Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Handa, Rajash K.; Johns, Edward J.

doi:10.1113/jphysiol.1985.sp015903

Cited by 62 publications

(39 citation statements)

References 32 publications

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“…Whether circulating angiotensin II levels are lowered with saline loading or captopril, the rise in sodium reabsorption with renal nerve stimulation is markedly blunted (18). Circulating angiotensin II may facilitate adrenergic transmission at the renal nerve-renal epithelial cell junction (14,18,19).…”

Section: Discussionmentioning

confidence: 99%

“…For example, the stimulatory effect of the renal nerves on renal sodium reabsorption requires production of circulating angiotensin II by the systemic renin-angiotensin system (14,18,19). The rise in sodium reabsorption accompanying renal nerve stimulation occurs only in the presence of physiological nonpressor levels of circulating angiotensin II (18).…”

Section: Discussionmentioning

confidence: 99%

“…Proximal tubule transport is also regulated by the renin-angiotensin system (8,14,28). The proximal tubule contains an autonomous renin-angiotensin system in which high levels of angiotensin II are synthesized and luminally secreted (7,17,23,25,(31)(32)(33).…”

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

Quan¹,

Baum

2002

American Journal of Physiology-Renal Physiology

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, P Ͻ 0.02, and 51.8 Ϯ 5.0 vs. 14.6 Ϯ 7.4%, P Ͻ 0.05, respectively). Renal nerve stimulation did not alter the glomerular filtration rate or renal blood flow. Renal nerve stimulation augments the stimulatory effect of intraluminal angiotensin II. The sympathetic renal nerves modulate the proximal tubule renin-angiotensin system and thereby regulate proximal tubule transport.renin-angiotensin system; enalaprilat; in vivo microperfusion THE SYMPATHETIC RENAL NERVES innervate the proximal tubule and participate in the regulation of proximal tubule sodium reabsorption (1,9,11,21,24). Renal nerve stimulation augments proximal tubule transport, whereas renal denervation decreases proximal tubule transport (3-5, 9, 12, 13). The renal nerves directly modulate proximal tubule transport independently of changes in the glomerular filtration rate (GFR), renal blood flow, and peritubular Starling forces (3-5, 9, 12, 13).Proximal tubule transport is also regulated by the renin-angiotensin system (8, 14, 28). The proximal tubule contains an autonomous renin-angiotensin system in which high levels of angiotensin II are synthesized and luminally secreted (7,17,23,25,(31)(32)(33).Inhibition of intraluminal angiotensin II production decreases proximal tubule volume reabsorption in hydropenic rats (2, 27, 28). These studies are consistent with the proximal tubule renin-angiotensin system modulating proximal tubule transport independently of circulating angiotensin II.The effect of angiotensin II on proximal tubule transport is regulated by acute changes in extracellular volume (29). Proximal tubule volume reabsorption is augmented by intraluminal angiotensin II to a greater degree during volume contraction than during volume expansion (29). However, the mechanism by which acute changes in extracellular volume are "translated" into changes in the proximal tubule volume reabsorptive rate, as mediated by intraluminal angiotensin II, is unknown.We have recently demonstrated that the sympathetic renal nerves modulate the effect of intraluminal angiotensin II on proximal tubule transport. In studies in which the renal nerves were disrupted in vivo, inhibition of proximal tubule angiotensin II production failed to decrease proximal tubule transport in hydropenic animals (30). However, similar inhibition of angiotensin II production in the normally innervated kidney decreases volume transport (27,30). These studies support a role for renal nerves in modulating the effect of angiotensin II on proximal tubule transport. To further examine whether renal nerves play a role in modulating the proximal tubule renin-angiotensin system, we examined whether renal nerve stimulation modulates the effect of the renin-angiotensin system on proximal tubule transport. MATERIALS AND METHODS Preparation of animals.Male Sprague-Dawley rats, 190-250 g, were used for this study. Rat surgical preparation and in vivo microperfusion were performed as described previously (27,29,30). After tracheostomy and jugular vein cannulation, 5% bovine serum albumin containi...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Quan¹,

Baum

2002

American Journal of Physiology-Renal Physiology

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“…5,6 When reninangiotensin system activity was stimulated by low dietary sodium intake, captopril completely eliminated the antinatriuretic response. 7 When renin-angiotensin system activity was suppressed by high dietary sodium intake, the antinatriuretic responses were absent but could be restored to (but not greater than) normal by Ang II given in nonpressor doses that did not affect baseline renal hemodynamic and excretory function.…”

Section: Intrarenal Interactionsmentioning

confidence: 99%

“…Subsequently, administration of the ACE inhibitor (ACEI) captopril or an Ang II receptor antagonist attenuated the antinatriuretic response to either low-frequency electrical or reflex renal sympathetic nerve stimulation in anesthetized rats consuming a normal dietary sodium intake. 5,6 When reninangiotensin system activity was stimulated by low dietary sodium intake, captopril completely eliminated the antinatriuretic response. 7 When renin-angiotensin system activity was suppressed by high dietary sodium intake, the antinatriuretic responses were absent but could be restored to (but not greater than) normal by Ang II given in nonpressor doses that did not affect baseline renal hemodynamic and excretory function.…”

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Nervous Kidney

DiBona

2000

Hypertension

162

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Abstract-Increases in renal sympathetic nerve activity regulate the functions of the nephron, the vasculature, and the renin-containing juxtaglomerular granular cells. Because increased activity of the renin-angiotensin system can also influence nephron and vascular function, it is important to understand the interactions between the renal sympathetic nerves and the renin-angiotensin system in the control of renal function. These interactions can be intrarenal, for example, the direct (by specific innervation) and indirect (by angiotensin II) contributions of increased renal sympathetic nerve activity to the regulation of renal function. The effects of increased renal sympathetic nerve activity on renal function are attenuated when the activity of the renin-angiotensin system is suppressed or antagonized with ACE inhibitors or angiotensin II-type AT 1 -receptor antagonists. The effects of intrarenal administration of angiotensin II are attenuated after renal denervation. These interactions can also be extrarenal, for example, in the central nervous system, wherein renal sympathetic nerve activity and its arterial baroreflex control are modulated by changes in activity of the renin-angiotensin system. In addition to the circumventricular organs, whose permeable blood-brain barrier permits interactions with circulating angiotensin II, there are interactions at sites behind the blood-brain barrier that depend on the influence of local angiotensin II. The responses to central administration of angiotensin II-type AT 1 -receptor antagonists into the ventricular system or microinjected into the rostral ventrolateral medulla are modulated by changes in activity of the renin-angiotensin system produced by physiological changes in dietary sodium intake. Similar modulation is observed in pathophysiological models wherein activity of both the renin-angiotensin and sympathetic nervous systems is increased (eg, congestive heart failure). Thus, both renal and extrarenal sites of interaction between the renin-angiotensin system and renal sympathetic nerve activity are involved in influencing the neural control of renal function. (Hypertension. 2000;36:1083-1088.)Key Words: renin-angiotensin system Ⅲ renal nerves Ⅲ rats T he renal sympathetic nerves innervate the tubules, the vessels, and the juxtaglomerular granular cells of the kidney. 1,2 In this way, changes in renal sympathetic nerve activity (RSNA) directly influence the functions of these innervated renal effector units. Increases in RSNA decrease urinary sodium and water excretion by increasing renal tubular water and sodium reabsorption throughout the nephron, decrease renal blood flow and glomerular filtration rate by constricting the renal vasculature, and increase activity of the renin-angiotensin system (angiotensin [Ang]II) by stimulating renin release from juxtaglomerular granular cells. Ang II, through direct actions on Ang II-type AT 1 receptors located on tubular and vascular segments, can also increase renal tubular sodium, chloride, and water reabsorption an...

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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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Interaction of the renin‐angiotensin system and the renal nerves in the regulation of rat kidney function.

Cited by 62 publications

References 32 publications

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

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

Nervous Kidney

Neural Control of Renal Function

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