Renal nerve stimulation augments effect of intraluminal angiotensin II on proximal tubule transport

Quan, Albert; Baum, Michel

doi:10.1152/ajprenal.00279.2001

Cited by 20 publications

(28 citation statements)

References 32 publications

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“…These results are consistent with others showing that norepinephrine modulates the effect of luminal ANG II on chloride transport, which is likely mediated by ␤-receptor activation and an increase in cAMP. These results are consistent with those found in the proximal tubule in which the effect of luminal ANG II is modulated by sympathetic nerve activity (31,32). …”

Section: Discussionsupporting

confidence: 92%

“…Of relevance to the present studies, in proximal tubules perfused in vivo from acutely and chronically denervated kidneys, there was no inhibition in proximal tubule sodium transport with luminal enalaprilat compared with the 40 -50% inhibition by luminal enalaprilat in innervated kidneys (31). Furthermore, renal nerve stimulation augmented the inhibition of volume absorption by luminal enalaprilat, which is consistent with an enhanced effect of endogenous luminal ANG II by increased sympathetic nerve activity (32). Luminal ANG II was found to stimulate sodium transport in both the early and late rat distal tubule perfused in vivo (39).…”

Section: Discussionsupporting

confidence: 77%

“…We had previously shown that luminal dopamine has no effect on transport in the proximal convoluted tubule but it inhibits transport in the presence of bath norepinephrine (5). As previously noted, the effect of luminal ANG II on proximal tubule transport is modulated by renal sympathetic nerve activity (31,32). Finally, we have shown that the inhibitory effect of bath ANG II on mTAL chloride transport is abrogated by bath norepinephrine (4).…”

Section: Discussionmentioning

confidence: 78%

“…Our laboratory has previously found that a synergistic effect of luminal ANG II and sympathetic nerve activity modulates proximal tubular transport of sodium (31,32). Because ANG II is secreted into the proximal tubule, we assessed the contribution of secreted ANG II to proximal tubule sodium transport by the decrement in volume absorption by adding either luminal enalaprilat or losartan (6,30).…”

Section: Discussionmentioning

confidence: 99%

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Luminal angiotensin II stimulates rat medullary thick ascending limb chloride transport in the presence of basolateral norepinephrine

Baum

2016

American Journal of Physiology-Renal Physiology

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Baum M. Luminal angiotensin II stimulates rat medullary thick ascending limb chloride transport in the in the presence of basolateral norepinephrine. Am J Physiol Renal Physiol 310: F294 -F299, 2016. First published December 9, 2015 doi:10.1152/ajprenal.00447.2015.-Angiotensin II (ANG II) is secreted by the proximal tubule resulting in a luminal concentration that is 100-to 1,000-fold greater than that in the blood. Luminal ANG II has been shown to stimulate sodium transport in the proximal tubule and distal nephron. Surprisingly, luminal ANG II inhibits NaCl transport in the medullary thick ascending limb (mTAL), a nephron segment responsible for a significant amount of NaCl absorption from the glomerular ultrafiltrate. We confirmed that addition of 10 Ϫ8 M ANG II to the lumen inhibited mTAL chloride transport (220 Ϯ 19 to 165 Ϯ 25 pmol·mm, P Ͻ 0.01) and examined whether an interaction with basolateral norepinephrine existed to simulate the in vivo condition of an innervated tubule. We found that in the presence of a 10 Ϫ6 M norepinephrine bath, luminal ANG II stimulated mTAL chloride transport from 298 Ϯ 18 to 364 Ϯ 42 pmol·mm NKCC2; chloride transport; norepinephrine; hormonal interaction; microperfusion ANGIOTENSIN II (ANG II) LEVELS INCREASE with volume depletion, which results in an increase in renal sodium absorption that helps to maintain a constant extracellular fluid volume. In addition to the systemic renin-angiotensin system, the proximal tubule has all of the metabolic machinery to generate the peptide hormone ANG II and secrete it into the tubular lumen (8,19,22,23,25). The concentration of ANG II in the blood is approximately 10 -100 pM (8, 25), whereas studies that have directly measured ANG II from the proximal tubule lumen using in vivo micropuncture demonstrate that the concentration of ANG II is 100-to 1,000-fold higher in the tubular lumen than in the blood (8,25,34). In vivo microperfusion studies in which the glomerular ultrafiltrate is blocked and an artificial ultrafiltrate is used to directly perfuse the proximal tubule have shown that the proximal tubule generates and secretes ANG II into the tubular lumen (8). The effect of luminal ANG II may thus play a significant role in the regulation of tubular transport. ANG II has been shown to stimulate transport of sodium in the proximal tubule when added to the bathing solution of proximal tubules perfused in vitro (33). Addition of ANG II had no effect on transport when added to the luminal perfusate of proximal tubules perfused in vitro, but it stimulated proximal tubule sodium transport when the endogenous production of ANG II was inhibited by enalaprilat, which is consistent with endogenous luminal secretion affecting proximal tubule transport of sodium (6). In vitro microperfusion studies of the distal convoluted tubule have also found that ANG II had a direct effect on the apical membrane by stimulating sodium transport (39). ANG II also increases sodium transport in the cortical collecting tubule, which is dependent on pendrin, an ap...

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

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Luminal angiotensin II stimulates rat medullary thick ascending limb chloride transport in the presence of basolateral norepinephrine

Baum

2016

American Journal of Physiology-Renal Physiology

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“…The AT 1 R-dependent but aldosterone-independent alteration in sodium excretion may occur in the proximal tubule, 26,36,37 where aldosterone receptors are not expressed. 38,39 Although aldosterone may have nongenomic effects in human proximal tubule cells, 40 such effects have not been described in rodents.…”

Section: Perspectivesmentioning

confidence: 99%

Differential Effects of Angiotensin II Type-1 Receptor Antisense Oligonucleotides on Renal Function in Spontaneously Hypertensive Rats

et al. 2005

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Abstract-The effect of selectively decreasing renal angiotensin II type 1 (AT 1 ) receptor expression on renal function and blood pressure has not been determined. Therefore, we studied the consequences of selective renal inhibition of AT 1 receptor expression in normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) in vivo. Vehicle, AT 1 receptor antisense oligodeoxynucleotides (AS-ODN), or scrambled oligodeoxynucleotides were infused chronically into the cortex of the remaining kidney of conscious, uninephrectomized WKY and SHR on a 4% NaCl intake. Basal renal cortical membrane AT 1 receptor protein was greater in SHR than in WKY. In WKY and SHR, AS-ODN decreased renal but not cardiac AT 1 receptors. AT 1 receptor AS-ODN treatment increased plasma renin activity to a greater extent in WKY than in SHR. However, plasma angiotensin II and aldosterone were increased by AS-ODN to a similar degree in both rat strains. In SHR, sodium excretion was increased and sodium balance was decreased by AS-ODN but had only a transient ameliorating effect on blood pressure. Urinary protein and glomerular sclerosis were markedly reduced by AS-ODN-treated SHR. In WKY, AS-ODN had no effect on sodium excretion, blood pressure, or renal histology but also modestly decreased proteinuria. The major consequence of decreasing renal AT 1 receptor protein in the SHR is a decrease in proteinuria, probably as a result of the amelioration in glomerular pathology but independent of systemic blood pressure and circulating angiotensin II levels. Key Words: receptors, angiotensin II Ⅲ rats Ⅲ kidney Ⅲ hypertension, essential Ⅲ proteinuria G enetic manipulations that increase the activity of the renin-angiotensin system (RAS) systemically 1-5 or in specific organs (eg, brain and kidney) elevate blood pressure. 6,7 For example, overexpression of angiotensinogen and renin in renal proximal tubules 6 or in neurons and glia cells in brain 7 increased blood pressure without increasing circulating renin levels. Systemic deletion or silencing of genes that regulate the RAS also decreases blood pressure. Thus, disrupting or silencing angiotensinogen 4 and angiotensinconverting enzyme 1 genes 8,9 or the angiotensin II type 1A receptor (AT 1A R) gene 10,11 in mice or rats decreases blood pressure. Decreasing the expression of liver angiotensinogen also decreases blood pressure in mice. 12 More recently, Crowley et al reported that nephrectomized AT 1A Ϫ/Ϫ mice with 1 transplanted AT 1A ϩ/ϩ kidney had higher blood pressures than those observed in unmanipulated AT 1A Ϫ/Ϫ mice or AT 1A Ϫ/Ϫ mice with a transplanted AT 1A Ϫ/Ϫ kidney but lower than the blood pressures in unmanipulated AT 1A ϩ/ϩ or AT 1A ϩ/ϩ mice with a transplanted AT 1A ϩ/ϩ kidney. 13 These studies showed the importance of renal and extrarenal factors in the regulation of blood pressure. However, there are no reports of the renal functional and blood pressure consequences of silencing the AT 1 R selectively in the kidney of rats with spontaneous hypertension. To test the ...

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Neural Control of Renal Function

Johns

Kopp

DiBona

2011

Comprehensive Physiology

247

186

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The kidney is innervated with efferent sympathetic nerve fibers that directly contact the vasculature, the renal tubules, and the juxtaglomerular granular cells. Via specific adrenoceptors, increased efferent renal sympathetic nerve activity decreases renal blood flow and glomerular filtration rate, increases renal tubular sodium and water reabsorption, and increases renin release. Decreased efferent renal sympathetic nerve activity produces opposite functional responses. This integrated system contributes importantly to homeostatic regulation of sodium and water balance under physiological conditions and to pathological alterations in sodium and water balance in disease. The kidney contains afferent sensory nerve fibers that are located primarily in the renal pelvic wall where they sense stretch. Stretch activation of these afferent sensory nerve fibers elicits an inhibitory renorenal reflex response wherein the contralateral kidney exhibits a compensatory natriuresis and diuresis due to diminished efferent renal sympathetic nerve activity. The renorenal reflex coordinates the excretory function of the two kidneys so as to facilitate homeostatic regulation of sodium and water balance. There is a negative feedback loop in which efferent renal sympathetic nerve activity facilitates increases in afferent renal nerve activity that in turn inhibit efferent renal sympathetic nerve activity so as to avoid excess renal sodium retention. In states of renal disease or injury, there is activation of afferent sensory nerve fibers that are excitatory, leading to increased peripheral sympathetic nerve activity, vasoconstriction, and increased arterial pressure. Proof of principle studies in essential hypertensive patients demonstrate that renal denervation produces sustained decreases in arterial pressure.

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Renal nerve stimulation augments effect of intraluminal angiotensin II on proximal tubule transport

Cited by 20 publications

References 32 publications

Luminal angiotensin II stimulates rat medullary thick ascending limb chloride transport in the presence of basolateral norepinephrine

Luminal angiotensin II stimulates rat medullary thick ascending limb chloride transport in the presence of basolateral norepinephrine

Differential Effects of Angiotensin II Type-1 Receptor Antisense Oligonucleotides on Renal Function in Spontaneously Hypertensive Rats

Neural Control of Renal Function

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