Secretin-dependent HCO3- secretion from pancreas and liver.
Ultrastructural studies performed on pigs revealed that numerous cytoplasmic tubulovesicles were present in resting pancreatic duct cells. Elevation of systemic arterial PCO2 from 5.5 to 11 kPa increased the number of vesicles more than twofold. Following secretin administration, concurrent with the onset of HCO3- secretion (JHCO3), 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 microtubules-inhibiting drug colchicine, secretin failed to reduce duct cell vesicle density, and JHCO3 was reduced by c. 50% compared to the control. These ultrastructural changes resemble those described in other H+/HCO3(-)-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 JHCO3.
Institute for Experimental Medical Research, University of Oslo, Norway.
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D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001652:Bile Ducts / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D001692:Biological Transport / Q000502:physiology; D066298:In Vitro Techniques; D008099:Liver / Q000378:metabolism*; D010183:Pancreatic Ducts / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D012633:Secretin / Q000502:physiology*; D013552:Swine
D001639:Bicarbonates; D012633:Secretin