Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | American Journal of Physiology: Regulatory, Integrative and Comparative Physiology |
| Vol/bind | 285 |
| Udgave nummer | 2 |
| Sider (fra-til) | R329-38 |
| ISSN | 0363-6119 |
| DOI | |
| Status | Udgivet - 2003 |
Bibliografisk note
Keywords: Animals; Captopril; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Indomethacin; Isoenzymes; Kidney; NG-Nitroarginine Methyl Ester; Nitric Oxide; Perfusion; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Inbred SHR; Renal Circulation; ReninAdgang til dokumentet
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NO mediates downregulation of RBF after a prolonged reduction of renal perfusion pressure in SHR. / Sørensen, Charlotte Mehlin; Leyssac, Paul Peter; Skott, Ole; Holstein-Rathlou, N.-H.
I: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Bind 285, Nr. 2, 2003, s. R329-38.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - NO mediates downregulation of RBF after a prolonged reduction of renal perfusion pressure in SHR.
AU - Sørensen, Charlotte Mehlin
AU - Leyssac, Paul Peter
AU - Skott, Ole
AU - Holstein-Rathlou, N.-H.
N1 - Keywords: Animals; Captopril; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Indomethacin; Isoenzymes; Kidney; NG-Nitroarginine Methyl Ester; Nitric Oxide; Perfusion; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Inbred SHR; Renal Circulation; Renin
PY - 2003
Y1 - 2003
N2 - The aim of the study was to investigate mechanisms underlying the downregulation of renal blood flow (RBF) after a prolonged reduction in renal perfusion pressure (RPP) in adult spontaneously hypertensive rats (SHR). We tested the effect on the RBF response of clamping plasma ANG II in sevoflurane-anesthetized SHR. We also tested the effect of general cyclooxygenase (COX) inhibition and inhibition of the inducible COX-2. Furthermore, we assessed the effect of clamping the nitric oxide (NO) system. A prolonged period (15 min) of reduced RPP induced a downregulation of RBF. This was unchanged after clamping of plasma ANG II concentrations, general COX inhibition, and specific inhibition of COX-2. In contrast, clamping the NO system diminished the ability of SHR to downregulate RBF to a lower level. The downregulation of RBF was not associated with a resetting of the lower limit of autoregulation in the control group, in the ANG II-clamped group, or the NO clamped group. However, general COX inhibition and specific COX-2 inhibition enabled downward resetting of the lower limit of autoregulation. In conclusion, in SHR the renin-angiotensin system does not appear to play a major role in the downregulation of RBF after prolonged reduction of RPP. This response appears to be mediated partly by the NO system. We hypothesize that, in SHR, lack of downward resetting of the lower limit of autoregulation in response to a prolonged lowering of RPP could be the result of increased COX-2-mediated production of vasoconstrictory prostaglandins.
AB - The aim of the study was to investigate mechanisms underlying the downregulation of renal blood flow (RBF) after a prolonged reduction in renal perfusion pressure (RPP) in adult spontaneously hypertensive rats (SHR). We tested the effect on the RBF response of clamping plasma ANG II in sevoflurane-anesthetized SHR. We also tested the effect of general cyclooxygenase (COX) inhibition and inhibition of the inducible COX-2. Furthermore, we assessed the effect of clamping the nitric oxide (NO) system. A prolonged period (15 min) of reduced RPP induced a downregulation of RBF. This was unchanged after clamping of plasma ANG II concentrations, general COX inhibition, and specific inhibition of COX-2. In contrast, clamping the NO system diminished the ability of SHR to downregulate RBF to a lower level. The downregulation of RBF was not associated with a resetting of the lower limit of autoregulation in the control group, in the ANG II-clamped group, or the NO clamped group. However, general COX inhibition and specific COX-2 inhibition enabled downward resetting of the lower limit of autoregulation. In conclusion, in SHR the renin-angiotensin system does not appear to play a major role in the downregulation of RBF after prolonged reduction of RPP. This response appears to be mediated partly by the NO system. We hypothesize that, in SHR, lack of downward resetting of the lower limit of autoregulation in response to a prolonged lowering of RPP could be the result of increased COX-2-mediated production of vasoconstrictory prostaglandins.
U2 - 10.1152/ajpregu.00063.2003
DO - 10.1152/ajpregu.00063.2003
M3 - Journal article
C2 - 12714352
VL - 285
SP - R329-38
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 2
ER -