Abstract-In animals, electric field stimulation of carotid baroreceptors elicits a depressor response through sympathetic inhibition. We tested the hypothesis that the stimulation acutely reduces sympathetic vasomotor tone and blood pressure in patients with drug treatment-resistant arterial hypertension. Furthermore, we tested whether the stimulation impairs the physiological baroreflex regulation. We studied 7 men and 5 women (ages 43 to 69 years) with treatment-resistant arterial hypertension. A bilateral electric baroreflex stimulator at the level of the carotid sinus (Rheos) was implanted Ն1 month before the study. We measured intra-arterial blood pressure, heart rate, muscle sympathetic nerve activity (microneurography), cardiac baroreflex sensitivity (cross-spectral analysis and sequence method), sympathetic baroreflex sensitivity (threshold technique), plasma renin, and norepinephrine concentrations. Measurements were performed under resting conditions, with and without electric baroreflex stimulation, for Ն6 minutes during the same experiment. Intra-arterial blood pressure was 193Ϯ9/94Ϯ5 mm Hg on medications. Acute electric baroreflex stimulation decreased systolic blood pressure by 32Ϯ10 mm Hg (range: ϩ7 to Ϫ108 mm Hg; Pϭ0.01). The depressor response was correlated with a muscle sympathetic nerve activity reduction (r 2 ϭ0.42; PϽ0.05). In responders, muscle sympathetic nerve activity decreased sharply when electric stimulation started. Then, muscle sympathetic nerve activity increased but remained below the baseline level throughout the stimulation period. Heart rate decreased 4.5Ϯ1.5 bpm with stimulation (PϽ0.05). Plasma renin concentration decreased 20Ϯ8% (PϽ0.05). Electric field stimulation of carotid sinus baroreflex afferents acutely decreased arterial blood pressure in hypertensive patients, without negative effects on physiological baroreflex regulation. The depressor response was mediated through sympathetic inhibition. (Hypertension. 2010;55:619-626.)

Neurohumoral activation has been shown to be present in hypoxic patients with chronic obstructive pulmonary disease (COPD). The aims of the present study were to investigate whether there is sympathetic activation in COPD patients in the absence of hypoxia and whether slow breathing has an impact on sympathoexcitation and baroreflex sensitivity.Efferent muscle sympathetic nerve activity, blood pressure, cardiac frequency and respiratory movements were continuously measured in 15 COPD patients and 15 healthy control subjects. Baroreflex sensitivity was analysed by autoregressive spectral analysis and the alpha-angle method.At baseline, sympathetic nerve activity was significantly elevated in COPD patients and baroreflex sensitivity was decreased (5.0¡0.6 versus 8.9¡0.8 ms?mmHg -1

Abstract-Involuntary apnea during sleep elicits sustained arterial hypertension through sympathetic activation; however, little is known about voluntary apnea, particularly in elite athletes. Their physiological adjustments are largely unknown.We measured blood pressure, heart rate, hemoglobin oxygen saturation, muscle sympathetic nerve activity, and vascular resistance before and during maximal end-inspiratory breath holds in 20 elite divers and in 15 matched control subjects. At baseline, arterial pressure and heart rate were similar in both groups. Key Words: baroreflex Ⅲ breath-hold diving Ⅲ chemoreflex Ⅲ diving response Ⅲ sympathetic nervous system . "I nvoluntary" sleep apnea episodes trigger sympathetically mediated blood pressure surges 1 and predispose to cardiovascular and cerebrovascular morbidity and mortality. [2][3][4] The state of affairs is disturbing, because healthy people, including underwater hockey players, synchronized swimmers, and elite breath-hold divers practice "voluntary" apnea on a regular basis. Freestyle swimmers may hold their breath throughout 50-m sprint competitions. Elite breath-hold divers can hold their breath for several minutes. In these unique individuals, arterial oxygen saturation may decrease to Ͻ50%, whereas alveolar carbon dioxide partial pressure increases substantially. 5 Typically, diving fish-catching competitions last for 5 hours with cumulative apnea duration of Ϸ1 hour.Breath holding elicits complex cardiovascular adaptations even before relevant changes in arterial blood gases occur. The response includes bradycardia, reduced cardiac output, and peripheral vasoconstriction through sympathetic activation. 6,7 The so-called diving response seems to conserve oxygen. 8 -10 Breath holding without water immersion also increases sympathetic vasomotor tone. [11][12][13][14][15][16][17][18][19]20 and hypercapnia 16,18 provide additional stimuli to the sympathetic nervous system through central and peripheral chemoreflex mechanisms. However, in untrained individuals, breath-hold duration is too short to elicit a relevant decrease in arterial oxygen saturation. 21 We tested the hypothesis that the sympathetic vasomotor response to maximal breath holding is increased in apnea divers compared with control subjects. Methods Study PopulationWe recruited 43 young white subjects. Twenty two were active apnea divers. Within the preceding months, they participated in Ն7 diving competitions and Ն70 training sessions, each consisting of 30 to 40 maximal apneas, separated by variable interapneic periods. Matched, untrained subjects served as controls. All of the participants were healthy nonsmokers and ingested no medications. The

5Catheter-based renal nerve ablation decreased renal norepinephrine spillover, reflecting efferent activity by 47%. 2 The mechanisms likely contribute to the blood pressure-lowering effect because efferent renal sympathetic nerves activate the renin-angiotensin system 6,7 and directly stimulate tubular sodium retention. 8,9 In addition, reduced afferent renal nerve traffic may have elicited a central nervous sympatholytic response. Indeed, massive reductions in muscle sympathetic nerve activity (MSNA) and systemic norepinephrine spillover have been reported in a single patient after renal nerve ablation.10 Similarly, removal of the diseased native kidney reduced MSNA in renal transplant recipients.11 These clinical observations translate the experimental finding that renal afferents convey signals to the brain, thus raising sympathetic activity and blood pressure 12,13 from animals to humans. See Editorial Commentary, pp 1385-1386Abstract-Endovascular renal nerve ablation has been developed to treat resistant hypertension. In addition to lowering efferent renal sympathetic activation, the intervention may attenuate central sympathetic outflow through decreased renal afferent nerve traffic, as evidenced by a recent case report. We tested the hypothesis in 12 nonpreselected patients with difficult-to-control hypertension (aged 45-74 years) admitted for renal nerve ablation. All patients received ≥3 antihypertensive medications at full doses, including a diuretic. Electrocardiogram, respiration, brachial and finger arterial blood pressure, and muscle sympathetic nerve activity were recorded before and 3 to 6 months after renal nerve ablation. Heart rate and blood pressure variability were analyzed in the time and frequency domain. Pharmacological baroreflex slopes were determined using the modified Oxford bolus technique. Resting heart rate was 61±3 bpm before and 58±2 bpm after ablation (P=0.4). Supine blood pressure was 157±7/85±4 mm Hg before and 157±6/85±4 mm Hg after ablation (P=1.0). Renal nerve ablation did not change resting muscle sympathetic nerve activity (before, 34±2 bursts per minute; after, 32±3 bursts per minute P=0.6), heart rate variability, or blood pressure variability. Pharmacological baroreflex control of heart rate and muscle sympathetic nerve activity did not change. We conclude that reduced central sympathetic inhibition may be the exception rather than the rule after renal nerve ablation in unselected patients with difficult-to-control arterial hypertension. (Hypertension. 2012;60:1485-1490.) • Online Data Supplement

ANP briskly stimulates lipid mobilization and oxidation at plasma concentrations that are encountered in conditions such as heart failure. Natriuretic-peptide induced lipid mobilization might contribute to cardiac cachexia. Drugs that interfere with the natriuretic peptide system should be evaluated for potential metabolic side effects.

Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail.

Abstract-The baroreflex receives less attention nowadays because most students of hypertension are convinced that faulty volume regulation by the kidneys is responsible for long-term blood pressure increases. However, unusual patients with bilateral destruction of the normal blood pressure-sensing mechanisms can develop profound chronic hypertension. We present 2 patients with baroreflex failure. Both had volatile hypertension with systolic readings up to 300 mm Hg documented over years. Both had muscle sympathetic nerve activity that was increased even while resting. Treating these patients was a stochastic challenge. The therapy is frequently based on medicines that are no longer commonly prescribed. Key Words: baroreflex Ⅲ sympathetic nervous system Ⅲ autonomic nervous system Ⅲ hypotension Ⅲ bradycardia T he arterial baroreflex buffers acute fluctuations in blood pressure that occur during posture, stress, or other maneuvers. When blood pressure rises, vascular distension is transduced into nervous electrical activity, triggering reflex parasympathetic activation and sympathetic inhibition. Heart rate is slowed and vascular resistance is decreased, buffering the increase in blood pressure. Conversely, baroreceptor activity decreases when blood pressure falls, producing a reflex-mediated increase in heart rate and peripheral resistance. Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained. However, the resetting of the baroreflex plays at least a permissive role in perpetuation of hypertension. Guyton argued that the baroreflex is responsible for the minute-to-minute regulation of blood pressure, but that the long-term blood pressure regulation is related to volume mechanisms adjusted by the kidneys. 1 However, faulty baroreflexes can occasionally influence long-term blood pressure regulation. An example is the condition of baroreflex failure. Such patients are a diagnostic challenge and a therapeutic nightmare. Case 1A 65-year-old woman was referred to our center for evaluation of possible baroreflex failure. Her chief symptom was volatile hypertension. The patient had a family history of arterial hypertension. Antihypertensive therapy was initiated at a young age and blood pressure readings were stable for many years. Twenty-two years before admission, a papillary thyroid cancer was diagnosed. She was successfully treated with thyroidectomy and local radiation followed by radioiodine treatment. Six years before admission, the patient experienced a neck trauma during a skiing accident. A left common carotid artery stenosis secondary to radiation injury was treated with angioplasty and stent implantation 4 years before admission. After the skiing accident, blood pressure became highly volatile. Systolic blood pressure values as high as 230 mm Hg had been recorded even during antihypertensive therapy with amlodipine, ramipril, spironolactone, metoprolol, and moxonidine. The hypertension was exacerba...

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