Effects of renal denervation on pressure-natriuresis in spontaneously hypertensive rats.

Kubota, Jiro; Nishimura, Hikaru; Ueyama, Masakuni; Kawamura, Keishiro

doi:10.1253/jcj.57.1097

Cited by 9 publications

(6 citation statements)

References 15 publications

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“…Accordingly, in some models of hypertension, complete renal denervation delayed the development of hypertension (23,(27)(28)(29)(30). These results indirectly support a role of afferent and efferent renal nerves in the pathogenesis of hypertension.…”

mentioning

confidence: 68%

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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confidence: 68%

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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“…During the physiological adaptation to altered sodium intake, the acute PN curve is modulated by hormonal and neuronal inputs: the renin–angiotensin system (Wadei & Textor, ) and RSNA are both major regulators (Kubota et al . ). In response to high sodium intake, for example, angiotensin II is suppressed, the PN curve is shifted to the left and the gradient becomes steeper.…”

Section: Time Line Of the Development Of Major Antihypertensive Theramentioning

confidence: 97%

Pressure natriuresis and the renal control of arterial blood pressure

Ivy

Bailey

2014

The Journal of Physiology

135

113

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The regulation of extracellular fluid volume by renal sodium excretion lies at the centre of blood pressure homeostasis. Renal perfusion pressure can directly regulate sodium reabsorption in the proximal tubule. This acute pressure natriuresis response is a uniquely powerful means of stabilizing long-term blood pressure around a set point. By logical extension, deviation from the set point can only be sustained if the pressure natriuresis mechanism is impaired, suggesting that hypertension is caused or sustained by a defect in the relationship between renal perfusion pressure and sodium excretion. Here we describe the role of pressure natriuresis in blood pressure control and outline the cascade of biophysical and paracrine events in the renal medulla that integrate the vascular and tubular response to altered perfusion pressure. Pressure natriuresis is impaired in hypertension and mechanistic insight into dysfunction comes from genetic analysis of blood pressure disorders. Transplantation studies in rats show that blood pressure is determined by the genotype of the kidney and Mendelian hypertension indicates that the distal nephron influences the overall natriuretic efficiency. These approaches and the outcomes of genome-wide-association studies broaden our view of blood pressure control, suggesting that renal sympathetic nerve activity and local inflammation can impair pressure natriuresis to cause hypertension. Understanding how these systems interact is necessary to tackle the global burden of hypertension.

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“…There are reports that neural stimulation elicits enhanced renal release of norepinephrine (Collis et al, 1980) and that renal norepinephrine turnover is elevated in young SHR (Patel et al, 1981). SHR kidneys exhibit a rightward shift of their pressurenatriuresis curve compared with normotensive WKy rats (Kubota et al, 1993). The significant decreased natriuretic response in young SHR compared with WKy may reflect differences in efferent renal nerve activity, which is reported to be higher in SHR as young as 5 weeks (Judy and Farrel, 1979).…”

Section: Introductionmentioning

confidence: 98%

Altered renal sodium handling in spontaneously hypertensive rats (SHR) after hypertonic saline intracerebroventricular injection: Role of renal nerves

Guadagnini

Gontijo

2006

Life Sciences

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Effects of renal denervation on pressure-natriuresis in spontaneously hypertensive rats.

Cited by 9 publications

References 15 publications

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

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

Pressure natriuresis and the renal control of arterial blood pressure

Altered renal sodium handling in spontaneously hypertensive rats (SHR) after hypertonic saline intracerebroventricular injection: Role of renal nerves

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