Experimental pancreatitis is mediated by low-affinity cholecystokinin receptors that inhibit digestive enzyme secretion.
AK Saluja, M Saluja, H Printz, A Zavertnik… - Proceedings of the …, 1989 - pnas.org
AK Saluja, M Saluja, H Printz, A Zavertnik, A Sengupta, ML Steer
Proceedings of the National Academy of Sciences, 1989•pnas.orgRats 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.
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