TY - JOUR
T1 - Prostaglandin regulation of H+ secretion in amphibian epithelia
AU - Yorio, T.
AU - Page, R. D.
AU - Frazier, L. W.
PY - 1991
Y1 - 1991
N2 - The role of prostaglandins in regulating H+ excretion in amphibian epithelia was investigated. The abdominal skin of the southern leopard frog Rana pipiens and the urinary bladder of the toad Bufo marinus were used to measure proton excretion across their mucosal surface. Prostaglandin F(2α) (PGF(2α)) produced a dose-dependent inhibition of H+ excretion across the frog skin. Frogs pretreated with ibuprofen (30 mg·kg-1·day-1 for 3 days) showed an enhanced proton excretion similar to that observed when frogs are placed in chronic metabolic acidosis. The number of mitochondria-rich cells, the cells responsible for proton excretion, was also increased in frog skins after chronic metabolic acidosis or ibuprofen treatment. Mezerein and the phorbol ester 4β-phorbol 12-myristate 13-acetate (4β-PMA), activators of protein kinase C (PCK), decreased H+ excretion in frog skin, whereas the inactive phorbol 4α-PMA was without an effect. The inhibition of proton excretion was similar to that observed with PGF(2α) and suggested that the effects of PGF(2α) and activation of PKC were mediated through a common pathway. Frogs pretreated with ibuprofen not only had an enhanced proton excretion rate but also had a decrease in cytosolic PKC activity. In another amphibian tissue, the toad urinary bladder, PGE2 inhibited proton excretion at low doses but enhanced H+ excretion at higher doses. Toads maintained under chronic metabolic acidosis had enhanced proton excretion rates and also had a threefold increase in cellular PGE2 concentration, which was consistent with the observation that PGE2 enhanced proton excretion at high doses. Collectively, these observations suggest that prostaglandins and activation of PKC may play a role in regulating basal H+ excretion in amphibian epithelia.
AB - The role of prostaglandins in regulating H+ excretion in amphibian epithelia was investigated. The abdominal skin of the southern leopard frog Rana pipiens and the urinary bladder of the toad Bufo marinus were used to measure proton excretion across their mucosal surface. Prostaglandin F(2α) (PGF(2α)) produced a dose-dependent inhibition of H+ excretion across the frog skin. Frogs pretreated with ibuprofen (30 mg·kg-1·day-1 for 3 days) showed an enhanced proton excretion similar to that observed when frogs are placed in chronic metabolic acidosis. The number of mitochondria-rich cells, the cells responsible for proton excretion, was also increased in frog skins after chronic metabolic acidosis or ibuprofen treatment. Mezerein and the phorbol ester 4β-phorbol 12-myristate 13-acetate (4β-PMA), activators of protein kinase C (PCK), decreased H+ excretion in frog skin, whereas the inactive phorbol 4α-PMA was without an effect. The inhibition of proton excretion was similar to that observed with PGF(2α) and suggested that the effects of PGF(2α) and activation of PKC were mediated through a common pathway. Frogs pretreated with ibuprofen not only had an enhanced proton excretion rate but also had a decrease in cytosolic PKC activity. In another amphibian tissue, the toad urinary bladder, PGE2 inhibited proton excretion at low doses but enhanced H+ excretion at higher doses. Toads maintained under chronic metabolic acidosis had enhanced proton excretion rates and also had a threefold increase in cellular PGE2 concentration, which was consistent with the observation that PGE2 enhanced proton excretion at high doses. Collectively, these observations suggest that prostaglandins and activation of PKC may play a role in regulating basal H+ excretion in amphibian epithelia.
KW - Frog skin
KW - Hydrogen ion transport
KW - Protein kinase C
KW - Urinary bladder
UR - http://www.scopus.com/inward/record.url?scp=0025831408&partnerID=8YFLogxK
U2 - 10.1152/ajpregu.1991.260.5.r866
DO - 10.1152/ajpregu.1991.260.5.r866
M3 - Article
C2 - 1903604
AN - SCOPUS:0025831408
SN - 0363-6119
VL - 260
SP - R866-R872
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 5 29-5
ER -