Renal denervation does not prevent hypertension in Lyon hypertensive rats

Boussairi, El Habib; Julien, Claude; Ducher, Michel; Barrès, Christian; Vincent, M; Sassard, J

doi:10.1152/ajpregu.1991.261.1.r20

Cited by 3 publications

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“…It has been demonstrated that renal denervation prevents or attenuates some forms of genetic and experimental hypertension in animals such as spontaneously hypertensive rats, 22,23 New Zealand genetically hypertensive rats, 24 2-kidney models of Goldblatt hypertensive rats, 25 lowsodium, 1-kidney hypertensive rats, 26 angiotensin-induced hypertensive rats, 27 and obesity-induced hypertensive dogs, 28 although negative results were reported in Dahl salt-sensitive rats 31 and Lyon hypertensive rats 32 and conflicting results were also obtained in hypertensive models induced by aortic coarctation, 33,34 NO synthase inhibition, 35,36 and deoxycorticosterone acetate salt treatment 37,38 and in the 1-kidney model of Goldblatt hypertensive rats. 39,40 In the present study, bilateral RD depleted the renal tissue NE content by 94% (measured at the end of the experiments, ie, 2 to 4 weeks after RD), suggesting that the denervation procedure was effective and that significant reinnervation had not yet occurred.…”

Section: Discussionmentioning

confidence: 99%

Renal Denervation Prevents and Reverses Hyperinsulinemia-Induced Hypertension in Rats

1998

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Abstract-Experiments were performed to evaluate the role of the renal nerves in hyperinsulinemia-induced hypertension.Male Sprague-Dawley rats were made hyperinsulinemic by insulin infusion via osmotic minipumps implanted subcutaneously (3.0 mU/kg per minute for 6 weeks). Rats with vehicle infusion served as controls. Bilateral renal denervation was performed either at the beginning of or 4 weeks after insulin infusion. The systolic blood pressure was measured by the tail-cuff method twice a week. Food and water intake and urine flow were measured daily. The results showed that sustained insulin infusion significantly increased plasma insulin concentrations from 277.7Ϯ25.8 pmol/L to 609.9Ϯ22.2 and 696.7Ϯ23.0 pmol/L by the end of weeks 4 and 6, respectively (PϽ0.05). Systolic blood pressure was significantly increased from 135Ϯ3 to 157Ϯ3 and 159Ϯ2 mm Hg (PϽ0.05) at the corresponding time points. There was a significant increase in the plasma norepinephrine concentration after insulin infusion, whereas no significant changes in plasma triglyceride and glucose concentrations, water intake, urine flow, sodium excretion, sodium gain, and body weight gain were observed. Bilateral renal denervation depleted renal norepinephrine stores and prevented the development of hyperinsulinemia-induced hypertension. After hyperinsulinemia-induced hypertension had been fully established (from 134Ϯ2 to 157Ϯ2 mm Hg), bilateral renal denervation reversed the elevated systolic blood pressure to normotensive levels within 2 weeks. Transient denervated diuresis and natriuresis were observed. These results indicate that chronic hyperinsulinemia-induced hypertension requires the presence of intact renal nerves in rats.(Hypertension. 1998;32:249-254.)Key Words: hyperinsulinemia Ⅲ insulin resistance Ⅲ renal nerve Ⅲ renal denervation Ⅲ denervated natriuresis N umerous studies have provided strong inferential evidence that positively associates hypertension with insulin resistance and hyperinsulinemia in humans and some genetically hypertensive rats.1-6 Sustained high carbohydrate feeding in rats results in hypertension that is also correlated with insulin resistance and hyperinsulinemia.7-9 Moreover, we and others have demonstrated that long-term insulin administration causes hypertension in rats.10 -13 The hyperinsulinemia-induced rise of blood pressure is reversible with termination of insulin infusion, thus denoting a specific effect of hyperinsulinemia. 10 These observations provide direct support for an important role for hyperinsulinemia or a hyperinsulinemia-associated mechanism in causing hypertension. However, the precise mechanism coupling hyperinsulinemia to the development of hypertension is not yet clear. Some short-term studies showed that insulin could increase the renal reabsorption of sodium and reduce sodium excretion in animals and humans.14,15 Also, acute or chronic elevation in plasma insulin level stimulates the sympathetic nervous system and increases plasma catecholamines. 16 -18 It follows that hyperinsulinemia may ...

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Section: Discussionmentioning

confidence: 99%

Renal Denervation Prevents and Reverses Hyperinsulinemia-Induced Hypertension in Rats

1998

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Pressure-dependent renin release and arterial pressure maintenance in conscious rats

Bertolino

Julien

Medeiros

et al. 1994

American Journal of Physiology-Regulatory, Integrative and Comp

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The relationship between pressure-dependent renin release and mean arterial pressure (MAP) level was assessed in normotensive intact (n = 10), sympathectomized (guanethidine at 1-13 wk of age; n = 8), and renal-denervated (1 wk before the study; n = 6) rats under normal-salt diet. MAP was recorded beat-to-beat for 2 h in conscious animals. Then plasma renin concentration (PRC) responses to graded reductions of MAP were determined using an aortic inflatable cuff. Neither sympathectomy nor renal denervation altered baseline MAP level and PRC. Lowering MAP below a threshold pressure induced large increases in PRC. Threshold pressure did not differ between intact (87 +/- 1 mmHg), sympathectomized (88 +/- 2 mmHg), and renal-denervated (83 +/- 2 mmHg) rats. MAP frequently fell below threshold pressure in sympathectomized but not in intact and renal-denervated rats. We conclude that in conscious normotensive quiet rats under normal-salt diet the pressure-dependent renin release is not activated spontaneously and is therefore unlikely to play a role in MAP maintenance. This regulatory mechanism develops and operates normally in the absence of sympathetic nerves.

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Comments on Point:Counterpoint: The dominant contributor to systemic hypertension: Chronic activation of the sympathetic nervous system vs. Activation of the intrarenal renin-angiotensin system

2010

Journal of Applied Physiology

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Renal denervation does not prevent hypertension in Lyon hypertensive rats

Cited by 3 publications

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Renal Denervation Prevents and Reverses Hyperinsulinemia-Induced Hypertension in Rats

Renal Denervation Prevents and Reverses Hyperinsulinemia-Induced Hypertension in Rats

Pressure-dependent renin release and arterial pressure maintenance in conscious rats

Comments on Point:Counterpoint: The dominant contributor to systemic hypertension: Chronic activation of the sympathetic nervous system vs. Activation of the intrarenal renin-angiotensin system

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