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Effect of reactive oxygen species (ROS) on the dynamics of renal autoregulation in Sprague‐Dawley (SDR) and spontaneously hypertensive rats (SHR)
Author(s) -
Sung Biin,
Siu Kin L.,
Chon Ki H.,
Moore Leon C.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a501
Subject(s) - isoflurane , autoregulation , chemistry , reactive oxygen species , cerebral autoregulation , kidney , medicine , endocrinology , blood pressure , renal blood flow , blood flow , anesthesia , biochemistry , organic chemistry
Our previous work has shown that isoflurane anesthesia is associated with a myogenic (MYO) dominant pattern of renal autoregulation in both SDR and SHR. Since others have shown increased levels of ROS in SHR and in animals treated with isoflurane, we tested the hypothesis that elevated ROS contributes to the increased MYO reactivity. Arterial blood pressure (BP) and renal blood flow (RBF) from SDR and SHR, anesthetized with isoflurane, were measured. The RBF measurements were made at two different sites: local cortical tissues (via laser‐Doppler velocimetry) and whole kidney (via an ultrasound flow probe). After baseline measurements, Tempol, a scavenger of ROS, was given for 1 hour. MYO compensation was calculated from vascular conductance before and after Tempol treatment, and in untreated time‐matched controls. Both cortical tissue and whole kidney measurements in both SDR and SHR show a decrease in the MYO compensation after Tempol treatment; time‐controls were unchanged. Moreover, damped MYO oscillations in cortical blood flow, typically seen after an abrupt rise in BP, were quenched by Tempol. Such damped MYO oscillations were not observed in the whole kidney recordings, possibly due to phase cancellation. These results suggest that elevated ROS enhances MYO reactivity and autoregulatory compensation in isoflurane anesthetized SHR and SDR.