Differential control of intrarenal blood flow during reflex increases in sympathetic nerve activity

Leonard, Bridget L.; Malpas, Simon C.; Denton, Kate M.; Madden, Anna C; Evans, Roger G.

doi:10.1152/ajpregu.2001.280.1.r62

Cited by 54 publications

(81 citation statements)

References 19 publications

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“…Body temperature was maintained between 37.0 and 38.0°C throughout the surgery and subsequent experiment by means of a heated table and infrared heating lamp. Baseline arterial PO2 (90 -110 mmHg) and PCO2 (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40) were maintained within the desired ranges by altering respiratory rate and volume and the level of positive end-expiratory pressure. Arterial hemoglobin saturation was monitored continuously by pulse oximetry (model 8600V; Nonin, Plymouth, MN).…”

Section: Animalsmentioning

confidence: 99%

“…However, previous studies investigating the effects of hypoxemia on renal V O 2 were performed in animals with intact renal nerves. Hypoxemia can activate renal sympathetic drive and so induce renal vasoconstriction (25). Consequently, none of these previous studies were able to demonstrate that renal V O 2 can be maintained in the face of hypoxemia-induced reductions in DO 2 .…”

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confidence: 94%

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Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Evans

Goddard

Eppel

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Evans RG, Goddard D, Eppel GA, O'Connor PM. Factors that render the kidney susceptible to tissue hypoxia in hypoxemia. Am J Physiol Regul Integr Comp Physiol 300: R931-R940, 2011. First published January 19, 2011 doi:10.1152/ajpregu.00552.2010To better understand what makes the kidney susceptible to tissue hypoxia, we compared, in the rabbit kidney and hindlimb, the ability of feedback mechanisms governing oxygen consumption (V O2) and oxygen delivery (DO 2 ) to attenuate tissue hypoxia during hypoxemia. In the kidney (cortex and medulla) and hindlimb (biceps femoris muscle), we determined responses of whole organ blood flow and V O2, and local perfusion and tissue PO2, to reductions in DO2 mediated by graded systemic hypoxemia. Progressive hypoxemia reduced tissue PO2 similarly in the renal cortex, renal medulla, and biceps femoris. Falls in tissue PO2 could be detected when arterial oxygen content was reduced by as little as 4 -8%. V O2 remained stable during progressive hypoxemia, only tending to fall once arterial oxygen content was reduced by 55% for the kidney or 42% for the hindlimb. Even then, the fall in renal V O2 could be accounted for by reduced oxygen demand for sodium transport rather than limited oxygen availability. Hindlimb blood flow and local biceps femoris perfusion increased progressively during graded hypoxia. In contrast, neither total renal blood flow nor cortical or medullary perfusion was altered by hypoxemia. Our data suggest that the absence in the kidney of hyperemic responses to hypoxia, and the insensitivity of renal V O2 to limited oxygen availability, contribute to kidney hypoxia during hypoxemia. The susceptibility of the kidney to tissue hypoxia, even in relatively mild hypoxemia, may have important implications for the progression of kidney disease, particularly in patients at high altitude or with chronic obstructive pulmonary disease. hyperemia; hypoxia; ischemia; kidney circulation; oxygen tension; skeletal muscle ONE OF THE GREAT PARADOXES of physiology is the susceptibility of the kidney to tissue hypoxia. The kidneys are among the most highly perfused organs in the body, receiving approximately one-quarter of the cardiac output at rest yet comprise Ͻ1% of total body weight (14). Thus renal oxygen delivery (DO 2 ) greatly exceeds oxygen consumption (V O 2 ). Yet the kidney is extremely susceptible to hypoxic damage, which in turn appears to be a crucial event in the pathogenesis of chronic kidney disease (8,19,32,35) and acute kidney injury (7, 20, 24) of diverse etiology. Therefore, it is imperative that we improve our understanding of the structural and functional characteristics of the kidney that make it susceptible to development of hypoxia.Most organs respond to a reduction in oxygenation by increasing local blood flow and so DO 2 (14). The increased DO 2 then acts to increase tissue oxygenation and so attenuate development of hypoxia and tissue injury. In this regard, the control of blood flow to the kidney is unique in that it appears to be dominated by the func...

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Section: Animalsmentioning

confidence: 99%

mentioning

confidence: 94%

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Evans

Goddard

Eppel

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…10,11,24,25 Anesthesia was induced with sodium pentobarbital (90 to 150 mg plus 30 to 50 mg/h). Artificial ventilation and infusion of maintenance solutions then continued for the entire experiment.…”

Section: Surgical Proceduresmentioning

confidence: 99%

“…25 Both kidneys were denervated and both ureters catheterized. 24,25 The left kidney was placed in a stable cup, and a renal artery was side-branch catheterized. Left kidney RBF, and cortical blood flow and MBF were monitored by transit-time ultrasound flowmetry and laser-Doppler flowmetry, respectively.…”

Section: Surgical Proceduresmentioning

confidence: 99%

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Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

et al. 2003

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Abstract-The contributions of angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors to the control of regional kidney blood flow were determined in pentobarbital-anesthetized rabbits. Intravenous candesartan (AT 1 antagonist; 10 g/kg plus 10 g · kg Ϫ1 · h Ϫ1) reduced mean arterial pressure (12%) and increased total renal blood flow (29%) and cortical laser-Doppler flux (18%) but not medullary laser-Doppler flux. Neither intravenous PD123319 (AT 2 antagonist; 1 mg/kg plus 1 mg · kg Ϫ1 · h Ϫ1 ) nor saline vehicle significantly affected these variables, and the responses to candesartan plus PD123319 were indistinguishable from those of candesartan alone. In vehicle-treated rabbits, renal-arterial infusions of angiotensin II (1 to 25 ng · kg Ϫ1 · min Ϫ1 ) and angiotensin III (5 to 125 ng · kg Ϫ1 · min Ϫ1) dose-dependently reduced renal blood flow (up to 51%) and cortical laser-Doppler flux (up to 50%) but did not significantly affect medullary laser-Doppler flux or arterial pressure. Angiotensin(1-7) (20 to 500 ng · kg Ϫ1 · min Ϫ1) had similar effects but of lesser magnitude. CGP42112A (20 to 500 ng · kg Ϫ1 · min Ϫ1) did not significantly affect these variables. After PD123319 administration, angiotensin II and angiotensin III dose-dependently increased medullary laser-Doppler flux (up to 84%), and reductions in renal blood flow in response to angiotensin II were enhanced. Candesartan abolished renal hemodynamic responses to the angiotensin peptides, even when given in combination with PD123319. We conclude that AT 2 receptor activation counteracts AT 1 -mediated vasoconstriction in the renal cortex but also counteracts AT 1 -mediated vasodilatation in vascular elements controlling medullary perfusion. These mechanisms might have an important effect on the control of medullary perfusion under conditions of activation of the renin-angiotensin system. Key Words: receptors, angiotensin Ⅲ kidney Ⅲ laser-Doppler flowmetry Ⅲ rabbits Ⅲ renal circulation T he medullary circulation contributes to the control of mean arterial pressure (MAP) and body fluid homeostasis. 1 However, the roles of angiotensin II type 1 (AT 1 ) and type 2 (AT 2 ) receptors in regulating regional kidney perfusion remain unclear. In rats and rabbits, infusions of angiotensin II reduce total renal blood flow (RBF) and cortical blood flow but have a lesser effect on medullary blood flow (MBF). [2][3][4][5] Angiotensin II can even increase MBF, especially when administered as a bolus. 6 -8 Nitric oxide synthase and/or cyclooxygenase blockade can enhance angiotensin II-induced reductions in MBF and abolish angiotensin II-induced increases in MBF, both of which are chiefly AT 1 mediated. 4,6 -12 However, the contributions of AT 2 receptors to these effects have received little attention, even though they are expressed in vessels that might contribute to MBF control (eg, afferent arterioles and vasa recta). 13 AT 2 -mediated counterregulatory vasodilatation can oppose AT 1 -mediated vasoconstriction. For example, in rat renalwrap hypertension, AT 2 re...

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Reproducibility of renal perfusion MR imaging in native and transplanted kidneys using non‐contrast arterial spin labeling

Artz

Sadowski

Wentland

et al. 2011

Magnetic Resonance Imaging

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Purpose: To examine both inter-visit and intra-visit reproducibility of a MR arterial spin labeling (ASL) perfusion technique in native and transplanted kidneys over a broad range of renal function. Materials and Methods:Renal perfusion exams were performed at 1.5 T in a total of 24 subjects: 10 with native and 14 with transplanted kidneys. Using a flowsensitive alternating inversion recovery (FAIR) ASL scheme, 32 control/tag pairs were acquired and processed using a single-compartment model. Two FAIR-ASL MR exams were performed at least 24 h apart on all the subjects to assess inter-visit reproducibility. ASL perfusion measurements were also repeated back-to-back within one scanning session in 8 native subjects and in 12 transplant subjects to assess intra-visit reproducibility. Intra-class correlations (ICCs) and coefficients of variation (CVs) were calculated as metrics of reproducibility.Results: Intra-visit ICCs ranged from 0.96 to 0.98 while CVs ranged from 4.8 to 6.0%. Inter-visit measurements demonstrated slightly more variation with ICCs from 0.89 to 0.94 and CVs from 7.6 to 13.1%. Medullary perfusion demonstrated greater variability compared with cortical blood flow: intra-visit ICCs from 0.72 to 0.78 and CVs from 16.7 to 26.7%, inter-visit ICCs from 0.13 to 0.63 and CVs from 19.8 to 37%. Conclusion:This study indicates that a FAIR-ASL perfusion technique is reproducible in the cortex of native and transplanted kidneys over a broad range in renal function. In contrast, perfusion measurements in the medulla demonstrated moderate to poor reproducibility for intravisit and inter-visit measures respectively.

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Differential control of intrarenal blood flow during reflex increases in sympathetic nerve activity

Cited by 54 publications

References 19 publications

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

Reproducibility of renal perfusion MR imaging in native and transplanted kidneys using non‐contrast arterial spin labeling

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Differential control of intrarenal blood flow during reflex increases in sympathetic nerve activity

Cited by 54 publications

References 19 publications

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Factors that render the kidney susceptible to tissue hypoxia in hypoxemia

Disparate Roles of AT 2 Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits

Reproducibility of renal perfusion MR imaging in native and transplanted kidneys using non‐contrast arterial spin labeling

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Disparate Roles of AT ₂ Receptors in the Renal Cortical and Medullary Circulations of Anesthetized Rabbits