Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.

Roman, Richard J.

doi:10.1161/01.hyp.12.2.177

Cited by 67 publications

(55 citation statements)

References 20 publications

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“…These studies suggest that the loop of Henle may play a compensatory role during the process of pressure natriuresis. In contrast, Roman 11 reported that alterations in medullary hemodynamics participate in the pressure-natriuretic response by inhibiting tubular reabsorption in the proximal tubule and the thin descending limb of the loop of Henle (or both) of juxtamedullary nephrons. Thus, changes in renal perfusion pressure within the autoregulatory range may elicit changes in tubular sodium reabsorption in multiple nephron segments.…”

Section: Discussionmentioning

confidence: 99%

Acute Angiotensin II Infusions Elicit Pressure Natriuresis in Mice and Reduce Distal Fractional Sodium Reabsorption

Zhao

Navar

2008

Hypertension

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Abstract-Acute angiotensin II (Ang II) infusions into mice increase arterial pressure (AP) and elicit pressure natriuresis.We used this model of pressure natriuresis to delineate the distal nephron responses to AP-mediated increases in distal sodium delivery. In the first group, we measured changes in urinary sodium excretion (U Na V) in male C57/BL6 anesthetized mice (nϭ9) before and during acute Ang II infusions (5 ng/g of body weight per minute). Acute Ang II infusions increased AP (98Ϯ3 to 126Ϯ5 mm Hg; PϽ0.001), urine flow (2.7Ϯ0.5 to 6.0Ϯ0.8 L/min; PϽ0.01), and U Na V (0.6Ϯ0.2 to 1.3Ϯ0.2 Eq/min; PϽ0.05). There were significant relationships between U Na V and urine flow (yϭ0.207xϩ0.030; PϽ0.0001) and between U Na V and AP (yϭ0.027xϪ2.100). In a separate series, distal sodium delivery and fractional reabsorption of distal sodium delivery were determined in control (nϭ12) and Ang II-infused mice (nϭ8) by comparing U Na V before and after blockade of the 2 major distal nephron sodium transporters with amiloride (5 mg/kg of body weight) plus bendroflumethiazide (12 mg/kg of body weight). A positive relationship was found between U Na V (yϭ0.015xϪ1.100; PϽ0.0001) or distal sodium delivery (yϭ0.027xϪ0.900; PϽ0.0001) and AP. An inverse relationship was found between fractional reabsorption of distal sodium delivery and AP (yϭϪ0.511xϩ128.300; PϽ0.01). These data indicate that Ang II-mediated pressure natriuresis involves an increase in distal sodium delivery combined with a reduced distal nephron fractional sodium reabsorption, suggesting that increased AP prevents the distal nephron transport mechanisms from accommodating the increased distal delivery. Key Words: Ang II Ⅲ arterial pressure Ⅲ renal sodium reabsorption Ⅲ distal nephron segments Ⅲ amiloride Ⅲ bendroflumethiazide Ⅲ fractional distal sodium reabsorption I t is well known that increases in arterial pressure (AP) lead to the increases in renal sodium excretion, a phenomenon commonly referred to as pressure natriuresis. [1][2][3][4][5][6][7][8] The changes in renal sodium excretion in response to changes in AP provide a link between the mechanisms regulating sodium excretion and those regulating AP. 1 Because glomerular filtration rate (GFR) and filtered sodium load are autoregulated over the same AP range, the mechanism of pressure natriuresis involves decreased tubular sodium reabsorption in response to increased AP; 6 however, the relative contributions of the various nephron segments responsible have not been fully defined. 5,9 -12 Acute angiotensin II (Ang II) infusions in mice and rats increase AP and elicit pressure natriuresis, suggesting that Ang II infusion is a useful model to delineate the relative contributions of the various nephron segments to increases in AP.The development of a mouse model with minimal surgical interventions to study pressure natriuresis would allow evaluation of the roles of specific tubular transport systems by using various gene targeted models. Although several studies have focused on the AP effects on proximal nephro...

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Section: Discussionmentioning

confidence: 99%

Acute Angiotensin II Infusions Elicit Pressure Natriuresis in Mice and Reduce Distal Fractional Sodium Reabsorption

Zhao

Navar

2008

Hypertension

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“…Moreover, NO appears to exert a tonic vasodilation of the vasa recta in the renal medulla. Variations in NO synthesis will be followed by proportional changes in renomedullary blood flow and thereby in renal interstitial pressure and will produce an inversely related change in sodium reabsorption (132). We will examine this mechanism later on.…”

Section: Intrarenal Functions Regulated By Ang II and Nomentioning

confidence: 99%

“…A group of investigators at the Medical College of Wisconsin has accumulated a significant amount of evidence showing that, in the rat, the integrity of the renal medullary circulation is very critical in maintaining pressure natriuresis (132). In fact, they found that increments in renal perfusion pressure above 78-85 mmHg produced proportional changes in renal papillary flow, whereas renal cortical flow does not change because it is effectively autoregulated (94).…”

Section: Role Of Oxst On Endothelial Function and On Medullary Circulmentioning

confidence: 99%

Role of oxidative stress in angiotensin-induced hypertension

Reckelhoff

Romero

2003

American Journal of Physiology-Regulatory, Integrative and Comp

167

133

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Reckelhoff, Jane F., and J. Carlos Romero. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol Regul Integr Comp Physiol 284: R893-R912, 2003; 10.1152/ajpregu.00491.2002.-Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.isoprostanes; endothelin; spontaneous hypertension; renovascular hypertension; sodium balance THREE DECADES AGO, the production of free radicals was thought to be the result of severe injuries or pathological insults such as those resulting from exposure to high-energy radiation or toxins such as carbon tetrachloride (127). However, in 1968, the discovery of superoxide dismutase (SOD) by McCord and Fridovich (96) strongly suggested that all aerobically metabolizing cells are capable of producing superoxide ions, which could play a role in normal metabolic processes. The concomitant discovery of the biology of nitric oxide (NO) strongly suggested that free radicals could constitute the basis of metabolic regulation (67,90,118). One of the first findings supporting such a notion was the demonstration that the inhibition of the synthesis of NO produced by the administration of an NO synthesis competitor, such as N -monomethyl-Larginine] or N G -nitro-L-arginine methyl ester (L-NAME), produced a marked vasoconstriction (13,136,173), sodium retention (82, 83), and thereby a sustained increase in mean arterial pressure (MAP) (13,82,83,136,173). The identification of a specific pathological situation in humans, where a decrease of NO may end up in an elevation of blood pressure was thought to be linked to endothelial dysfunction (105), such as those involved in aging, arteriosclerosis, etc., but the specific metabolic alterations involved in this process were poorly understood. However, the relationship betw...

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“…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.…”

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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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Pressure-diuresis in volume-expanded rats. Tubular reabsorption in superficial and deep nephrons.

Cited by 67 publications

References 20 publications

Acute Angiotensin II Infusions Elicit Pressure Natriuresis in Mice and Reduce Distal Fractional Sodium Reabsorption

Acute Angiotensin II Infusions Elicit Pressure Natriuresis in Mice and Reduce Distal Fractional Sodium Reabsorption

Role of oxidative stress in angiotensin-induced hypertension

Autoregulation of renal medullary blood flow in rabbits

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