TY - JOUR
T1 - Prostaglandin E2 synthesis in the inner medullary collecting duct of the rat
T2 - Implications for vasopressin‐dependent cyclic AMP formation
AU - Jackson, Brian A.
PY - 1986/10
Y1 - 1986/10
N2 - The effects of osmolality on prostaglandin E2 (PGE2) biosynthetic capacity and the interaction between endogenous PGE2 synthesis and vasopressin (AVP)‐dependent cyclic AMP generation were examined in papillary collecting ducts (PCD) microdissected from collagenase‐digested rat kidneys. Increasing medium osmolality with NaCl:urea (1:2 molar ratio) progressively increased PGE2 synthesis in PCD up to 1,500 mOsm. Addition of NaCl:urea or NaCI alone were equally effective in stimulating PGE2 biosynthetic capacity in PCD. In contrast, addition of urea alone had a much smaller stimulatory effect on PGE2 synthesis. Inhibition of endogenous PGE2 synthesis with naproxen (10−5M) suppressed AVP‐dependent cAMP formation in PCD when incubated in 300 mOsm medium but had no effect when incubated in 1,500 mOsm medium. Addition of 2.5×10−5 M PGE2 also suppressed AVP‐dependent cAMP formation in PCD only when incubated in 300 mOsm medium. The present study suggests that the PCD is a site of active PGE2 synthesis that is modulated by osmolality. Our results do not support the concept that endogenous PGE2 antagonizes vasopressin action via inhibition of AVP‐dependent cAMP formation.
AB - The effects of osmolality on prostaglandin E2 (PGE2) biosynthetic capacity and the interaction between endogenous PGE2 synthesis and vasopressin (AVP)‐dependent cyclic AMP generation were examined in papillary collecting ducts (PCD) microdissected from collagenase‐digested rat kidneys. Increasing medium osmolality with NaCl:urea (1:2 molar ratio) progressively increased PGE2 synthesis in PCD up to 1,500 mOsm. Addition of NaCl:urea or NaCI alone were equally effective in stimulating PGE2 biosynthetic capacity in PCD. In contrast, addition of urea alone had a much smaller stimulatory effect on PGE2 synthesis. Inhibition of endogenous PGE2 synthesis with naproxen (10−5M) suppressed AVP‐dependent cAMP formation in PCD when incubated in 300 mOsm medium but had no effect when incubated in 1,500 mOsm medium. Addition of 2.5×10−5 M PGE2 also suppressed AVP‐dependent cAMP formation in PCD only when incubated in 300 mOsm medium. The present study suggests that the PCD is a site of active PGE2 synthesis that is modulated by osmolality. Our results do not support the concept that endogenous PGE2 antagonizes vasopressin action via inhibition of AVP‐dependent cAMP formation.
UR - http://www.scopus.com/inward/record.url?scp=0022930039&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0022930039&partnerID=8YFLogxK
U2 - 10.1002/jcp.1041290109
DO - 10.1002/jcp.1041290109
M3 - Article
C2 - 3020064
AN - SCOPUS:0022930039
SN - 0021-9541
VL - 129
SP - 60
EP - 64
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
IS - 1
ER -