physiology of the biliary tree motility of the gallbl bladder-part 1

An incomplete picture has emerged of the complex means by which gallbladder motility is controlled under normal and pathophysiological conditions. In the first part of this review an overall account is presented. The mechanisms of cholecystokinin release, its stimulation by dietary factors and peptides elaborated by both pancreas and small intestine are discussed. The inhibition of cholecystokinin release by bile acids and proteases is also described. In the second part attention is focussed on other peptides affecting motility. These include [a] octreotide, effective for treatment of acromegaly, [b] peptide YY, contributing to a "colonic brake", [c] motilin, associated with interdigestive contractions, analogues of which possibly correct gallbaldder hypomotility, and d] substance P and calcitonin gene- related peptide, which facilitate ganglionic transmission after release from exrinsic sensory neurones and alter gallbladder responses to vagal stimulation. The sympathetic nervous system and diabetes mellitus also influence vagal responses. The former, acting presynaptically, may provide a "brake" to prevent vagal overactivity. The latter could cause hypomotility via autonomic neuropathy, although hyperglycaemia, itself, may play a role. The role of nitric oxide, released from neurones also producing vasoactive intestinal peptide is recognized. Both lengthen muscle, the former producing responses without requiring plasma membrane receptors. Gallbaldder motility also changes during pregnancy and stone formation. Progesterone and cholesterol can limit G protein actions, thus impairing contractions. Inflammation is associated with abnormal motility. The production of reactive Oxygen metabolites, acting directly or releasing prokinetic prostaglandins, may be responsible. It has been proposed that the gastrointestinal tract may be normally in a state of controlled inflamation, primed to react to harmful challenges

Avances en Hormonas Gastro-Intestinales:Colecistoquinina / Advances in gastrointestinal hormones: Cholecystokinin

Colecistoquinina(CCK) y gastrina integran una familia importante de polipéptidos gastroenteropancreáticos. La divesidad de funciones ejercidas por CCK se explica por su distribución en el aparato digestivo y el sistema nervioso tanto central como periférico; más que una hormona clásica es un neurotransmisor peptidérgico. CCK interviene preponderantemente en múltiples funciones digestivas:contracción y vaciamiento de la vesícula biliar, estimulación de la secreción pancreática, de enzimas, detención del vaciamiento gástrico, disminución de la secreción gástrica, regulación de la secreción de insulina, relajación transitoria del esfínter cardial y disminución de la ingestión alimentaria. En todas esta áreas he habido confusión entre los efectos farmacológicos y los fisiológicos. Los procedimientos tecnológicos modernos han producido avances considerables: biotitulación plasmática confiable, entendimiento de la heterogeneidad molecular, identificación y caracterización de los receptorres con sus biotipos, agonistas y antagonistas accesibles para estudios experimentales y clínicos. Los resultados permiten mejorar la perspectiva integradora de la fisiología normal y patológica. La aplicación terapéutica de CCK y sus derivados a algunos problemas específicos, como obesidad y anorexia, es aún incipiente y limitada