Volume natriuresis vs. pressure natriuresis

Bie, Peter; Wamberg, S.; Kjølby, Mads

doi:10.1111/j.1365-201x.2004.01323.x

Cited by 50 publications

(57 citation statements)

References 36 publications

(68 reference statements)

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“…Investigators from Odense and Berlin have argued that the pressure natriuresis mechanism is not always operative during modest changes in arterial pressure. 19,20 In regard to the present study, if this interpretation were correct, and the concomitant neurohumoral responses did not enhance pressure natriuresis, this would indicate that renal excretory function adapts to changes in arterial pressure and that reductions in either cardiac output or peripheral resistance could be causal mechanisms that account for long-term reductions in arterial pressure during prolonged baroreflex activation. Additional long-term studies are needed to provide greater insight into this controversy.…”

Section: Discussionmentioning

confidence: 94%

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Lohmeier

Hildebrandt²,

Dwyer³

et al. 2007

Hypertension

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Abstract-Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean arterial pressure and plasma norepinephrine concentration were 95Ϯ2 mm Hg and 96Ϯ12 pg/mL, respectively. During day 1 of baroreflex activation, mean arterial pressure decreased 13Ϯ1 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean arterial pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with sustained decreases in plasma norepinephrine concentration (Ϸ50%) and plasma renin activity (30% to 40%). All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean arterial pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were comparable to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were similar to those observed before renal denervation. These findings demonstrate that the presence of the renal nerves is not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex. Key Words: baroreflex Ⅲ arterial pressure Ⅲ renal nerves Ⅲ sympathetic nervous system Ⅲ norepinephrine Ⅲ renin-angiotensin system Ⅲ sodium excretion N ovel experimental approaches in chronically instrumented animals have recently provided greater insight into the role of baroreflexes in long-term control of arterial pressure. 1-10 These studies, conducted over several weeks, indicate that baroreflex resetting is incomplete in experimental models of hypertension. They also indicate that during chronic increases in arterial pressure, there is sustained baroreflex-mediated suppression of renal sympathetic nerve activity and attendant increments in renal excretory function, responses expected to attenuate the severity of hypertension. However, the quantitative importance of renal sympathoinhibition in mediating the chronic blood pressure-lowering effects of sustained baroreflex activation remains unclear.We have recently developed methodology that is ideal for evaluating the time dependency and underlying mechanisms of the blood pressure-lowering effects of the baroreflex. 6,10 To activate the carotid baroreflex, an externally adjustable pulse generator is used to electrically stimulate electrodes chronically implanted around both c...

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Section: Discussionmentioning

confidence: 94%

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Lohmeier

Hildebrandt²,

Dwyer³

et al. 2007

Hypertension

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“…Our data confirm that even modest blood pressure increases are important to the acute regulation of the renal sodium excretion in the rat. In the absence of blood pressure changes, other mediators, such as RSNA and nNOS-derived NO, are operative and functionally important; studies in dogs and humans (3,27,28) have shown that marked natriuresis may result from acute salt loading, which does not affect mean arterial blood pressure at all. One of the conclusions of the present investigation, therefore, is that the neurohumoral control of renal excretion in the conscious rat should be studied by procedures that do not generate changes in renal arterial blood pressure, i.e., under conditions emulating the normal homeostatic regulation.…”

Section: Perspectives and Significancementioning

confidence: 99%

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Kompanowska-Jezierska

Wolff²,

Kuczeriszka³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kompanowska-Jezierska E, Wolff H, Kuczeriszka M, Gramsbergen JB, Walkowska A, Johns EJ, Bie P. Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats. Am J Physiol Regul Integr Comp Physiol 294: R1130-R1139, 2008. First published January 30, 2008 doi:10.1152/ajpregu.00908.2007.-It was hypothesized that renal sympathetic nerve activity (RSNA) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading (NaLoad) and that RSNA participates in the regulation of arterial blood pressure (MABP). This was tested by NaLoad after chronic renal denervation with and without inhibition of nNOS by S-methyl-thiocitrulline (SMTC). In addition, the acute effects of renal denervation on MABP and sodium balance were assessed. Rats were investigated in the conscious, catheterized state, in metabolic cages, and acutely during anesthesia. NaLoad was performed over 2 h by intravenous infusion of hypertonic solution (50 mol ⅐ min Ϫ1 ⅐ kg body mass Ϫ1 ) at constant body volume conditions. SMTC was coinfused in amounts (20 g ⅐ min Ϫ1 ⅐ kg Ϫ1 ) reported to selectively inhibit nNOS. Directly measured MABPs of acutely and chronically denervated rats were less than control (15% and 9%, respectively, P Ͻ 0.005). Plasma renin concentration (PRC) was reduced by renal denervation (14.5 Ϯ 0.2 vs. 19.3 Ϯ 1.3 mIU/l, P Ͻ 0.005) and by nNOS inhibition (12.4 Ϯ 2.3 vs. 19.6 Ϯ 1.6 mlU/l, P Ͻ 0.005). NaLoad reduced PRC (P Ͻ 0.05) and elevated MABP modestly (P Ͻ 0.05) and increased sodium excretion six-fold, irrespective of renal denervation and SMTC. The metabolic data demonstrated that renal denervation lowered sodium balance during the first days after denervation (P Ͻ 0.001). These data show that renal denervation decreases MABP and renin secretion. However, neither renal denervation nor nNOS inhibition affects either the renin downregulation or the natriuretic response to acute sodium loading. Acute sodium-driven renin regulation seems independent of RSNA and nNOS under the present conditions. plasma renin concentration; total body sodium; blood pressure; sodium excretion THE INTERRELATIONSHIP BETWEEN blood pressure changes and acute variations in water and sodium excretion is not well defined. Arterial blood pressure is controlled by multiple systems, which differ widely in their time of activation. Neural systems react within seconds, while the hormonal and paracrine systems are more sluggish, requiring minutes to hours, or even days, to respond with full capacity. Neurogenic factors have long been hypothesized to be important in the initiation and maintenance of high blood pressure. There is considerable evidence suggesting that enhanced sympathetic drive to the heart and peripheral circulation is involved in the development of persistent blood pressure elevation or maintains the blood pressure elevation originally induced by nonneurogenic mechanisms (11). Moreover, it is known that electrical stimulation of the renal ...

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“…[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.…”

mentioning

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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Volume natriuresis vs. pressure natriuresis

Cited by 50 publications

References 36 publications

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Renal Denervation Does Not Abolish Sustained Baroreflex-Mediated Reductions in Arterial Pressure

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

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

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