Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat

Kopp, Ulla C.; Olson, Lar̀s; DiBona, Gerald F.

doi:10.1152/ajprenal.1984.246.1.f67

Cited by 97 publications

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“…2,4 Increased ipsilateral ARNA subsequently induces a contralateral diuresis and natriuresis via an inhibition on contralateral efferent renal nerve activity, which is known as the renorenal reflex. 2,4 The vanilloid receptor (VR1), also known as the capsaicin receptor or a member of the transient receptor potential vanilloid subfamily, was cloned by the use of the "hot" pepper-derived vanilloid compound, capsaicin, as a ligand. 5 The VR1 receptor, a ligand gate ion channel, is mainly expressed in a subpopulation of primary sensory afferents and functions to integrate multiple stimuli including proton, heat, and vanilloid compounds such as capsacin.…”

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Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats

Zhu

Wang

2005

Hypertension

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Abstract-To test the hypothesis that activation of the vanilloid receptor 1 (VR1) expressed in sensory nerves innervating the renal pelvis leads to diuresis and natriuresis, a selective VR1 receptor agonist, capsaicin (2.4 nmol), or vehicle was perfused intravenously or into the left renal pelvis of anesthetized rats at a rate without changing renal perfusion pressure. Mean arterial pressure was not altered by capsaicin administered intravenously or into the renal pelvis. Capsaicin perfusion into the left renal pelvis but not intravenously caused significant increases in urine flow rate and urinary sodium excretion bilaterally in a dose-dependent manner, which were abolished by capsazepine, a selective VR1 receptor antagonist, given ipsilaterally to the renal pelvis or by ipsilateral renal denervation. Capsaicin given intravenously or into the left renal pelvis increased plasma calcitonin gene-related peptide levels to the same extent. Increased plasma calcitonin gene-related peptide levels induced by capsaicin (68.9Ϯ2.8 pg/mL) perfusion into the renal pelvis was prevented either by capsazepine (22.5Ϯ10.1 pg/mL) given ipsilaterally into the renal pelvis or by ipsilateral renal denervation (25.9Ϯ2.3 pg/mL). Taken together, our data show that unilateral activation of VR1-positive sensory nerves innervating the renal pelvis leads to bilateral diuresis and natriuresis via a mechanism that is independent of plasma calcitonin gene-related peptide levels. These data suggest that VR1-positive sensory nerves in the kidney enhance renal excretory function, a mechanism that may be critically involved in sodium and fluid homeostasis. Key Words: natriuresis Ⅲ diuresis Ⅲ sensory nerves Ⅲ vanilloid receptor 1 Ⅲ capsaicin Ⅲ renal pelvis T he renal pelvis is heavily innervated by primary sensory afferent nerves with their nerve terminals distributing in mucous and in proximity to the epithelial cells. 1 The renal pelvis therefore is considered as a sensory organ sensing mechano-stimuli and chemo-stimuli leading to altered renal excretory function such as diuresis and natriuresis. 2,3 Previous studies have shown that ipsilateral obstruction to urine flow or elevation of pressure in the renal pelvis activates renal mechano-sensitive neurons, which results in an increase in ipsilateral afferent renal nerve activity (ARNA). 2,4 Increased ipsilateral ARNA subsequently induces a contralateral diuresis and natriuresis via an inhibition on contralateral efferent renal nerve activity, which is known as the renorenal reflex. 2,4 The vanilloid receptor (VR1), also known as the capsaicin receptor or a member of the transient receptor potential vanilloid subfamily, was cloned by the use of the "hot" pepper-derived vanilloid compound, capsaicin, as a ligand. 5 The VR1 receptor, a ligand gate ion channel, is mainly expressed in a subpopulation of primary sensory afferents and functions to integrate multiple stimuli including proton, heat, and vanilloid compounds such as capsacin. 6 -7 VR1-positive sensory nerves have been implicated to play an...

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Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats

Zhu

Wang

2005

Hypertension

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“…However, this is very unlikely because, in dogs, studies have shown that raising renal venous pressure up to 28 mm Hg failed to activate a renorenal reflex. 44 In fact, increasing ureteral pressure to approximately 63 mm Hg illicited only very small changes in contralateral renal blood flow (approximately -3%) and sodium excretion (approximately -10%). 44 In addition, attempts to elicit a renorenal reflex via chemoreceptor stimulation by retrograde ureteropelvic perfusion with 0.9 M NaCI failed to produce any changes in contralateral renal function.…”

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confidence: 94%

“…44 In fact, increasing ureteral pressure to approximately 63 mm Hg illicited only very small changes in contralateral renal blood flow (approximately -3%) and sodium excretion (approximately -10%). 44 In addition, attempts to elicit a renorenal reflex via chemoreceptor stimulation by retrograde ureteropelvic perfusion with 0.9 M NaCI failed to produce any changes in contralateral renal function. 44 Therefore, based on the available evidence, it seems likely that the neural influences are the same to each kidney under the conditions of our experiment.…”

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“…44 In addition, attempts to elicit a renorenal reflex via chemoreceptor stimulation by retrograde ureteropelvic perfusion with 0.9 M NaCI failed to produce any changes in contralateral renal function. 44 Therefore, based on the available evidence, it seems likely that the neural influences are the same to each kidney under the conditions of our experiment.…”

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confidence: 94%

“…This was done by chronically altering renal perfusion pressure of the two kidneys (in the same animal) to different levels while using a split bladder technique to determine renal by guest on May 12, 2018 http://hyper.ahajournals.org/ Downloaded from hemodynamics and excretory function of each kidney separately.…”

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Role of pressure natriuresis in long-term control of renal electrolyte excretion.

et al. 1993

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If pressure natriuresis is to play an important role in arterial pressure control, renal perfusion pressure must have a long-term effect on urinary sodium excretion. The aim of this study was to quantitate the importance of renal perfusion pressure per se in controlling renal hemodynamics and electrolyte excretion chronically. Female mongrel dogs (n=6) were instrumented with bilateral renal artery catheters for measurement of renal perfusion pressure and occluders on both renal arteries for servo-control of renal perfusion pressure at different levels; the urinary bladder was split for determination of renal clearances and electrolyte excretion from each kidney separately. Because both kidneys were exposed to the same neurohumoral influences, any changes in renal function could be attributed to differences in renal perfusion pressure between the two kidneys. After 5 days of control, renal perfusion pressure to one kidney was reduced from 86.7 ±0.2 to 74.2 ±0.6 mm Hg for 12 days, and pressure in the contralateral kidney increased to 91.5±0.4 mm Hg. Sodium excretion decreased from 41±2 to 25±1 mmol/d in the servo-controlled kidney and increased from 41 ±1 to 55 ±1 mmol/d in the contralateral kidney during 12 days of servo-control. Urine volume, chloride excretion, and potassium excretion exhibited similar patterns during servo-control. In addition, autoregulation of effective renal plasma flow and glomerular filtration rate was relatively well maintained; however, in the low-pressure kidney, glomerular filtration rate was slightly but significantly lower (-8%) than in the contralateral kidney. In summary, long-term changes in renal perfusion pressure caused sustained alterations in renal electrolyte excretion. These results suggest that renal perfusion pressure is an important long-term controller of sodium and water excretion. over the long-term by complex interactions J~ A . between the various neurohumoral control systems and the ability of the kidneys to excrete salt and water. Guyton and colleagues 1 (see References 2 through 5 for review) have emphasized renal-body fluid feedback as the dominant control system for long-term blood pressure control. A key component of this feedback is the effect of arterial pressure on renal excretion of sodium, often referred to as pressure natriuresis. In most instances, this mechanism is believed to stabilize blood pressure in response to various perturbations that would tend to cause hypertension or hypotension.The validity of this concept depends on the assumption that arterial pressure has a long-term influence on renal excretion of sodium and water, a premise that has been difficult to test experimentally. Numerous investigators have demonstrated that acute changes in arterial pressure markedly alter sodium and water excretion, 69 but the long-term effects of pressure per se on renal excretion are largely unknown. Long-term pressurenatriuresis curves are usually determined indirectly by

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Pelviureteral inhibitory reflex and ureteropelvic excitatory reflex: Role of the two reflexes in regulation of urine flow from the renal pelvis to the ureter

Shafik

1997

Neurourol. Urodyn.

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The mechanism by which the ureteropelvic junction (UPJ) regulates the passage of urine from the renal pelvis to the ureter, and prevents urinary backflow from the ureter to the renal pelvis, is not completely understood. The current communication studies this mechanism in 18 dogs. With the dogs under anesthesia, nephrostomy was done through which two catheters (one pressure and one balloon‐tipped) were introduced into the UPJ and the renal pelvis, respectively. Renal pelvis distension with a balloon filled with 1 ml of saline effected a rise of renal pelvic pressure from a mean basal pressure of 4.8 ± 1.2 cm H2O to 6.9 ± 2.3 cm H2O (P < 0.05). The basal UPJ pressure of 12.6 ± 2.7 cm H2O showed no significant change with 1 ml distention of the renal pelvic balloon (P > 0.05). Renal pelvic distension with 2, 3, and 4 ml caused a significant rise of renal pelvic pressure to 8.4 ± 2.7 (P < 0.05), 10.6 ± 2.2 (P < 0.01), and 11.8 ± 1.9 (P < 0.01) cm H2O, respectively, and a significant drop of UPJ pressure to 4.8 ± 1.2, 4.7 ± 1.1, and 4.6 ± 1.2 cm H2O (P < 0.01), respectively. Ureteric distension with a balloon filled with 0.5 ml of saline significantly raised the ureteric pressure from a mean basal value of 4.3 ± 1.4 cm H2O to 14.7 ± 3.3 cm H2O (P < 0.01) and the UPJ pressure to a mean of 20.8 ± 3.8 (P < 0.05). Ureteric distension with 1 and 1.5 ml of saline led to an elevation of ureteric and UPJ pressure which was not significantly different from that observed with distension with 0.5 ml (P > 0.05). In contrast, the UPJ showed no significant pressure change upon distension of the locally anesthetized renal pelvis or ureter, respectively. Likewise, the locally anesthetized UPJ exhibited no significant pressure response to renal pelvic or ureteric distension. The study demonstrates that urine might have to accumulate in the renal pelvis up to a certain volume and pressure so as to effect UPJ opening, which occurs at its maximum irrespective of the distending volume. UPJ opening upon renal pelvic distension postulates a reflex relationship which we call “pelviureteral inhibitory reflex.” This reflex is believed to regulate the passage of urine from the renal pelvis to the ureter. Ureteric distension closes the UPJ we call this reflex action the “ureteropelvic excitatory reflex” as it seems to prevent reflux of urine through the UPJ and thus protects the kidney. The concept that the UPJ acts as a physiologic sphincter is put forward. Neurourol. Urodynam. 16:315–325, 1997. © 1997 Wiley‐Liss, Inc.

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Renorenal reflex responses to mechano- and chemoreceptor stimulation in the dog and rat

Cited by 97 publications

References 0 publications

Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats

Diuresis and Natriuresis Caused by Activation of VR1-Positive Sensory Nerves in Renal Pelvis of Rats

Role of pressure natriuresis in long-term control of renal electrolyte excretion.

Pelviureteral inhibitory reflex and ureteropelvic excitatory reflex: Role of the two reflexes in regulation of urine flow from the renal pelvis to the ureter

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