Basal vascular tone in the kidney. Evaluation from the static pressure-flow relationship under normal autoregulation and at maximal dilation in the dog.

Gross, R; Kirchheim, H. R.; Brandstetter, K

doi:10.1161/01.res.38.6.525

Cited by 20 publications

(6 citation statements)

References 27 publications

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“…This is in contrast to studies in the dog which acetylcholine specifically has been shown to lower RVR at reduced perfusion pressures (31,44). Our observations suggest that mannitol may act on the rat renal vasculature by a mechanism totally unrelated to that of other potent vasodilators.…”

Section: Methodscontrasting

confidence: 97%

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Johnston¹,

Bernard²,

Donohoe³

et al. 1979

J. Clin. Invest.

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A B S T R A C T The hemodynamics of the rat kidney were studied during reduction ofrenal arterial pressure to 35-40 mm Hg (H), and after volume expansion at that pressure with 0.9% NaCl (IS), 1.7% NaCl (HS), 5% mannitol in 0.9% NaCl (MS), 5% mannitol in water (MW), or 50 mM mannitol + 125 mM NaCl. During H, left renal blood flow (RBF) was 0.8±0.1 ml/min. Expansion with IS did not alter RBF, but expansion with HS, MS, MW, and 50 + 125 mM NaCl elevated RBF to 200-250% of hypoperfusion values. Glomerular capillary pressure rose significantly from 15.7±0.7 mm Hg during H to 22.3+1.1, 24.4±0.7, and 26.6±0.7 mm Hg following expansion with HS, MS, or MW, respectively. Efferent arteriolar pressure also rose significantly to 6.9+0.5, 9.7±0.8, and 9.5±0.9 mm Hg, respectively. Preglomerular resistance fell to 18-24% of H values, and postglomerular resistance fell to 58-74% of H values after expansion with HS, MS, or MW. Glomerular filtration (GFR) could not be detected during H or after IS expansion. HS and mannitol-containing solutions restored GFR to 0.10±0.02-0.15±0.02 ml/min, and single nephron glomerular filtration to 6-12 nl/min. Papaverine, acetylcholine, and kinins had no effect on RBF or GFR at a perfusion pressure of 35-40 mm Hg. We conclude that mannitol and HS have the capacity to augment RBF during hypoperfusion by reducing arteriolar resistance. The mechanism of the rise in RBF is uncertain; it may be due to changes in effective osmolality of the extracellular fluid or to a direct action of mannitol on vascular smooth muscle. Other potent vasodilators were ineffective during hypoperfusion.

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Section: Methodscontrasting

confidence: 97%

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Johnston¹,

Bernard²,

Donohoe³

et al. 1979

J. Clin. Invest.

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“…This proposed role for NO is at variance with a recent publication showing that an effect of L-NAME on the myogenic response similar to that reported here was reversed by cGMP formation induced by continual pharmacological stimulation of sGC (19). Overall steady-state RBF autoregulation efficiency was attenuated by up to 33%, although most investigators report that NO donors, L-arginine, or acetylcholine do not affect the efficiency of overall steady-state autoregulation (28,45,67,68). Adding to controversy in this area are the puzzling results on mice deficient in the various NOS isoforms from which Dautzenberg et al (20) concluded that eNOS activity attenuates the myogenic response in a manner independent of NO production.…”

Section: Discussionsupporting

confidence: 53%

Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O₂⁻ dismutation on renal autoregulation in the time and frequency domains

Moss

Gentle

Arendshorst

2016

American Journal of Physiology-Renal Physiology

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Moss NG, Gentle TK, Arendshorst WJ. Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O 2 Ϫ dismutation on renal autoregulation in the time and frequency domains. Am J Physiol Renal Physiol 310: F832-F845, 2016. First published January 28, 2016 doi:10.1152/ajprenal.00461.2015.-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 [N G -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. renal circulation; perfusion pressure; renal vascular resistance; admittance gain; afferent arteriole MOST VASCULAR BEDS REGULATE blood flow according to metabolic conditions to provide adequate nutrient delivery and effective waste removal. Control of renal blood flow (RBF) is unique among peripheral vascular beds, as the principal goal is not to satisfy metabolic demands, but rather to stabilize glomerular capillary pressure at a level that provides an adequate glomerular filtration rate. This is achieved by an efficient autoregulatory mechanism(s) that adjusts glomerular afferent arteriolar diameter in response to fluctuations in renal perfusion pressure (RPP). Of equal importance, this process protects glomerular capillaries from excessive pressures that can cause barotrauma, glomerular injury, and renal failure. Several intrinsic mechanisms regulate renal vascular resistance (RVR) in response to changes in RPP (3, 13). In common with most organs, changes in RPP invoke an intrinsic myogenic mechanism in the vascular smooth muscle cells (VSMC) of renal resistance vessels, which stabilizes dow...

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“…but did not affect the autoregulatory capacity [41. 42], However, if much higher doses o f acetylcholine [43,44] or exogenous NO [45] are given, the autoregulation may be impaired, al though not always entirely abolished [43], In the abovementioned studies, autoregulation was tested as the re sponse to stepwise artificially induced changes in perfusion pressure. However, since shear stress is a major stimulus for the release of NO [46,47], the influence of NO on the auto regulatory function may be more important if this function is challenged by dynamic fluctuations in blood pressure oc curring under physiological conditions.…”

Section: Influence Of N O On Rbfmentioning

confidence: 99%

Nitric Oxide and Renal Autoregulation

Just

1997

Kidney Blood Press Res

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Basal vascular tone in the kidney. Evaluation from the static pressure-flow relationship under normal autoregulation and at maximal dilation in the dog.

Cited by 20 publications

References 27 publications

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O₂⁻ dismutation on renal autoregulation in the time and frequency domains

Nitric Oxide and Renal Autoregulation

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Basal vascular tone in the kidney. Evaluation from the static pressure-flow relationship under normal autoregulation and at maximal dilation in the dog.

Cited by 20 publications

References 27 publications

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Effect of Volume Expansion on Hemodynamics of the Hypoperfused Rat Kidney

Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O2− dismutation on renal autoregulation in the time and frequency domains

Nitric Oxide and Renal Autoregulation

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Modulation of the myogenic mechanism: concordant effects of NO synthesis inhibition and O₂⁻ dismutation on renal autoregulation in the time and frequency domains