Adrenergic pathway in the inhibition of pancreatic secretion by peptide YY in dogs.
Adrenergic pathway in the inhibition of pancreatic secretion by peptide YY in dogs.
复制标题
肽 YY 抑制狗胰腺分泌的肾上腺素能途径。
DOI：
10.1016/0016-5085(88)90412-x
复制
发表时间：
1988
期刊：
影响因子：
29.4
通讯作者：
W. Domschke
中科院分区：
文献类型：
--
作者：
S. Konturek;J. Bilski;W. Pawlik;J. Tasler;W. Domschke
肽YY（PYY）通过用油酸盐灌注回结肠段而释放，并且抑制胰腺外分泌。本研究旨在确定肾上腺素能途径在PYY诱导的胰腺分泌抑制中的作用。PYY静脉给药后，有剂量依赖性抑制胰腺HCO 3和蛋白质的反应，促胰液素，胆囊收缩素，清醒的狗和胰腺血流量减少麻醉动物喂养。PYY对胰腺分泌和血流量的这些抑制作用在酚妥拉明和普萘洛尔联合存在下被消除。回肠灌注油酸酯引起血浆PYY水平升高，与静脉输注外源性PYY后观察到的结果相似。联合α-和β-肾上腺素能阻滞剂也可拮抗油酸酯回肠灌注对激素和餐后胰腺分泌的影响。我们的结论是外源性PYY或内源性PYY释放回肠油酸抑制胰腺分泌反应外源性促胰液素，胆囊收缩素，或一顿饭，并导致胰腺血管收缩。这两种作用至少部分是由肾上腺素能途径介导的。
Peptide YY (PYY) is released by perfusion of an ileocolonic segment with oleate and inhibits exocrine pancreatic secretion. This study was designed to determine the role of the adrenergic pathway in the PYY-induced inhibition of pancreatic secretion. After intravenous administration of PYY, there was a dose-dependent inhibition of pancreatic HCO3and protein responses to secretin, cholecystokinin, and feeding in conscious dogs and a reduction in pancreatic blood flow in anesthetized animals. These inhibitory effects of PYY on pancreatic secretion and blood flow were abolished in the presence of combined phentolamine and propranolol. Ileal perfusion with oleate caused a rise in plasma PYY levels similar to that observed after intravenous infusion of exogenous PYY. Combined α- and β-adrenergic blockade also antagonized the effects of ileal perfusion with oleate on hormonal and postprandial pancreatic secretion. We conclude that exogenous PYY or endogenous PYY released by ileal oleate inhibits pancreatic secretory responses to exogenous secretin, cholecystokinin, or a meal and causes pancreatic vasoconstriction. Both these effects are mediated, at least in part, by the adrenergic pathway.
影响因子：
29.4
作者：
I. Taylor
通讯作者：
I. Taylor
肽 YY 抑制膳食刺激的胰腺和胃分泌。
DOI：
10.1152/ajpgi.1985.248.1.g118
发表时间：
1985
期刊：
The American journal of physiology
影响因子：
--
作者：
Pappas,TN;Debas,HT;Goto,Y;Taylor,IL
通讯作者：
Taylor,IL