Experimental pancreatitis is mediated by low-affinity cholecystokinin receptors that inhibit digestive enzyme secretion.
AK Saluja, M Saluja, H Printz… - Proceedings of the …, 1989 - National Acad Sciences
AK Saluja, M Saluja, H Printz, A Zavertnik, A Sengupta, ML Steer
Proceedings of the National Academy of Sciences, 1989•National Acad SciencesRats infused with a supramaximally stimulating dose of the cholecystokinin (CCK) analog
caerulein develop acute edematous pancreatitis. Using CCK-JMV-180, a recently
developed CCK analog that acts as an agonist at high-affinity CCK receptors but
antagonizes the effect of CCK at low-affinity receptors, we have determined that caerulein
induces pancreatitis by interacting with low-affinity CCK receptors. Those low-affinity
receptors mediate CCK-induced inhibition of digestive enzyme secretion from the pancreas …
caerulein develop acute edematous pancreatitis. Using CCK-JMV-180, a recently
developed CCK analog that acts as an agonist at high-affinity CCK receptors but
antagonizes the effect of CCK at low-affinity receptors, we have determined that caerulein
induces pancreatitis by interacting with low-affinity CCK receptors. Those low-affinity
receptors mediate CCK-induced inhibition of digestive enzyme secretion from the pancreas …
Rats infused with a supramaximally stimulating dose of the cholecystokinin (CCK) analog caerulein develop acute edematous pancreatitis. Using CCK-JMV-180, a recently developed CCK analog that acts as an agonist at high-affinity CCK receptors but antagonizes the effect of CCK at low-affinity receptors, we have determined that caerulein induces pancreatitis by interacting with low-affinity CCK receptors. Those low-affinity receptors mediate CCK-induced inhibition of digestive enzyme secretion from the pancreas. Our observations, therefore, suggest that this form of experimental pancreatitis results from the inhibition of pancreatic digestive enzyme secretion.
National Acad Sciences