive intestinal peptide Rattus norvegicus 70-73 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 310-321 vasoactive intestinal peptide Rattus norvegicus 75-104 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 310-321 vasoactive intestinal peptide Rattus norvegicus 70-73 1575904-4 1992 The response to the perfused doses of 0.15 to 2.4 nmol.100 g-1.h-1 of VIP (vasoactive intestinal peptide) differed qualitatively and quantitatively in the 3 segments: VIP increased bicarbonate secretion and induced chloride secretion in the duodenum, induced chloride secretion in the jejunum without changing bicarbonate minimal influx, induced bicarbonate secretion and suppressed chloride absorption in the ileum. Bicarbonates 310-321 vasoactive intestinal peptide Rattus norvegicus 75-104 2383321-1 1990 Vasoactive intestinal peptide (VIP) is a potent stimulant of duodenal HCO3- secretion and may, like prostaglandins, have a stimulatory role in the local duodenal HCO3- response to luminal HCl. Bicarbonates 70-74 vasoactive intestinal peptide Rattus norvegicus 31-34 2383321-1 1990 Vasoactive intestinal peptide (VIP) is a potent stimulant of duodenal HCO3- secretion and may, like prostaglandins, have a stimulatory role in the local duodenal HCO3- response to luminal HCl. Bicarbonates 162-166 vasoactive intestinal peptide Rattus norvegicus 31-34 2383321-6 1990 Inhibition of prostaglandin synthesis by indomethacin augmented the HCl-stimulated luminal release of VIP, as well as the HCO3- response to exogenous VIP. Bicarbonates 122-126 vasoactive intestinal peptide Rattus norvegicus 150-153 2383321-9 1990 Released VIP may contribute to the HCO3- response at pH less than or equal to 3. Bicarbonates 35-39 vasoactive intestinal peptide Rattus norvegicus 9-12 6149978-3 1984 Somatostatin infused at doses of 1, 10, 100 and 1000 ng/kg/h against a background of VIP 100 ng/kg/h inhibited in dose-dependent fashion the stimulated epidermal growth factor and bicarbonate outputs from rat Brunner"s gland pouches. Bicarbonates 180-191 vasoactive intestinal peptide Rattus norvegicus 85-88 3860926-0 1985 Effects of some opiates and vasoactive intestinal peptide (VIP) on duodenal surface epithelial bicarbonate secretion in the rat. Bicarbonates 95-106 vasoactive intestinal peptide Rattus norvegicus 28-57 3860926-0 1985 Effects of some opiates and vasoactive intestinal peptide (VIP) on duodenal surface epithelial bicarbonate secretion in the rat. Bicarbonates 95-106 vasoactive intestinal peptide Rattus norvegicus 59-62 3860926-6 1985 The results suggest a role of endogenous opioid peptides and VIP in the humoral and/or nervous control of duodenal surface epithelial bicarbonate secretion and mucosal protection. Bicarbonates 134-145 vasoactive intestinal peptide Rattus norvegicus 61-64 2719108-0 1989 Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion. Bicarbonates 70-81 vasoactive intestinal peptide Rattus norvegicus 10-13 2719108-0 1989 Effect of VIP antagonist on VIP-, PGE2-, and acid-stimulated duodenal bicarbonate secretion. Bicarbonates 70-81 vasoactive intestinal peptide Rattus norvegicus 28-31 2719108-1 1989 Vasoactive intestinal peptide (VIP), prostaglandin E2 (PGE2), and luminal acidification are each potent stimulants of duodenal mucosal bicarbonate secretion. Bicarbonates 135-146 vasoactive intestinal peptide Rattus norvegicus 31-34 2719108-2 1989 The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. Bicarbonates 165-176 vasoactive intestinal peptide Rattus norvegicus 83-86 2719108-2 1989 The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. Bicarbonates 165-176 vasoactive intestinal peptide Rattus norvegicus 117-120 2719108-2 1989 The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. Bicarbonates 165-176 vasoactive intestinal peptide Rattus norvegicus 117-120 2719108-2 1989 The present experiments were performed to determine whether the recently described VIP antagonist, [4Cl-D-Phe6,Leu17]VIP, suppresses VIP-stimulated duodenal mucosal bicarbonate secretion and to determine whether VIP serves as a mediator of bicarbonate secretion stimulated by acid or PGE2. Bicarbonates 165-176 vasoactive intestinal peptide Rattus norvegicus 117-120 2719108-4 1989 The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. Bicarbonates 38-49 vasoactive intestinal peptide Rattus norvegicus 4-7 2719108-4 1989 The VIP antagonist inhibited duodenal bicarbonate secretion stimulated by both intravenous VIP and luminal acidification but not luminal PGE2. Bicarbonates 38-49 vasoactive intestinal peptide Rattus norvegicus 91-94 2719108-5 1989 These findings suggest that VIP could be one mediator of acid-induced duodenal bicarbonate secretion and that the mechanism of PGE2-stimulated bicarbonate secretion is independent of VIP. Bicarbonates 79-90 vasoactive intestinal peptide Rattus norvegicus 28-31 6548570-0 1984 Secretin, VIP, and PHI stimulate rat proximal duodenal surface epithelial bicarbonate secretion in vivo. Bicarbonates 74-85 vasoactive intestinal peptide Rattus norvegicus 10-13 6548570-5 1984 Compared to the saline control, each dose of VIP produced a significant increase in duodenal bicarbonate secretion in a dose-response manner. Bicarbonates 93-104 vasoactive intestinal peptide Rattus norvegicus 45-48 6548570-8 1984 It is concluded that secretin and VIP stimulate proximal duodenal bicarbonate secretion and are more potent than PHI. Bicarbonates 66-77 vasoactive intestinal peptide Rattus norvegicus 34-37 6149978-7 1984 It is concluded that VIP stimulates secretion of epidermal growth factor and bicarbonate from Brunner"s glands, an effect which is inhibited by somatostatin. Bicarbonates 77-88 vasoactive intestinal peptide Rattus norvegicus 21-24 30978113-12 2019 Based on the results from the present study, xenin-25-induced Cl-/ HCO3- secretion is involved in NTSR1 activation on intrinsic and extrinsic afferent neurons, followed by the release of SP and subsequent activation of NK1 expressed on noncholinergic VIP secretomotor neurons. Bicarbonates 67-71 vasoactive intestinal peptide Rattus norvegicus 251-254 30978113-13 2019 Finally, the secreted VIP may activate VPAC1 on epithelial cells to induce Cl-/ HCO3- secretion in the rat ileum. Bicarbonates 80-84 vasoactive intestinal peptide Rattus norvegicus 22-25 30978113-16 2019 We have found that nutrient-stimulated xenin-25 release may activate noncholinergic vasoactive intestinal polypeptide (VIP) secretomotor neurons to promote Cl-/ HCO3- secretion through the activation of VIP receptor 1 on epithelial cells. Bicarbonates 161-165 vasoactive intestinal peptide Rattus norvegicus 84-117 30978113-16 2019 We have found that nutrient-stimulated xenin-25 release may activate noncholinergic vasoactive intestinal polypeptide (VIP) secretomotor neurons to promote Cl-/ HCO3- secretion through the activation of VIP receptor 1 on epithelial cells. Bicarbonates 161-165 vasoactive intestinal peptide Rattus norvegicus 119-122