Regression of left ventricular hypertrophy after bilateral nephrectomy

Getts, Roger; Hazlett, Shawn M.; Sharma, Sandeep; McGill, Rita L.; Biederman, Robert W; Marcus, Richard J.; Sandroni, Stephen

doi:10.1093/ndt/gfi321

Cited by 10 publications

(9 citation statements)

References 11 publications

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“…Pertinently, renal denervation decreased (by 50%) kidney renin secretion in uncontrolled hypertensive patients ) and attenuated the elevated expression of the angiotensin II type 1 (AT 1 ) receptor in the kidney of our Ren-2 STZ model (Yao et al 2014) and in rabbits with pacing-induced heart failure (Clayton et al 2011). Consequently, BRD intervention in our model may have reduced levels of circulating angiotensin II and aldosterone, both of which are well known to contribute to cardiac remodelling (Privratsky et al 2003;Getts et al 2006). Thus, an important finding of our study is that BRD reduced not only the hypertension, but also the hypertension-induced concentric hypertrophic cardiac remodelling, independently of the presence of diabetes as a co-morbidity.…”

Section: H P a Thaung And Othersmentioning

confidence: 86%

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Chronic bilateral renal denervation reduces cardiac hypertrophic remodelling but not β‐adrenergic responsiveness in hypertensive type 1 diabetic rats

Thaung

Yao

Bussey

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study?Can bilateral renal denervation, an effective antihypertensive treatment in clinical and experimental studies, improve cardiac β-adrenoceptor responsiveness in a diabetic model with underlying hypertension? r What is the main finding and its importance?Bilateral renal denervation did not affect β-adrenergic responsiveness in the diabetic hypertensive rat heart, but denervation reduced the hypertension-induced concentric hypertrophic remodelling. This suggests that the positive haemodynamic changes induced by renal denervation are most likely to reflect an attenuation of sympathetic effects on the systemic vasculature and/or the renal function rather than direct sympathetic modulation of the heart. Bilateral renal denervation (BRD) has been shown to normalise blood pressure in clinical and experimental studies of hypertension by reducing systemic sympathetic output. This study determined the effect of BRD on cardiac β-adrenoceptor (AR) responsiveness in a diabetic model with underlying hypertension using the transgenic (mRen-2)27 rats. Bilateral renal denervation or sham surgeries were conducted repeatedly at 3, 6 and 9 weeks in Ren-2 rats with or without streptozotocin (STZ)-induced diabetes (4 × n = 7); Sprague-Dawley rats (n = 6) served as control animals. Cardiac function was determined in isolated hearts at 18 weeks of age. Normalised left ventricular developed pressure and relaxation was recorded in response to incremental concentrations of the β-AR agonist isoprenaline (from 10−10 to 10−7 m) or the β 3 -AR agonist BRL37344 (from 10 −13 to 10 −6 m). Expression levels of β 1 -AR were determined by Western blot. Both inotropic and lusitropic β-AR responsiveness was reduced in the hypertensive diabetic hearts, but these responses were unaltered after BRD. Expression levels of β 1 -AR were increased after BRD (Sham, 0.85 ± 0.11 versus 1.01 ± 0.05 a.u.; BRD, 1.45 ± 0.11 versus 1.46 ± 0.07 a.u.; Ren-2 versus Ren-2 STZ, P < 0.05 versus Sham). No effect of β 3 -AR agonist stimulation with BRL37344 was observed. Interestingly, BRD increased left ventricular diastolic volume in both the Ren-2 and the Ren-2 STZ groups. Bilateral renal denervation did not restore the attenuated cardiac β-AR responsiveness in the diabetic hypertensive rats, but it reduced the extent of hypertension-induced concentric hypertrophic remodelling. Thus, the haemodynamic

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Section: H P a Thaung And Othersmentioning

confidence: 86%

“…; Getts et al . ). Thus, an important finding of our study is that BRD reduced not only the hypertension, but also the hypertension‐induced concentric hypertrophic cardiac remodelling, independently of the presence of diabetes as a co‐morbidity.…”

Section: Discussionmentioning

confidence: 97%

Chronic bilateral renal denervation reduces cardiac hypertrophic remodelling but not β‐adrenergic responsiveness in hypertensive type 1 diabetic rats

Thaung

Yao

Bussey

et al. 2015

Experimental Physiology

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“…Reports of nephrectomy in patients with ESRD, maintained on dialysis or posttransplantation, confirm the potential value of renal denervation of the native kidney, which was associated with consistent reduction in blood pressure and total systemic vascular resistance. 56 The potential therapeutic use of denervation of the native kidney in ESRD patients with hypertension and left ventricular hypertrophy has been highlighted recently in a case report demonstrating a decrease of left ventricular mass of 54 g within 4 months after bilateral nephrectomy, 57 supporting the concept of heightened sympathetic outflow, particularly to the heart, being a main contributor to hypertensive left ventricular hypertrophy. 19 …”

Section: Blood Pressure Regulation In Esrd: Nephrectomy Of Native Nonmentioning

confidence: 98%

Renal Denervation as a Therapeutic Approach for Hypertension

et al. 2009

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“…Furthermore, nephrectomy in patients with end-stage renal disease is associated with consistent reductions in blood pressure and total systemic vascular resistance [46], perhaps indicating the potential therapeutic utility of denervation of the native kidney for blood pressure lowering and target-organ protection in these patients. Indeed, a recent case report demonstrated a substantial 54-gram decrease in left ventricular mass within 4 months following bilateral nephrectomy [47], supporting the concept that heightened sympathetic outflow, particularly to the heart, is a main contributor to hypertensive left ventricular hypertrophy [48].…”

Section: The Role Of Renal Sympathetic Nerves In Other Conditions Commentioning

confidence: 89%

Renal Sympathetic Nerve Ablation: The New Frontier in the Treatment of Hypertension

Schlaich

Krum

Sobotka

2010

Current Science Inc

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The sympathetic nervous system plays an important role in circulatory and metabolic control and has clearly been established as a major contributor to the development of hypertension, as elevated sympathetic nerve activity initiates and sustains the elevation of blood pressure. Increased sympathetic outflow to the heart, resulting in increased cardiac output and neurally mediated vasoconstriction of peripheral blood vessels, is an obvious example of a neural pathophysiologic pathway leading to elevated blood pressure. The consequences of increased sympathetic outflow to the kidneys, perhaps most important in this context, are sodium and water retention, increased renin release, and alterations of renal blood flow-effects that contribute substantially to both acute and long-term blood pressure elevations. Accordingly, renal sympathetic nerve ablation appears to be a logical therapeutic approach for the treatment of hypertension. Recent reports on a novel catheter-based renal nerve ablation procedure reviewed in this article are promising.

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Regression of left ventricular hypertrophy after bilateral nephrectomy

Cited by 10 publications

References 11 publications

Chronic bilateral renal denervation reduces cardiac hypertrophic remodelling but not β‐adrenergic responsiveness in hypertensive type 1 diabetic rats

Chronic bilateral renal denervation reduces cardiac hypertrophic remodelling but not β‐adrenergic responsiveness in hypertensive type 1 diabetic rats

Renal Denervation as a Therapeutic Approach for Hypertension

Renal Sympathetic Nerve Ablation: The New Frontier in the Treatment of Hypertension

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