Whang E E, Hines O J, Reeve J R, Grandt D, Moser J A, Bilchik A J, Zinner M J, McFadden D W, Ashley S W
Department of Surgery, UCLA School of Medicine, USA.
Dig Dis Sci. 1997 Jun;42(6):1121-7. doi: 10.1023/a:1018869116284.
Peptide YY (PYY) is a potent regulator of intestinal secretion. These studies investigated the role of Y1 and Y2 receptor subtypes in mediating the antisecretory effects of PYY on mucosa-submucosa preparations of rat distal colon. Addition of vasoactive intestinal peptide (VIP) to these tissues resulted in a 140 +/- 18% increase in basal short-circuit current (Isc) and the induction of Cl- secretion. VIP-stimulated increases in Isc were abolished by the addition of each of PYY, (Pro34)-PYY, a Y1 receptor-selective agonist, and PYY-(3-36), an endogenous Y2 receptor-selective ligand. However, when tissue neural transmission was blocked with tetrodotoxin, neither PYY nor its receptor subtype-selective analogs were able to inhibit VIP-stimulated increases in Isc. These results suggest that in the rat distal colon, the antisecretory actions of PYY are mediated through a combination of Y1 and Y2 receptor subtypes or through a novel receptor subtype that is unable to discriminate between (Pro34)-PYY and PYY-(3-36).
肽YY（PYY）是肠道分泌的一种有效调节剂。这些研究调查了Y1和Y2受体亚型在介导PYY对大鼠远端结肠黏膜-黏膜下层制剂的抗分泌作用中的作用。向这些组织中添加血管活性肠肽（VIP）导致基础短路电流（Isc）增加140±18%，并诱导氯离子分泌。添加PYY、（Pro34）-PYY（一种Y1受体选择性激动剂）和PYY-（3-36）（一种内源性Y2受体选择性配体）均可消除VIP刺激引起的Isc增加。然而，当用河豚毒素阻断组织神经传递时，PYY及其受体亚型选择性类似物均不能抑制VIP刺激引起的Isc增加。这些结果表明，在大鼠远端结肠中，PYY的抗分泌作用是通过Y1和Y2受体亚型的组合介导的，或者是通过一种无法区分（Pro34）-PYY和PYY-（3-36）的新型受体亚型介导的。
