TY - JOUR
T1 - Vasopressin release during ventriculo cisternal perfusion with prostaglandin E2 in the dog
AU - Yamamoto, M.
AU - Share, L.
AU - Shade, R. E.
PY - 1976
Y1 - 1976
N2 - In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo cisternal system of anesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76.4 ng/min (0.19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152.8 ng/min (0.19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9.0±2.2 (S.E.M.) to 18.8±3.9 μu./ml at 10 min and to 41.0±16.7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.
AB - In an attempt to determine whether prostaglandin E2 (PGE2) can act centrally to affect the release of vasopressin (ADH), the ventriculo cisternal system of anesthetized dogs was perfused with PGE2. When PGE2 was perfused at a rate of 76.4 ng/min (0.19 ml/min), the plasma ADH concentration was unchanged. However, perfusion of PGE2 at a rate of 152.8 ng/min (0.19 ml/min) resulted in a significant increase in the plasma ADH concentration from the control value of 9.0±2.2 (S.E.M.) to 18.8±3.9 μu./ml at 10 min and to 41.0±16.7 μu./ml at 30 min after the start of the perfusion. There were no changes in arterial blood pressure, rectal temperature, plasma osmolality, and the plasma concentrations of sodium and potassium. In additional experiments, i.v. injection of indomethacin (2 or 20 mg/kg) decreased the plasma ADH concentration by approximately 50%. Although this finding is consistent with a role of PGE2 in the control of ADH release, it could also have been due to the observed increases in arterial blood pressure and effective left atrial pressure. Plasma renin activity was unchanged in the indomethacin experiments. It is concluded that PGE2 can act in the central nervous system to stimulate ADH release.
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U2 - 10.1677/joe.0.0710325
DO - 10.1677/joe.0.0710325
M3 - Article
C2 - 1003062
AN - SCOPUS:0017172048
VL - 71
SP - 325
EP - 331
JO - Journal of Endocrinology
JF - Journal of Endocrinology
SN - 0022-0795
IS - 3
ER -