Abstract
The role of the renin angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin II, [1 sarcosine, 8 glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70 to 90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.
Original language | English (US) |
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Title of host publication | American Journal of Physiology |
Pages | 731-736 |
Number of pages | 6 |
Volume | 229 |
Edition | 3 |
State | Published - 1975 |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
Effect of β adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation. / Anderson, R. J.; Taher, M. S.; Cronin, R. E.; McDonald, K. M.; Schrier, R. W.
American Journal of Physiology. Vol. 229 3. ed. 1975. p. 731-736.Research output: Chapter in Book/Report/Conference proceeding › Chapter
}
TY - CHAP
T1 - Effect of β adrenergic blockade and inhibitors of angiotensin II and prostaglandins on renal autoregulation
AU - Anderson, R. J.
AU - Taher, M. S.
AU - Cronin, R. E.
AU - McDonald, K. M.
AU - Schrier, R. W.
PY - 1975
Y1 - 1975
N2 - The role of the renin angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin II, [1 sarcosine, 8 glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70 to 90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.
AB - The role of the renin angiotensin system and prostaglandins in renal autoregulation was investigated in dog kidneys in situ. Renal autoregulation during decreases in renal arterial pressure (RAP) was examined in animals pretreated with a competitive antagonist of angiotensin II, [1 sarcosine, 8 glycine] angiotensin II, or one of two chemically dissimilar inhibitors of prostaglandin synthetase, indomethacin and meclofenamate. Because of recent evidence suggesting a role for an intrarenal beta receptor in regulating renin release, renal autoregulation was also examined in animals treated with the beta adrenergic blocking agent propranolol. In all groups of animals constancy of glomerular filtration rate (GFR) and renal blood flow (RBF) was observed after substantial decreases in RAP to a range of 70 to 90 mmHg. These studies therefore do not provide evidence in support of a role for angiotensin II, prostaglandins, or an intrarenal beta receptor as mediators of the renal autoregulation of GFR or total RBF.
UR - http://www.scopus.com/inward/record.url?scp=0016717951&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0016717951&partnerID=8YFLogxK
M3 - Chapter
C2 - 813531
AN - SCOPUS:0016717951
VL - 229
SP - 731
EP - 736
BT - American Journal of Physiology
ER -