The Relation Between Pancreatic Secretion and Local Blood Flow: A Review

Tankel, H. I.; Hollander, Franklin

doi:10.1016/s0016-5085(57)80059-6

Cited by 42 publications

(13 citation statements)

References 14 publications

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“…Tankel et al (49) hypothesized that reductions in pancreatic microvascular blood flow (PMBF) can reduce pancreatic secretion. NOS inhibition has been shown to reduce in vivo stimulated pancreatic protein secretion and PMBF (24,41), although the association between secretory and circulatory events was secretagogue dependent (41).…”

Section: Discussionmentioning

confidence: 99%

Secretagogue-stimulated pancreatic secretion is differentially regulated by constitutive NOS isoforms in mice

DiMagno¹,

Hao²,

Tsunoda³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Nitric oxide (NO) and NO synthase (NOS) play controversial roles in pancreatic secretion. NOS inhibition reduces CCK-stimulated in vivo pancreatic secretion, but it is unclear which NOS isoform is responsible, because NOS inhibitors lack specificity and three NOS isoforms exist: neuronal (nNOS), endothelial (eNOS), and inducible (iNOS). Mice having individual NOS gene deletions were used to clarify the NOS species and cellular interactions influencing pancreatic secretion. In vivo secretion was performed in anesthetized mice by collecting extraduodenal pancreatic duct juice and measuring protein output. Nonselective NOS blockade was induced with N(omega)-nitro-L-arginine (L-NNA; 10 mg/kg). In vivo pancreatic secretion was maximal at 160 pmol.kg(-1).h(-1) CCK octapeptide (CCK-8) and was reduced by NOS blockade (45%) and eNOS deletion (44%). Secretion was unaffected by iNOS deletion but was increased by nNOS deletion (91%). To determine whether the influence of NOS on secretion involved nonacinar events, in vitro CCK-8-stimulated secretion of amylase from isolated acini was studied and found to be unaltered by NOS blockade and eNOS deletion. Influence of NOS on in vivo secretion was further examined with carbachol. Protein secretion, which was maximal at 100 nmol.kg(-1).h(-1) carbachol, was reduced by NOS blockade and eNOS deletion but unaffected by nNOS deletion. NOS blockade by L-NNA had no effect on carbachol-stimulated amylase secretion in vitro. Thus constitutive NOS isoforms can exert opposite effects on in vivo pancreatic secretion. eNOS likely plays a dominant role, because eNOS deletion mimics NOS blockade by inhibiting CCK-8 and carbachol-stimulated secretion, whereas nNOS deletion augments CCK-8 but not carbachol-stimulated secretion.

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Section: Discussionmentioning

confidence: 99%

Secretagogue-stimulated pancreatic secretion is differentially regulated by constitutive NOS isoforms in mice

DiMagno¹,

Hao²,

Tsunoda³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…In a review of the subject Tankel and Hollander (1957) concluded, from the evidence then available, that there were insufficient data to establish any association between pancreatic secretion and an increase in blood flow to the gland. More recent studies on this subject, however, point strongly to an association between pancreatic secretion and increased blood flow.…”

mentioning

confidence: 99%

Relationship between pancreatic secretion and pancreatic blood flow

Goodhead¹,

Himal²,

Zanbilowicz³

1970

Gut

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“…The influence of vasomotor reactions in the pancreas on the secretary function of the gland is still an open question. It has been suggested that, above a critical level, blood flow does not interfere with the secretary response to stimulants (Tankel & Hollander, 1957). However, it is logical to suppose that any increase in blood flow will raise the amount ofstimulant flowing into the pancreas (Thomas, 1967).…”

Section: Discussionmentioning

confidence: 99%

Relationships between blood flow and secretion in the isolated perfused canine pancreas

Augier¹,

Boucard²,

Pascal³

et al. 1972

The Journal of Physiology

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SUMMARY1. Stimulation by a continuous intra-arterial infusion of secretin caused a marked vasodilatation in the pancreato-duodenal preparation or in the isolated pancreas perfused with whole heparinized blood. There was no difference in the vasomotor effects of two unequally purified preparations of secretin. The fact that the vasodilatation was still observed when the duodenum was removed proved that the haemodynamic effect of secretin was initiated in the pancreas itself.2. The secretary response of the pancreas to a given dose of secretin was larger when the blood pressure was kept constant by increasing the blood flow than when the blood pressure was allowed to fall by maintaining the blood flow at a fixed value. It is concluded that the vasodilatation plays a role in the functional regulation of the pancreatic response to secretin. 3. The correlation between blood flow and arterial pressure on the one hand, and the secretary response to secretin on the other, was not mediated by the control of respiration since there was no variation in oxygen uptake in response to a variation in the blood flow. This correlation was still observed when the venous blood was discarded and therefore could not be explained by variations in the rate of recirculation of secretin. It was observed too in experiments where the duodenum was removed, the pancreas alone being introduced into the perfusion apparatus, which indicated that this effect was not mediated by a control of the release of secretin by the duodenum.

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The Relation Between Pancreatic Secretion and Local Blood Flow: A Review

Cited by 42 publications

References 14 publications

Secretagogue-stimulated pancreatic secretion is differentially regulated by constitutive NOS isoforms in mice

Secretagogue-stimulated pancreatic secretion is differentially regulated by constitutive NOS isoforms in mice

Relationship between pancreatic secretion and pancreatic blood flow

Relationships between blood flow and secretion in the isolated perfused canine pancreas

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