Short- and Long-Term Neuroadrenergic Effects of Moderate Dietary Sodium Restriction in Essential Hypertension

Dell’Oro, Raffaella; Seravalle, Gino; Foglia, Gerardo; Trevano, Fosca Quarti; Mancia, Giuseppe

doi:10.1161/01.cir.0000033519.45615.c7

Cited by 120 publications

(101 citation statements)

References 30 publications

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“…However, in clinical situations with sustained low BP, such as heart failure, resting sympathetic activity is elevated (19). A recent study showed that MSNA remained consistently elevated over 8 wk in hypertensive subjects who switched to a low-salt diet (20). Clearly, changes in volume status and BP have a sustained effect on sympathetic activity.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic Nerve Activity Is Inappropriately Increased in Chronic Renal Disease

Klein¹,

Ligtenberg²,

Neumann³

et al. 2003

Journal of the American Society of Nephrology

155

136

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Abstract. The hypothesis that in hypertensive patients with renal parenchymal disease sympathetic activity is "inappropriately" elevated and that this overactivity is a feature of renal disease and not of a reduced number of nephrons per se is addressed. Fifty seven patients with renal disease (various causes, no diabetes, all on antihypertensive medication) were studied, age range 18 to 62, creatinine clearance 10 to 114 ml/min per 1.73 m 2 . Antihypertensives were stopped, but diuretics were allowed, to prevent overhydration. Matched control subjects were also studied. The effect of changes in fluid status was examined in seven patients while on and after stopping diuretics and in eight control subjects while on lowand high-sodium diet. Seven kidney donors were studied before and after unilateral nephrectomy. Sympathetic activity was quantified as muscle sympathetic nerve activity (MSNA) in the peroneal nerve. Mean arterial pressure, MSNA, and plasma renin activity were higher in patients than in control subjects, respectively (115 Ϯ 12 and 88 Ϯ 11 mmHg, 31 Ϯ 15 and 18 Ϯ 10 bursts/min, and 500 [20 to 6940] and 220 [40 to 980] fmol/L per s; P Ͻ 0.01 for all items). Extracellular fluid volume (bromide distribution) did not differ. Seven patients were studied again after stopping diuretics. MSNA decreased from 34 Ϯ 18 to 19 Ϯ 18 bursts/min (P Ͻ 0.01). Eight healthy subjects were studied during low-and high-sodium diet. MSNA was 26 Ϯ 12 and 13 Ϯ 7 bursts/min (P Ͻ 0.01). The curves relating extracellular fluid volume to MSNA were parallel in the two groups but shifted to a higher level of MSNA in the patients. In the kidney donors, creatinine clearance reduced by 25%, but MSNA was identical before and after donation. It is concluded that in hypertensive patients with renal parenchymal disease, sympathetic activity is inappropriately high for the volume status and that reduction of nephron number in itself does not influence sympathetic activity.

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Section: Discussionmentioning

confidence: 99%

Sympathetic Nerve Activity Is Inappropriately Increased in Chronic Renal Disease

Klein¹,

Ligtenberg²,

Neumann³

et al. 2003

Journal of the American Society of Nephrology

155

136

View full text Add to dashboard Cite

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“…[32][33][34] They additionally include the evidence that the HT-related adrenergic overdrive retains an humoral origin, namely that it is triggered by the central and/or peripheral sympathoexcitatory effects exerted by angiotensin II, leptin, insulin 9,28,35,36 (ie, substances whose circulating plasma levels are all increased in HT). Finally, evidence has been provided that nutritional or behavioral factors, such as low sodium intake or increased alcohol consumption, may trigger marked sympathoexcitatory effects, 37,38 which may be responsible, at least in part, for the HT-related adrenergic overdrive.…”

Section: Mechanisms Responsible For the Adrenergic Overdrivementioning

confidence: 99%

Assessment of Sympathetic Cardiovascular Drive in Human Hypertension

2009

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Abstract-Methodological refinements in the assessment of human sympathetic cardiovascular drive have allowed throughout the years to better define the role of the sympathetic nervous system in the pathophysiology of hypertension.Earlier studies have provided evidence that indirect markers of adrenergic drive, such as plasma or urinary norepinephrine as well as heart rate, often display an increase in the hypertensive state. Direct recording of efferent postganglionic muscle sympathetic nerve traffic via microneurography and regional norepinephrine spillover technique have conclusively documented the occurrence of an adrenergic overdrive in hypertension, showing that the sympathetic activation is directly related to the severity of the hypertensive state and is widespread to different cardiovascular districts. The present review will focus on some major features of the "neuroadrenergic hypothesis of hypertension." In particular it will examine the mechanisms responsible for the adrenergic overdrive, the relationships between the sympathetic activation and the metabolic disarray of frequent detection in the hypertensive state, and the participation of neuroadrenergic factors at the development of the hypertension-related target organ damage. Further issues addressed will be the contribution of the hyperadrenergic state to the different patterns of the 24-hour blood pressure profile as well as to the day/night blood pressure variability described in the hypertensive state and the behavior of the sympathetic function in the hypertensive states complicated by the presence of other cardiovascular or metabolic disease. Finally, the clinical and therapeutic implications of the neuroadrenergic abnormalities occurring in hypertension, as well as the areas worthy of future research, will be highlighted. Key Words: sympathetic nervous system Ⅲ hypertension Ⅲ target organ damage Ⅲ 24-hour ambulatory blood pressure Ⅲ cardiometabolic risk T he role of the sympathetic nervous system (SNS) in the pathogenesis of hypertension (HT) has been remarkably changed over the past 50 years. Indeed, until a few decades ago it was believed that sympathetic neural influences were almost univocally involved in the short-term blood pressure (BP) control, with limited or even no impact at all on long-term BP regulation and development of high BP. This concept, however, has drastically changed over the past 20 years, thanks to the development of methodological approaches allowing direct assessment of systemic and regional sympathetic cardiovascular drive in humans. [1][2][3] This review will focus on the changing face of the SNS in HT. This will be done by reviewing how technical refinements in the assessment of human adrenergic function have substantially modified our thinking on this issue. The review will also examine the most recent data collected in the field, allowing to better define the role of the SNS in the pathophysiology of HT-related target organ damage, the relationships with clinic, home, and ambulatory BP as well as the links wit...

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“…Results regarding the effects of acute antihypertensive treatment on sympathetic baroreflex function are few and controversial. Enhanced, 7 attenuated, 8,9 or unchanged 10 baroreflex sensitivity has been reported. There have been fewer studies on baroreflex regulation of muscle sympathetic nerve activity (MSNA) during chronic antihypertensive therapy, with similarly contradictory findings.…”

mentioning

confidence: 99%

Persistent Sympathetic Activation During Chronic Antihypertensive Therapy

Zhang

Witkowski

et al. 2005

Hypertension

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Abstract-Previous studies have demonstrated that antihypertensive treatment resets baroreflex control of heart rate (HR) and increases cardiac vagal baroreflex sensitivity. However, it is uncertain whether baroreflex control of muscle sympathetic nerve activity (MSNA) also resets after treatment. We tested the hypothesis that chronic antihypertensive therapy alters baroreflex regulation of MSNA in patients with untreated moderate hypertension. Seven newly diagnosed patients with systolic blood pressure (BP) of 159Ϯ5 mm Hg (meanϮSE) and diastolic BP of 103Ϯ4 mm Hg were studied before and after 1 to 2 weeks´and 3 months (chronic) of antihypertensive treatment with losartan-hydrochlorothiazide (Hyzaar). MSNA and hemodynamics were measured supine, during a Valsalva maneuver (VM), and at 70°h ead-up tilt (HUT) for 10 minutes. Data were compared with those obtained in 7 age-matched healthy controls. We found that Hyzaar lowered mean BP acutely and chronically by 20Ϯ4 and 23Ϯ3 mm Hg (both PϽ0.01) but did not change HR. Supine MSNA increased by 43Ϯ11% and 34Ϯ11% after acute and chronic treatment (both PϽ0.01). However, MSNA responses to VM and HUT did not differ after treatment compared with before treatment, indicating unchanged reflex control. These data indicate that sympathetic neural activity was augmented substantially by antihypertensive treatment with Hyzaar, consistent with an ongoing baroreflex unloading, and did not return to baseline or "reset" after 3 months of therapy. We speculate that persistent and marked sympathetic activation by the baroreflex may be a potential mechanism for hypertension that is refractory to antihypertensive therapy and may provide a target mechanism for persistent morbidity despite adequate BP control. Key Words: baroreceptors Ⅲ autonomic nervous system Ⅲ renin-angiotensin system L owering blood pressure (BP) by antihypertensive agents decreases morbidity and mortality in patients with hypertension. 1 However, the risk of stroke, myocardial infarction, or congestive heart failure remains high in such patients, even with adequate BP control. 2 Moreover, many patients have inadequate BP control despite medical therapy often involving multiple drug regimens. 3 One potential mechanism for both of these problems may be persistent or even augmented sympathetic activation by the baroreflex.Previous studies have demonstrated that antihypertensive treatment resets the vagally mediated baroreflex control of heart rate (HR) to a lower pressure level and increases cardiac vagal baroreflex sensitivity acutely and chronically. 4 -6 However, it is uncertain whether baroreflex control of sympathetic neural activity also resets after antihypertensive therapy. Results regarding the effects of acute antihypertensive treatment on sympathetic baroreflex function are few and controversial. Enhanced, 7 attenuated, 8,9 or unchanged 10 baroreflex sensitivity has been reported. There have been fewer studies on baroreflex regulation of muscle sympathetic nerve activity (MSNA) during chronic antihypertensi...

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Short- and Long-Term Neuroadrenergic Effects of Moderate Dietary Sodium Restriction in Essential Hypertension

Cited by 120 publications

References 30 publications

Sympathetic Nerve Activity Is Inappropriately Increased in Chronic Renal Disease

Sympathetic Nerve Activity Is Inappropriately Increased in Chronic Renal Disease

Assessment of Sympathetic Cardiovascular Drive in Human Hypertension

Persistent Sympathetic Activation During Chronic Antihypertensive Therapy

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