Responses Of Regional Kidney Perfusion To Vasoconstrictors In Anaesthetized Rabbits: Dependence On Agent And Renal Artery Pressure

Evans, Roger G.; Correia, Anabela G.; Weekes, Simon R; Madden, Anna C

doi:10.1046/j.1440-1681.2000.03377.x

Cited by 10 publications

(11 citation statements)

References 29 publications

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“…The results of our present study confirm previous observations by ourselves 2–4,17 and others 5,6,10,12,14,18–20 showing that vasoactive stimuli have diverse effects on regional kidney blood flow. Our major novel finding was that indomethacin abolished increases in MBF following bolus renal arterial administration of ET‐1 and AngII.…”

Section: Discussionsupporting

confidence: 93%

“…Increases in MBF in response to AngII and ET‐1 have been observed previously by ourselves 2,23,27,28 and others 10,11,14,20 under a variety of experimental conditions. Our present results indicate that release of vasodilator COX products mediates vasodilatation of the vascular elements that control MBF in response to ET‐1 and AngII, because both AngII‐ and ET‐1‐induced increases in MBF were abolished by indomethacin.…”

Section: Discussionsupporting

confidence: 76%

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Effects of indomethacin on responses of regional kidney perfusion to vasoactive agents in rabbits

Oliver

Rajapakse

Evans

2002

Clin Exp Pharma Physio

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1. To determine whether differential release of products of arachidonic acid metabolism, via the cyclo-oxygenase pathway, underlies the diversity of responses of regional kidney perfusion to vasoactive agents, we tested the effects of intravenous indomethacin on responses to renal arterial bolus doses of vasoactive agents in pentobarbitone-anaesthetized rabbits. 2. Total renal blood flow (RBF) and regional kidney perfusion were determined by transit time ultrasound flowmetry and laser-Doppler flowmetry, respectively. 3. Responses of regional kidney blood flow to vasoactive agents were diverse: noradrenaline reduced cortical but not medullary perfusion, [Phe 2,Ile 3,Orn 8]-vasopressin reduced medullary perfusion more than cortical perfusion, endothelin-1 and angiotensin II increased medullary perfusion in the face of reduced cortical perfusion, while acetylcholine, bradykinin and the nitric oxide donor methylamine hexamethylene methylamine (MAHMA) NONOate all increased both cortical and medullary perfusion. 4. Indomethacin administration was followed by reductions in total RBF (17 +/- 6%), cortical perfusion (13 +/- 5%) and medullary perfusion (40 +/- 8%). Angiotensin II- and endothelin-1-induced increases in medullary perfusion were abolished by indomethacin, but indomethacin had no significant effects on responses of regional kidney perfusion to acetylcholine, bradykinin, MAHMA NONOate, noradrenaline and [Phe 2,Ile 3,Orn 8]-vasopressin. 5. Our results suggest that vasodilator cyclo-oxygenase products contribute to the maintenance of resting renal vascular tone, particularly in vascular elements controlling medullary perfusion. Cyclo-oxygenase products also appear to mediate endothelin-1- and angiotensin II-induced increases in medullary perfusion. However, regionally specific engagement of cyclo-oxygenase-dependent arachidonic acid metabolism does not appear to contribute to the differential effects of noradrenaline and [Phe 2,Ile 3,Orn 8]-vasopressin on cortical and medullary perfusion.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 76%

Effects of indomethacin on responses of regional kidney perfusion to vasoactive agents in rabbits

Oliver

Rajapakse

Evans

2002

Clin Exp Pharma Physio

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“…Nevertheless, this seems to be a less serious problem for MBF (than for CBF), because the slope of the MLDF-RBF relationship in the isolated kidney was only slightly Ͻ1. We can also be confident that we can detect increases in MBF with the techniques used here, because we previously detected increases in CLDF and MLDF in response to vasodilators such as acetylcholine and bradykinin (30,33) and increases in MLDF in response to angiotensin II and endothelin-1 in a standard anesthetized rabbit preparation and in the extracorporeal circuit preparation (10)(11)(12). For example, in our standard rabbit preparation, a bolus of bradykinin into the renal artery has been shown to increase MLDF by ϳ100% from a baseline of ϳ100 units.…”

Section: Strengths and Limitations Of Laser-doppler Flowmetry For Estmentioning

confidence: 68%

“…The extracorporeal circuit has been described in detail (5,7,11,43). Briefly, blood was withdrawn at 90 ml/min from the aorta with a roller pump (Masterflex model 7521-45, Barnant, Barrington, IL) and returned to the rabbit via the vena cava and renal artery.…”

Section: Extracorporeal Circuitmentioning

confidence: 99%

Autoregulation of renal medullary blood flow in rabbits

Eppel

Bergström

Anderson

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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We examined the extent of renal medullary blood flow (MBF) autoregulation in pentobarbital-anesthetized rabbits. Two methods for altering renal arterial pressure (RAP) were compared: the conventional method of graded suprarenal aortic occlusion and an extracorporeal circuit that allows RAP to be increased above systemic arterial pressure. Changes in MBF were estimated by laser-Doppler flowmetry, which appears to predominantly reflect erythrocyte velocity, rather than flow, in the kidney. We compared responses using a dual-fiber needle probe held in place by a micromanipulator, with responses from a single-fiber probe anchored to the renal capsule, to test whether RAP-induced changes in kidney volume confound medullary laser-Doppler flux (MLDF) measurements. MLDF responses were similar for both probe types and both methods for altering RAP. MLDF changed little as RAP was altered from 50 to Ն170 mmHg (24 Ϯ 22% change). Within the same RAP range, RBF increased by 296 Ϯ 48%. Urine flow and sodium excretion also increased with increasing RAP. Thus pressure diuresis/natriuresis proceeds in the absence of measurable increases in medullary erythrocyte velocity estimated by laser-Doppler flowmetry. These data do not, however, exclude the possibility that MBF is increased with increasing RAP in this model, because vasa recta recruitment may occur.laser-Doppler flowmetry; pressure diuresis; renal blood flow; renal perfusion pressure; renal medulla PRESSURE DIURESIS/NATRIURESIS is a key mechanism in the long-term control of arterial pressure. There is strong evidence that this mechanism is mediated, at least in part, by a direct relationship between renal arterial pressure (RAP) and renal interstitial hydrostatic pressure, which in turn profoundly influences tubular sodium reabsorption (13,25,34,35). However, there is still much controversy as to the mechanism(s) by which increased RAP increases renal interstitial hydrostatic pressure, because total renal blood flow (RBF) and glomerular filtration rate are well autoregulated. One proposition is that increased RAP increases vasa recta capillary blood flow and pressure, which in turn increases renal interstitial hydrostatic pressure (8). This hypothesis is supported by observations, particularly in volume-expanded rats, of poor autoregulation of medullary blood flow (MBF) (13,18,21,28,35,39,40). In contrast, however, other studies have demonstrated efficient autoregulation of MBF in rats and dogs (6,9,17,(23)(24)(25)(26)(27)29), even under conditions of volume expansion (24). These and other observations have led to an alternative hypothesis: that increased RAP increases the renal production of nitric oxide, which in turn mediates the increase in renal interstitial hydrostatic pressure (25). Thus the issue of MBF autoregulation remains central to elucidating the precise mechanisms mediating pressure diuresis/natriuresis. Therefore, in this study, we used laser-Doppler flowmetry to examine the degree of MBF autoregulation in anesthetized rabbits. We paid particular attention t...

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“…Secondly, given that vasoactive hormones can differentially affect blood flow in the renal cortex and medulla (Evans et al 2000b), it seems reasonable to hypothesize that they might also differentially affect responses to activation of the renal nerves in these vascular territories, yet this hypothesis has not previously been tested. Therefore, in the present study we determined the effects of renal arterial infusions of a range of vasodilator (the NO donor methylamine hexamethylene NONOate (MAHMA NONOate), acetylcholine and adrenomedullin) and vasoconstrictor agents (angiotensin II and the vasopressin V ]-vasopressin can reduce medullary but not cortical perfusion (Evans et al , 2000a. In pilot studies, we were unable to demonstrate selective effects of vasodilators within specific renal vascular territories, so agents were chosen that might potentially act through different signalling cascades.…”

mentioning

confidence: 99%

Interactions Between Neural and Hormonal Mediators of Renal Vascular Tone in Anaesthetized Rabbits

Guild

Barrett

Evans

et al. 2003

Experimental Physiology

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Many studies have investigated the various neural and hormonal factors that influence the renal circulation. As a result, we now have a relatively good understanding of how these regulatory mechanisms operate in isolation from each other DiBona & Kopp, 1997). However, since the sympathetic nervous system and hormonal factors act in concert to regulate renal vascular tone, an understanding of how these mechanisms interact is warranted.Previous studies have provided evidence for interactions between the renal nerves and hormonal regulatory factors. For example, blockade of nitric oxide (NO) synthase has been shown to enhance renal vasoconstriction in response to electrical stimulation of the renal nerves in the rat isolated perfused kidney (Reid & Rand, 1992). There is also considerable evidence that the renin-angiotensin system can profoundly influence vascular responses to activation of the sympathetic nervous system, chiefly by facilitation of noradrenaline release (Zimmerman, 1978).However, there remain a number of issues that require resolution. Firstly, the degree to which vasoactive agents can modulate responses to activation of the renal nerves through direct actions mediated by specific signalling cascades, rather than through indirect actions such as alterations in resting renal vascular tone, remains unknown. Secondly, given that vasoactive hormones can differentially affect blood flow in the renal cortex and medulla (Evans et al. 2000b), it seems reasonable to hypothesize that they might also differentially affect responses to activation of the renal nerves in these vascular territories, yet this hypothesis has not previously been tested. Therefore, in the present study we determined the effects of renal arterial infusions of a range of vasodilator (the NO donor methylamine hexamethylene NONOate (MAHMA NONOate), Interactions between neural and hormonal mediators of renal vascular tone in anaesthetized rabbits

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Responses Of Regional Kidney Perfusion To Vasoconstrictors In Anaesthetized Rabbits: Dependence On Agent And Renal Artery Pressure

Cited by 10 publications

References 29 publications

Effects of indomethacin on responses of regional kidney perfusion to vasoactive agents in rabbits

Effects of indomethacin on responses of regional kidney perfusion to vasoactive agents in rabbits

Autoregulation of renal medullary blood flow in rabbits

Interactions Between Neural and Hormonal Mediators of Renal Vascular Tone in Anaesthetized Rabbits

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