Effects of complete renal denervation and selective afferent renal denervation on the hypertension induced by intrarenal norepinephrine infusion in conscious rats

Janssen, Ben J. A.; Essen, Helma van; Vervoort-Peters, L. H. T. M.; Thijssen, H. H. W.; Derkx, F. H. M.; Struyker‐Boudier, H. A. J.; Smits, J. F. M.

doi:10.1097/00004872-198906000-00003

Cited by 9 publications

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“…Similar to the current studies, Janssen at al 36 showed that conscious MAP was similar in DRX and sham-DRX rats fed an NNa diet. Furthermore, they showed that arterial pressure was lower in rats with total renal denervation than in sham-denervated rats.…”

Section: Are Differential Mechanisms Involved In Activation Of Renal supporting

confidence: 88%

“…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%

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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: Are Differential Mechanisms Involved In Activation Of Renal supporting

confidence: 88%

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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“…However, selective deafferentation has been performed in several experiments and, to our knowledge, did not cause a notable decrease in arterial pressure in normal rats. Interestingly, in a recent study (24) where rats were subjected to either complete renal denervation, selective deafferentation, or sham surgery, MAP was significantly lower in complete renal denervation compared with selective renal deafferentation or sham-operated rats. Furthermore, in the spontaneously hypertensive rat model, selective deafferentation by dorsal rhizotomy did not attenuate the subsequent increase in arterial pressure.…”

Section: Potential Mechanisms Of Hypotension In Rdnx Ratsmentioning

confidence: 93%

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

Jacob

Ariza

Osborn

2003

American Journal of Physiology-Heart and Circulatory Physiology

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.-The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX (n ϭ 11) and sham (n ϭ 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n ϭ 6, sham; n ϭ 5). In protocol 1, AP was lower in RDNX (91 Ϯ 1 mmHg) compared with sham (101 Ϯ 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased Ͻ5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 Ϯ 2 mmHg) compared with sham (105 Ϯ 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats. sympathetic nervous system; angiotensin II; renal vascular resistance THE KIDNEYS PLAY A PROMINENT role in fluid and electrolyte regulation and therefore arterial pressure homeostasis. One mechanism by which the kidneys are thought to maintain fluid homeostasis is by the renal sympathetic nerves. Fluctuations in the degree of renal sympathetic nerve activity (RSNA) modulate renin secretion from juxtaglomerular cells, sodium reabsorption from renal tubular cells, and renal hemodynamics (13).Many lines of evidence have implicated sympathetically mediated mechanisms in the development of hypertension in several rat models (23,26,27,46). Accordingly, in some models of hypertension, complete renal denervation delayed the development of hypertension (23, 27-30). These results indirectly support a role of afferent and efferent renal nerves in the pathogenesis of hypertension. However, evidence suggesting that renal nerves are important in the long-term control of blood pressure in normotensive rats is not well established. For example, under conditions of increases in dietary sodium intake, is the reduction of RSNA important in the maintenance of a normotensive state? Although this is a crucial question, it has not been answered due to technical limitations for long-term recording of sympathetic nerve activity in conscious rats.The results of several studies (6, 33) tend to suggest that RSNA is modulated by changes in baroreceptor afferent nerve activity. The role of the baroreflex in regulating RSNA is in part sup...

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“…49 Moreover, dorsal rhizotomy has no effect on hypertension induced by infusion of norepinephrine into the renal artery or by wrapping and compressing 1 kidney with a suture (renal wrap model). 50,51 Taken together, studies employing dorsal rhizotomy suggest that afferent renal nerves contribute to some, but not all, experimental models of hypertension.…”

Section: Rdn For the Treatment Of Hypertension: Experimental Evidencementioning

confidence: 99%

Sympathetic Pathophysiology in Hypertension Origins: The Path to Renal Denervation

Esler,

Osborn,

Schlaich

2024

Hypertension

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The importance of the sympathetic nervous system in essential hypertension has been recognized in 2 eras. The first was in early decades of the 20 th century, through to the 1960s. Here, the sympathetic nervous system was identified as a target for the treatment of hypertension, and an extensive range of antiadrenergic therapies were developed. Then, after a period of lapsed interest, in a second era from 1985 on, the development of precise measures of human sympathetic nerve firing and transmitter release allowed demonstration of the importance of neural mechanisms in the initiation and maintenance of the arterial blood pressure elevation in hypertension. This led to the development of a device treatment of hypertension, catheter-based renal denervation, which we will discuss.

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Effects of complete renal denervation and selective afferent renal denervation on the hypertension induced by intrarenal norepinephrine infusion in conscious rats

Cited by 9 publications

References 0 publications

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

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

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

Sympathetic Pathophysiology in Hypertension Origins: The Path to Renal Denervation

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