Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O2− dismutation on renal autoregulation in the time and frequency domains
Autor: | Nicholas G. Moss, William J. Arendshorst, Tayler K. Gentle |
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Rok vydání: | 2016 |
Předmět: |
Male
0301 basic medicine medicine.medical_specialty Afferent arterioles Physiology Myogenic mechanism 030204 cardiovascular system & hematology Kidney Two stages Renal Circulation Cyclic N-Oxides Mice 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Animals Homeostasis Autoregulation Enzyme Inhibitors Renal circulation Superoxide Dismutase Chemistry Muscle Smooth Editorial Focus Anatomy Arginine Vasopressin Mice Inbred C57BL NG-Nitroarginine Methyl Ester 030104 developmental biology medicine.anatomical_structure Renal blood flow Cardiology Spin Labels Vascular Resistance Nitric Oxide Synthase Perfusion |
Zdroj: | American Journal of Physiology-Renal Physiology. 310:F832-F845 |
ISSN: | 1522-1466 1931-857X |
Popis: | Renal blood flow autoregulation was investigated in anesthetized C57Bl6 mice using time- and frequency-domain analyses. Autoregulation was reestablished by 15 s in two stages after a 25-mmHg step increase in renal perfusion pressure (RPP). The renal vascular resistance (RVR) response did not include a contribution from the macula densa tubuloglomerular feedback mechanism. Inhibition of nitric oxide (NO) synthase [ NG-nitro-l-arginine methyl ester (l-NAME)] reduced the time for complete autoregulation to 2 s and induced 0.25-Hz oscillations in RVR. Quenching of superoxide (SOD mimetic tempol) during l-NAME normalized the speed and strength of stage 1 of the RVR increase and abolished oscillations. The slope of stage 2 was unaffected by l-NAME or tempol. These effects of l-NAME and tempol were evaluated in the frequency domain during random fluctuations in RPP. NO synthase inhibition amplified the resonance peak in admittance gain at 0.25 Hz and markedly increased the gain slope at the upper myogenic frequency range (0.06–0.25 Hz, identified as stage 1), with reversal by tempol. The slope of admittance gain in the lower half of the myogenic frequency range (equated with stage 2) was not affected by l-NAME or tempol. Our data show that the myogenic mechanism alone can achieve complete renal blood flow autoregulation in the mouse kidney following a step increase in RPP. They suggest also that the principal inhibitory action of NO is quenching of superoxide, which otherwise potentiates dynamic components of the myogenic constriction in vivo. This primarily involves the first stage of a two-stage myogenic response. |
Databáze: | OpenAIRE |
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