The Renal Microcirculation

Navar, L. Gabriel; Arendshorst, William J.; Pallone, Thomas L.; Inscho, Edward W.; Imig, John D.; Bell, P. Darwin

doi:10.1016/b978-0-12-374530-9.00015-2

Cited by 40 publications

(67 citation statements)

References 1,636 publications

(1,966 reference statements)

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“…In the kidney, complete autoregulatory responses reflect the combined influences of tubuloglomerular feedback and the myogenic mechanism (51,53). The inhibition observed in this report likely represents inhibition of myogenic responses as the diameter measurements were made in the first half of afferent arteriolar length (47-52% of the arterioles length), well removed from the tubuloglomerular feedback-sensitive region.…”

Section: Discussionmentioning

confidence: 94%

“…Autoregulation is a critical function of afferent arterioles (37,44,51,53,61). Setting preglomerular resistance appropriately is essential for maintenance of a stable renal blood flow and glomerular filtration rate.…”

Section: Discussionmentioning

confidence: 99%

“…P2 receptors; P2X 1 receptors; ATP; Y-27632; autoregulation RENAL PERFUSION IS CONTROLLED by agonist-induced and pressure-mediated adjustments in preglomerular resistance (51). Accurate regulation of preglomerular resistance is central to the maintenance of glomerular capillary pressure.…”

mentioning

confidence: 99%

“…Accurate regulation of preglomerular resistance is central to the maintenance of glomerular capillary pressure. Afferent arterioles are the main vascular elements responsible for pressure-mediated autoregulatory adjustments in preglomerular resistance for the regulation of renal blood flow and glomerular filtration rate (9,51,53). Autoregulatory changes in renal vascular resistance are calcium dependent and involve the combined influences of the myogenic and tubuloglomerular feedback mechanisms (4,12,21,28,49,52,53,58,61).…”

mentioning

confidence: 99%

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Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter

Inscho¹,

Cook²,

Webb³

et al. 2009

American Journal of Physiology-Renal Physiology

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Preglomerular resistance is regulated by calcium influx- and mobilization-dependent mechanisms; however, the role of Rho-kinase in calcium sensitization in the intact kidney has not been carefully examined. Experiments were performed to test the hypothesis that Rho-kinase inhibition blunts pressure-mediated afferent arteriolar autoregulatory behavior and vasoconstrictor responses evoked by angiotensin II and P2X1 receptor activation. Rat kidneys were studied in vitro using the blood-perfused juxtamedullary nephron technique. Autoregulatory behavior was assessed before and during Rho-kinase inhibition with Y-27632 (1.0 microM; n = 5). Control diameter averaged 14.3 +/- 0.8 microm and increased to 18.1 +/- 0.9 microm (P < 0.05) during Y-27632 treatment. In the continued presence of Y-27632, reducing perfusion pressure to 65 mmHg slightly increased diameter to 18.7 +/- 1.0 microm. Subsequent pressure increases to 130 and 160 mmHg yielded afferent arteriolar diameters of 17.5 +/- 0.8 and 16.6 +/- 0.6 microm (P < 0.05). This 11% decline in diameter is significantly smaller than the 40% decrease obtained in untreated kidneys. The inhibitory effects of Y-27632 on autoregulatory behavior were concentration dependent. Angiotensin II responses were blunted by Y-27632. Angiotensin II (1.0 nM) reduced afferent diameter by 17 +/- 1% in untreated arterioles and by 6 +/- 2% during exposure to Y-27632. The P2X1 receptor agonist, alpha, beta-methylene ATP, reduced afferent arteriolar diameter by 8 +/- 1% but this response was eliminated during exposure to Y-27632. Western blot analysis confirms expression of the Rho-kinase signaling pathway. Thus, Rho-kinase may be important in pressure-mediated autoregulatory adjustments in preglomerular resistance and responsiveness to angiotensin II and autoregulatory P2X1 receptor agonists.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter

Inscho¹,

Cook²,

Webb³

et al. 2009

American Journal of Physiology-Renal Physiology

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“…Since the cortex is responsible for 90% of RBF, the outer medulla 8% and the inner medulla 2% [19][20][21][22]. Both the RPR and β values were weighted as follows:…”

Section: Data Analysis Methodsmentioning

confidence: 99%

Improving the quantitative ability of contrast enhanced ultrasound perfusion imaging: effect of contrast administration rate and imaging plane orientation

Johnson

Kogan

Feingold

et al. 2011

2011 IEEE International Ultrasonics Symposium

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Contrast-enhanced ultrasound (CEUS) has demonstrated utility in the monitoring of blood flow in tissues, organs, and tumors. Current CEUS methods typically provide only relative image-derived measurements, rather than quantitative values of blood flow in milliliters/minute per gram of tissue. The purpose of this study is to validate CEUS-derived measurements of renal blood flow (RBF) with absolute values of ml/min per gram of tissue based on a calibrated flow probe. New information about the effects of parameters such as contrast agent administration rate and transducer positioning on two different image-derived measurements are provided.

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Physiology of Endothelin and the Kidney

Kohan

Inscho

Wesson

et al. 2011

Comprehensive Physiology

104

136

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Since its discovery in 1988 as an endothelial cell-derived peptide that exerts the most potent vasoconstriction of any known endogenous compound, endothelin (ET) has emerged as an important regulator of renal physiology and pathophysiology. This review focuses on how the ET system impacts renal function in health; it is apparent that ET regulates multiple aspects of kidney function. These include modulation of glomerular filtration rate and renal blood flow, control of renin release, and regulation of transport of sodium, water, protons and bicarbonate. These effects are exerted through ET interactions with almost every cell type in the kidney, including mesangial cells, podocytes, endothelium, vascular smooth muscle, every section of the nephron, and renal nerves. In addition, while not the subject of the current review, ET can also indirectly affect renal function through modulation of extrarenal systems, including the vasculature, nervous system, adrenal gland, circulating hormones and the heart. As will become apparent, these pleiotropic effects of ET are of fundamental physiologic importance in the control of renal function in health. In addition, to help put these effects into perspective, we will also discuss, albeit to a relatively limited extent, how alterations in the ET system can contribute to hypertension and kidney disease.

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The Renal Microcirculation

Cited by 40 publications

References 1,636 publications

Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter

Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter

Improving the quantitative ability of contrast enhanced ultrasound perfusion imaging: effect of contrast administration rate and imaging plane orientation

Physiology of Endothelin and the Kidney

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