Endogenous angiotensin modulates PGE<sub>2</sub>-mediated release of substance P from renal mechanosensory nerve fibers

Kopp, Ulla C.; Cicha, Michael Z.; Smith, Lori

doi:10.1152/ajpregu.2002.282.1.r19

Cited by 34 publications

(128 citation statements)

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“…Rats were placed on NNa pellets (Na ϩ ϭ163 meq/kg, Teklad) with 0.9% NaCl drinking fluid (HNa diet, nϭ38) or tap water drinking fluid (NNa diet, nϭ20). 5 Nine days later, the rats were placed in metabolic cages for 10 days for measurements of daily urinary sodium excretion.…”

Section: Animals and Experimental Designmentioning

confidence: 99%

“…A PE-50 catheter placed in the left ureter was used to increase renal pelvic pressure by elevating its free end above the kidney. 1,5,11 ARNA was recorded from the peripheral portion of the cut end of 1 renal nerve. ARNA integrated over 1-second intervals was expressed as a percentage of that at baseline.…”

Section: Recording Of Pulsatile Arterial Pressure In Conscious Ratsmentioning

confidence: 99%

“…12 The responsiveness of renal sensory nerves is modulated by dietary sodium, being suppressed by a low and enhanced by a high sodium (HNa) diet. 5 The altered responsiveness of renal sensory nerves is mediated by changes in angiotensin II (Ang II) levels in the renal pelvic wall. Ang II inhibits the PGE 2 -mediated release of substance P from the renal sensory nerves.…”

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confidence: 99%

“…3,4 The renal sensory nerves are activated by increases in renal pelvic pressure within the physiologic range. 5 The increase in afferent renal nerve activity (ARNA) produced by the increased renal pelvic pressure leads to a reflex decrease in efferent renal sympathetic nerve activity (ERSNA) and diuresis and natriuresis, ie, a renorenal reflex response. 6 Increasing renal pelvic pressure elicits a series of events eventually leading to increases in ARNA.…”

mentioning

confidence: 99%

“…5 The low activation threshold of renal mechanosensory nerves together with the natriuretic nature of the renorenal reflexes suggest that activation of these reflexes is an important component of the spectrum of renal mechanisms involved in the renal control of water and sodium homeostasis.…”

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Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

2003

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Abstract-In rats fed high sodium diet, increasing renal pelvic pressure Ն3 mm Hg activates renal mechanosensory nerves, resulting in a renorenal reflex-induced increase in urinary sodium excretion. The low activation threshold of the renal mechanosensory nerves suggests a role for natriuretic renorenal reflexes in the regulation of arterial pressure and sodium balance. If so, interruption of the afferent renal innervation by dorsal rhizotomy (DRX) at T 9 -L 1 would impair urinary sodium excretion and/or increase arterial pressure during high dietary sodium intake. DRX and sham-DRX rats were fed either a high or a normal sodium diet for 3 weeks. Mean arterial pressure measured in conscious rats was higher in DRX than in sham-DRX rats fed a high sodium diet, 130Ϯ2 vs 100Ϯ3 mm Hg (PϽ0.01). However, mean arterial pressure was similar in DRX and sham-DRX rats fed a normal sodium diet, 115Ϯ1 and 113Ϯ1 mm Hg, respectively. Steady-state urinary sodium excretion was similar in DRX and sham-DRX rats on high (17.9Ϯ2.2 and 16.4Ϯ1.8 mmol/24 h, respectively) and normal (4.8Ϯ0.3 and 5.0Ϯ0.4 mmol/24 h, respectively) sodium diets. Studies in anesthetized rats showed a lack of an increase in afferent renal nerve activity in response to increased renal pelvic pressure and impaired prostaglandin E 2 -mediated release of substance P from the renal pelvic nerves in DRX rats fed either a high or a normal sodium diet, suggesting that DRX resulted in decreased responsiveness of peripheral renal sensory nerves. In conclusion, when the afferent limb of the renorenal reflex is interrupted, a high sodium diet results in increased arterial pressure to facilitate the natriuresis and maintenance of sodium balance. Key Words: renal nerves Ⅲ hypertension, sodium dependent Ⅲ sodium, dietary Ⅲ urine Ⅲ natriuresis I n the kidney, the majority of renal sensory nerves containing substance P are located in the renal pelvic wall. 1,2 The afferent renal nerves project to the ipsilateral dorsal root ganglia at the T 6 -L 2 level, with the majority of cell bodies of the afferent renal nerves being at the T 9 -L 1 level. 3,4 The renal sensory nerves are activated by increases in renal pelvic pressure within the physiologic range. 5 The increase in afferent renal nerve activity (ARNA) produced by the increased renal pelvic pressure leads to a reflex decrease in efferent renal sympathetic nerve activity (ERSNA) and diuresis and natriuresis, ie, a renorenal reflex response. 6 Increasing renal pelvic pressure elicits a series of events eventually leading to increases in ARNA. Among the various mechanisms activated by increased renal pelvic pressure is stimulation of bradykinin-2 receptors that activate protein kinase C, which leads to activation of cyclooxygenase-2 and increased prostaglandin E 2 (PGE 2 ) synthesis. 7-9 PGE 2 activates cAMP, which leads to a calcium-dependent release of substance P from the renal sensory nerves. 10,11 Substance P increases ARNA by stimulating neurokinin-1 receptors. 12 The responsiveness of renal sensory nerves is modulated by...

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Section: Animals and Experimental Designmentioning

confidence: 99%

Section: Recording Of Pulsatile Arterial Pressure In Conscious Ratsmentioning

confidence: 99%

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Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

2003

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Physiology of Endothelin and the Kidney

Kohan

Inscho

Wesson

et al. 2011

Comprehensive Physiology

103

136

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Since its discovery in 1988 as an endothelial cell-derived peptide that exerts the most potent vasoconstriction of any known endogenous compound, endothelin (ET) has emerged as an important regulator of renal physiology and pathophysiology. This review focuses on how the ET system impacts renal function in health; it is apparent that ET regulates multiple aspects of kidney function. These include modulation of glomerular filtration rate and renal blood flow, control of renin release, and regulation of transport of sodium, water, protons and bicarbonate. These effects are exerted through ET interactions with almost every cell type in the kidney, including mesangial cells, podocytes, endothelium, vascular smooth muscle, every section of the nephron, and renal nerves. In addition, while not the subject of the current review, ET can also indirectly affect renal function through modulation of extrarenal systems, including the vasculature, nervous system, adrenal gland, circulating hormones and the heart. As will become apparent, these pleiotropic effects of ET are of fundamental physiologic importance in the control of renal function in health. In addition, to help put these effects into perspective, we will also discuss, albeit to a relatively limited extent, how alterations in the ET system can contribute to hypertension and kidney disease.

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Neural Control of Renal Function

Johns

Kopp

DiBona

2011

Comprehensive Physiology

243

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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Endogenous angiotensin modulates PGE₂-mediated release of substance P from renal mechanosensory nerve fibers

Cited by 34 publications

References 50 publications

Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

Physiology of Endothelin and the Kidney

Neural Control of Renal Function

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Endogenous angiotensin modulates PGE2-mediated release of substance P from renal mechanosensory nerve fibers

Cited by 34 publications

References 50 publications

Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

Dietary Sodium Loading Increases Arterial Pressure in Afferent Renal–Denervated Rats

Physiology of Endothelin and the Kidney

Neural Control of Renal Function

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Endogenous angiotensin modulates PGE₂-mediated release of substance P from renal mechanosensory nerve fibers