Renal denervation chronically lowers arterial pressure  independent of dietary sodium intake in normal rats

Jacob, Frédéric; Ariza, Pilar; Osborn, John W.

doi:10.1152/ajpheart.01029.2002

Cited by 77 publications

(93 citation statements)

References 46 publications

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“…During the control period, CGx rats had reduced MAP while eating 2% NaCl Figure 2. Similar to the effect observed with CGx, and consistent with previous reports, 27 bilateral RDx lowered MAP in normotensive rats independent of salt diet. During the control period, MAP was lower in RDx rats fed 2% NaCl (sham: 103Ϯ1 mm Hg; RDx: 97Ϯ2 mm Hg; PϽ0.05) and in rats fed 0.4% NaCl (sham: 101Ϯ1 mm Hg; RDx: 96Ϯ2 mm Hg; PϽ0.05).…”

Section: Radiotelemetrysupporting

confidence: 92%

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Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

2007

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Abstract-Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively disrupt sympathetic innervation to the splanchnic circulation, would attenuate arterial pressure (AP), and venous tone increases in Ang II salt hypertension. Rats fed 2% or 0.4% NaCl were instrumented to allow AP measurement by radiotelemetry at the same time as surgical CGx or sham operation. Ang II was delivered by minipump (150 ng/kg per minute) for 14 days. CGx reduced AP independent of salt diet during control. CGx markedly attenuated Ang II hypertension in rats on 2% NaCl but had little effect in rats fed 0.4% NaCl. To test the possibility that CGx exerted its effects via renal denervation, rats were subjected to the same protocol but received selective bilateral renal denervation. Renal denervation decreased AP during control but had no protective effect on Ang II hypertension and actually tended to exacerbate the pressor response. Finally, separate groups of rats underwent CGx or sham operation and were instrumented to allow repeated measures of mean circulatory filling pressure, an index of venous tone. In addition to attenuating Ang II salt hypertension, CGx completely prevented Ang II salt-induced increases in mean circulatory filling pressure and substantially attenuated depressor responses to acute ganglion blockade. We conclude that, in the presence of high salt, Ang II activates the splanchnic sympathetic nervous system to increase venomotor tone and AP. Key Words: angiotensin II Ⅲ sympathetic nervous system Ⅲ splanchnic circulation Ⅲ venomotor tone Ⅲ renal denervation W e have shown recently, using repeated measures of mean circulatory filling pressure (MCFP) in conscious undisturbed rats, that chronic infusion of angiotensin II (Ang II), only when administered in combination with a high-salt diet, activates the sympathetic nervous system (SNS) to increase venomotor tone. 1 This increase in venomotor tone may contribute to the pathogenesis of Ang II salt hypertension by increasing central blood volume, resulting in a translocation of blood from the highly compliant venous system to the less compliant arterial circulation. 1 This redistribution of blood volume and the well-documented impairment of renal excretory function caused by Ang II 2 would be major factors in increasing arterial pressure (AP) in this model. [3][4][5] Splanchnic veins and venules account for most of the active capacitance responses in the circulation and are richly innervated by the SNS. 6 -8 In fact, it has been estimated that innervation to the nonhepatic splanchnic organs accounts for half of the total norepinephrine (NE) released in the entire body. 9 Therefore, our recent observations in Ang II salt hypertension of neurog...

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Section: Radiotelemetrysupporting

confidence: 92%

“…Bilateral RDx was performed using established methods in the rat. 27 Briefly, the renal vessels were exposed, and all of the visible nerves, fat, and connective tissue were removed. The renal vessels were then painted with 10% phenol.…”

Section: Cgx Rdx and Radiotelemetry Implantationmentioning

confidence: 99%

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

2007

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“…Also, previous studies that examined the effects of HNa and NNa diets on arterial pressure in the same rat provided no evidence for the HNa diet to have a depressor effect. 18,19 Whereas the current studies suggest a role for renorenal reflexes in the long-term regulation of sodium balance during an HNa diet, a role for the renorenal reflexes has also been demonstrated in the short-term regulation of sodium balance during sodium restriction. 20 Measurements of urinary sodium excretion for 24 hours showed a transient sodium loss from the DRX kidneys when sodium delivery was restricted.…”

Section: Arterial Pressure Versus Urinary Sodium Excretion In Drx Andmentioning

confidence: 54%

“…Furthermore, they showed that arterial pressure was lower in rats with total renal denervation than in sham-denervated rats. These studies suggested that the antihypertensive effect of afferent plus efferent renal denervation 19,36 is related to interruption of the efferent renal nerve pathway in rats fed an NNa diet. The study by Jacob et al 19 further showed lack of a significant increase in arterial pressure in renal-denervated rats fed an HNa diet.…”

Section: Are Differential Mechanisms Involved In Activation Of Renal mentioning

confidence: 99%

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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“…Hypertension occurs commonly and early in renal disease and is paralleled by increases in sympathetic nerve activity, as indicated by increased muscle sympathetic nerve activity and circulating norepinephrine. This appears to be driven by the diseased kidneys, because nephrectomy or denervation has been shown to correct blood pressure and sympathetic nerve activity both in human and animal studies [Jacob, et al 2003]. …”

Section: Sympathetic Nerve Hyperactivity In Patients With Esrdmentioning

confidence: 99%

Cardiovascular and Renal Complications in Obesity and Obesity-Related Medical Conditions: Role of Sympathetic Nervous Activity and Insulin Resistance

Masuo¹,

Lambert²

2012

Insulin Resistance

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Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats

Cited by 77 publications

References 46 publications

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

Splanchnic Circulation Is a Critical Neural Target in Angiotensin II Salt Hypertension in Rats

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

Cardiovascular and Renal Complications in Obesity and Obesity-Related Medical Conditions: Role of Sympathetic Nervous Activity and Insulin Resistance

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