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Secretin‐dependent HCO 3 − secretion from pancreas and liver
Author(s) -
GROTMOL T.,
BUANES T.,
VEEL T.,
RŒDER M.
Publication year - 1990
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/j.1365-2796.1990.tb01471.x
Subject(s) - secretin , vesicle , secretion , medicine , endocrinology , cytoplasm , pancreas , colchicine , stimulation , epithelial polarity , nephron , duct (anatomy) , chemistry , biology , epithelium , microbiology and biotechnology , membrane , pathology , biochemistry , kidney
. Ultrastructural studies performed on pigs revealed that numerous cytoplasmic tubulovesicles were present in resting pancreatic duct cells. Elevation of systemic arterial P CO2 from 5.5 to 11 kPa increased the number of vesicles more than twofold. Following secretin administration, concurrent with the onset of HCO 3 − secretion (J HCO3 ). the cytoplasm became devoid of vesicles, and the basolateral plasma membrane surface area more than doubled. Similar phenomena were observed in bile duct cells. After pretreatment with the microtubulus‐inhibiting drug colchicine, secretin failed to reduce duct cell vesicle density, and J HCO3 was reduced by c. 50% compared to the control. These ultrastructural changes resemble those described in other H + /HCO 3 − ‐transporting organs such as the distal nephron and the urinary bladder. Our findings are compatible with the notion that cytoplasmic vesicles containing H + ‐ATPases are incorporated into the basolateral plasma membrane of secretory cells during secretin stimulation. Active transport of H + into interstitial fluid might therefore be the driving force underlying J HCO3 .