TY - JOUR
T1 - Effect of atriopeptin III on renin release in vitro
AU - Henrich, William L.
AU - Needleman, Philip
AU - Campbell, William B.
N1 - Funding Information:
Acknowledeements Support for these studies was provided by the Research Service of the Veterans Adminlstration and a grant from the National Heart, Lung and Blood Institute (HL-21066). Dr. Campbell is the reclplent of a Research Career Development Award of the National Institutes of Health (KO4-HLO00801). Ns. Virginia Mitchell provided expert secretarial assistance. The authors wish to thank Dr. Scott of the Nonsanto Co., St. Louis, MO for provldlng the Atrlopeptln III.
PY - 1986/9/15
Y1 - 1986/9/15
N2 - The ability of atriopeptin III (AP) to directly inhibit renal renin release has not been resolved. This issue was examined in a series of experiments performed in a system of rat renal cortical slices (dry weight 1.91 mg) in which the goal was to explore the effects of Ap on renin release induced by cyclic AMP (cAMP)-coupled stimuli or by agents which are believed to decrease intracellular calcium (Cai). Concentration response relationships were initially established for all test agents. The cAMP stimuli utilized were isoproterenol (10-5M), forskolin (10-5M), and dibutyryl cAMP (3 × 10-4M); each of these agents produced a significant increase in renin release in the system (with isoproterenol a 50% increase, with forskolin 37%, and with dibutyryl cAMP 52%). The addition of AP (2.09 × 10-8,M, a minimum inhibitory concentration derived from preliminary studies) significantly blunted these increases; in the case of the dibutyryl cAMP-stimulated renin release, the inhibition was partial as a significant 25% increase in renin occured in the presence of AP. The addition of the calcium channel blocking agent in diltiazem (10-4M) resulted in a significant increase in renin release (364 to 567 ng.mg-1, p<.05) which was not blocked by the addition of AP. Similarly, TMB-8 (0.6 × 10-4M), another agent thought to lower Cai, also resulted in increased renin release (455 to 810 ng.mg-1), p<.01) which.
AB - The ability of atriopeptin III (AP) to directly inhibit renal renin release has not been resolved. This issue was examined in a series of experiments performed in a system of rat renal cortical slices (dry weight 1.91 mg) in which the goal was to explore the effects of Ap on renin release induced by cyclic AMP (cAMP)-coupled stimuli or by agents which are believed to decrease intracellular calcium (Cai). Concentration response relationships were initially established for all test agents. The cAMP stimuli utilized were isoproterenol (10-5M), forskolin (10-5M), and dibutyryl cAMP (3 × 10-4M); each of these agents produced a significant increase in renin release in the system (with isoproterenol a 50% increase, with forskolin 37%, and with dibutyryl cAMP 52%). The addition of AP (2.09 × 10-8,M, a minimum inhibitory concentration derived from preliminary studies) significantly blunted these increases; in the case of the dibutyryl cAMP-stimulated renin release, the inhibition was partial as a significant 25% increase in renin occured in the presence of AP. The addition of the calcium channel blocking agent in diltiazem (10-4M) resulted in a significant increase in renin release (364 to 567 ng.mg-1, p<.05) which was not blocked by the addition of AP. Similarly, TMB-8 (0.6 × 10-4M), another agent thought to lower Cai, also resulted in increased renin release (455 to 810 ng.mg-1), p<.01) which.
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U2 - 10.1016/0024-3205(86)90288-2
DO - 10.1016/0024-3205(86)90288-2
M3 - Article
C2 - 3018407
AN - SCOPUS:0022454049
VL - 39
SP - 993
EP - 1001
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 11
ER -