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We describe a patient compound heterozygous for a novel deletion and a previously described frame shift mutation in the I CHRNA3 i gene resulting in a rare hereditary form of life-long autonomic failure with severe orthostatic hypotension. Keywords: autonomic failure; autonomic nervous system; CHRNA3; ganglionic acetylcholine receptor EN autonomic failure autonomic nervous system CHRNA3 ganglionic acetylcholine receptor e137 e139 3 07/27/23 20230801 NES 230801 The alpha-3 subunit encoded by the I CHRNA3 i gene is a crucial component of ganglionic acetylcholine receptors, which convey efferent sympathetic and parasympathetic activity to postganglionic autonomic neurons and are required to maintain blood pressure while standing. [Extracted from the article]

[Figure: see text]. [ABSTRACT FROM AUTHOR]

Orthostatic hypertension, which appears to be mediated through excess neurohumoral activation while standing, is a common blood pressure trait among patients with and without arterial hypertension. However, lack of consensus regarding the definition of orthostatic hypertension makes it difficult to assess the true prevalence of this condition. Orthostatic hypertension appears to predict the risk for progression to arterial hypertension in younger and risk of cardiovascular morbidity and mortality in older persons. Yet, the risk may differ between populations. Whether orthostatic hypertension indicates a generally increased risk of death, constitutes an intermediate variable in the causal pathway of cardiovascular risk factors, a simple measure of disease severity, or an independently acting mechanism is not known. Since both orthostatic hypotension and orthostatic hypertension herald increased risk of cardiovascular disease, it appears reasonable to screen the patients for abnormal orthostatic blood pressure responses using simple orthostatic testing. However, how presence of orthostatic hypertension may affect clinical management decisions such as the choice of antihypertensive drugs is currently difficult to ascertain. Clearly, this issue deserves more attention. [ABSTRACT FROM AUTHOR]

Kallistatin (KST), also known as SERPIN A4, is a circulating, broadly acting human plasma protein with pleiotropic properties. Clinical studies in humans revealed reduced KST levels in obesity. The exact role of KST in glucose and energy homeostasis in the setting of insulin resistance and type 2 diabetes is currently unknown. Kallistatin mRNA expression in human subcutaneous white adipose tissue (sWAT) of 47 people with overweight to obesity of the clinical trial "Comparison of Low Fat and Low Carbohydrate Diets With Respect to Weight Loss and Metabolic Effects (B-SMART)" was measured. Moreover, we studied transgenic mice systemically overexpressing human KST (hKST-TG) and wild type littermate control mice (WT) under normal chow (NCD) and high-fat diet (HFD) conditions. In sWAT of people with overweight to obesity, KST mRNA increased after diet-induced weight loss. On NCD, we did not observe differences between hKST-TG and WT mice. Under HFD conditions, body weight, body fat and liver fat content did not differ between genotypes. Yet, during intraperitoneal glucose tolerance tests (ipGTT) insulin excursions and HOMA-IR were lower in hKST-TG (4.42 ± 0.87 AU, WT vs. 2.20 ± 0.27 AU, hKST-TG, p < 0.05). Hyperinsulinemic euglycemic clamp studies with tracer-labeled glucose infusion confirmed improved insulin sensitivity by higher glucose infusion rates in hKST-TG mice (31.5 ± 1.78 mg/kg/min, hKST-TG vs. 18.1 ± 1.67 mg/kg/min, WT, p < 0.05). Improved insulin sensitivity was driven by reduced hepatic insulin resistance (clamp hepatic glucose output: 7.7 ± 1.9 mg/kg/min, hKST-TG vs 12.2 ± 0.8 mg/kg/min, WT, p < 0.05), providing evidence for direct insulin sensitizing effects of KST for the first time. Insulin sensitivity was differentially affected in skeletal muscle and adipose tissue. Mechanistically, we observed reduced Wnt signaling in the liver but not in skeletal muscle, which may explain the effect. KST expression increases after weight loss in sWAT from people with obesity. Furthermore, human KST ameliorates diet-induced hepatic insulin resistance in mice, while differentially affecting skeletal muscle and adipose tissue insulin sensitivity. Thus, KST may be an interesting, yet challenging, therapeutic target for patients with obesity and insulin resistance. • Kallistatin is expressed in human subcutaneous white adipose tissue. • Kallistatin mRNA expression increases by weight loss in humans with obesity. • Human Kallistatin improves hepatic insulin sensitivity in diet induced obese mice. • Kallistatin may contribute to the beneficial metabolic effects of weight loss. [ABSTRACT FROM AUTHOR]

It is noteworthy that the prevalence of hypertension in patients with neck cancer is 60% at the time of diagnosis and increases to 80% after 5 years.[9] It is not known, however, whether baroreflex impairment contributes to this finding. The authors argue that heart rate changes may seem to be intact because patients had an exaggerated depressor response during phase 2, but they also exhibited an attenuated pressor response during phase 4. Likely, the severity of baroreflex impairment was variable in this patient cohort, with some having definitive afferent baroreflex failure, while others may have labile hypertension exacerbated by treatment-induced baroreflex impairment. [Extracted from the article]

Arterial baroreflex activation through electrical carotid sinus stimulation has been developed for the treatment of resistant hypertension. Previous studies suggested that the peripheral chemoreflex is tonically active in hypertensive patients and may inhibit baroreflex responses. We hypothesized that peripheral chemoreflex activation attenuates baroreflex efficacy evoked by electrical carotid sinus stimulation. We screened 35 patients with an implanted electrical carotid sinus stimulator. Of those, 11 patients with consistent acute depressor response were selected (7 men/4 women, age: 67±8 years, body mass index: 31.6±5.2 kg/m2, 6±2 antihypertensive drug classes). We assessed responses to electrical baroreflex stimulation during normoxia, isocapnic hypoxia (SpO2: 79.0±1.5%), and hyperoxia (40% end-tidal O2 fraction) by measuring heart rate, blood pressure, ventilation, oxygen saturation, end-tidal CO2 and O2 fractions, and muscle sympathetic nerve activity. During normoxia, baroreflex activation reduced systolic blood pressure from 164±27 to 151±25 mm Hg (mean±SD, P<0.001), heart rate from 64±13 to 61±13 bpm (P=0.002), and muscle sympathetic nerve activity from 42±12 to 36±12 bursts/min (P=0.004). Hypoxia increased systolic blood pressure 8±12 mm Hg (P=0.057), heart rate 10±6 bpm (P<0.001), muscle sympathetic nerve activity 7±7 bursts/min (P=0.031), and ventilation 10±7 L/min (P=0.002). However, responses to electrical carotid sinus stimulation did not differ between hypoxic and hyperoxic conditions: systolic blood pressure: -15±7 versus -14±8 mm Hg (P=0.938), heart rate: -2±3 versus -2±2 bpm (P=0.701), and muscle sympathetic nerve activity: -6±4 versus -4±3 bursts/min (P=0.531). We conclude that moderate peripheral chemoreflex activation does not attenuate acute responses to electrical baroreflex activation therapy in patients with resistant hypertension. These patients provided insight into human baroreflex-chemoreflex interactions that could not be gained otherwise. [ABSTRACT FROM AUTHOR]

BACKGROUND: Voice analysis offers an unobtrusive approach for psychological monitoring. We demonstrate the relationship between voice parameters and cognitive performance in: 1) a task with psychological test character, and 2) performance in an operational, mission-relevant task. The central methodological aim was to verify the usefulness of voice commands and counting in providing anchor values for the step-function model of voice pitch. METHODS: During a 22-yr period, 42 cosmonauts participated in the Russian space experiment "Pilot", which was a hand-controlled docking maneuver. As reference the experiment included the cognitive task"Manometer."This task was controlled through voice commands. These voice commands were stored and are the basis for the present analysis. RESULTS: Cosmonauts differed in their working style and respective performance during the Manometer task. Clustered groups can be assumed to represent different effort. Importantly, these groups differed in the changes o f voice pitch among mission phases and among task repetitions. However, there were no differences between these motivation groups and performance in the professional task. DISCUSSION: The differing effort is the effect of different motivation of cosmonauts for experimental test tasks vs. mission-relevant professional tasks. Latter ones provide a more reliable chance to assess the real actual state and skills of a cosmonaut. Voice pitch measurement seems to be reliable and useful under space conditions for m onitoring this volitional effort. [ABSTRACT FROM AUTHOR]

B See related article, pp 1234-1244 b The study by Stewart et al[1] in this issue, which was conducted in patients with the postural tachycardia syndrome (POTS), reminds us that parasympathetic activity could be modulated to treat human cardiovascular disease. Despite these issues, the authors have to be congratulated for conducting an involved physiological study in POTS patients that provides insight in underlying mechanisms and potential treatment targets for POTS. [Extracted from the article]

Background: Essential arterial hypertension is one of the main treatable cardiovascular risk factors. In Germany, approximately 13% of women and 18% of men have uncontrolled high blood pressure (≥ 140/90 mmHg). Methods: This review is based on pertinent publications retrieved by a selective literature search in PubMed. Results: Arterial hypertension is diagnosed when repeated measurements in a doctor's office yield values of 140/90 mmHg or higher. The diagnosis should be confirmed by 24-hour ambulatory blood pressure monitoring or by home measurement. Further risk factors and end-organ damage should be considered as well. According to the current European guidelines, the target blood pressure for all patients, including those with diabetes mellitus or renal failure, is <140/90 mmHg. If the treatment is well tolerated, further lowering of blood pressure, with a defined lower limit, is recommended for most patients. The main non-pharmacological measures against high blood pressure are reduction of salt in the diet, avoidance of excessive alcohol consumption, smoking cessation, a balanced diet, physical exercise, and weight loss. The first-line drugs for arterial hypertension include long-acting dihydropyridine calcium channel blockers, angiotensin-converting enzyme inhibitors or angiotensin-receptor blockers, and thiazide-like diuretics. Mineralocorticoid-receptor blockers are effective in patients whose blood pressure cannot be brought into acceptable range with first-line drugs. Conclusion: In most patients with essential hypertension, the blood pressure can be well controlled and the cardiovascular risk reduced through a combination of lifestyle interventions and first-line antihypertensive drugs. [ABSTRACT FROM AUTHOR]

The article discusses the role of natriuretic peptides in the treatment of cardiovascular and metabolic disease, association between glucose metabolism and type 2 diabetes mellitus, and obesity caused due to natriuretic peptides' deficiency.

Sacubitril/valsartan (LCZ696), a novel angiotensin receptor-neprilysin inhibitor, was recently approved for the treatment of heart failure with reduced ejection fraction. Neprilysin degrades several peptides that modulate lipid metabolism, including natriuretic peptides. In this study, we investigated the effects of 8 weeks' treatment with sacubitril/valsartan on whole-body and adipose tissue lipolysis and lipid oxidation during defined physical exercise compared with the metabolically neutral comparator amlodipine. This was a multicenter, randomized, double-blind, active-controlled, parallel-group study enrolling subjects with abdominal obesity and moderate hypertension (mean sitting systolic blood pressure ≥130-180 mm Hg). Lipolysis during rest and exercise was assessed by microdialysis and [1,1,2,3,3-2H]-glycerol tracer kinetics. Energy expenditure and substrate oxidation were measured simultaneously using indirect calorimetry. Plasma nonesterified fatty acids, glycerol, insulin, glucose, adrenaline and noradrenaline concentrations, blood pressure, and heart rate were also determined. Exercise elevated plasma glycerol, free fatty acids, and interstitial glycerol concentrations and increased the rate of glycerol appearance. However, exercise-induced stimulation of lipolysis was not augmented on sacubitril/valsartan treatment compared with amlodipine treatment. Furthermore, sacubitril/valsartan did not alter energy expenditure and substrate oxidation during exercise compared with amlodipine treatment. In conclusion, sacubitril/valsartan treatment for 8 weeks did not elicit clinically relevant changes in exercise-induced lipolysis or substrate oxidation in obese patients with hypertension, implying that its beneficial cardiovascular effects cannot be explained by changes in lipid metabolism during exercise.Clinical Trial Registration: URL: https://www.clinicaltrials.gov. Unique identifier: NCT01631864. [ABSTRACT FROM AUTHOR]

Inhibition of sodium glucose cotransporter 2 with empagliflozin results in caloric loss by increasing urinary glucose excretion and has a mild diuretic effect. Diuretic effects are usually associated with reflex-mediated increases in sympathetic tone, whereas caloric loss is associated with decreased sympathetic tone. In an open-label trial, muscle sympathetic nerve activity (MSNA) (burst frequency, burst incidence, and total MSNA) was assessed using microneurography performed off-treatment and on day 4 of treatment with empagliflozin 25 mg once daily in 22 metformin-treated patients with type II diabetes (mean [range] age 54 [40–65] years). Systolic and diastolic blood pressure (BP), heart rate, urine volume, and body weight were assessed before and on day 4 (BP, heart rate), day 5 (urine volume), or day 6 (body weight) of treatment with empagliflozin. After 4 days of treatment with empagliflozin, no significant changes in MSNA were apparent despite a numerical increase in urine volume, numerical reductions in BP, and significant weight loss. There were no clinically relevant changes in heart rate. Empagliflozin is not associated with clinically relevant reflex-mediated sympathetic activation in contrast to increases observed with diuretics in other studies. Our study suggests a novel mechanism through which sodium glucose cotransporter 2 inhibition affects human autonomic cardiovascular regulation. [ABSTRACT FROM AUTHOR]

Aliskiren penetrates adipose and skeletal muscle in hypertensive patients with abdominal obesity and reduces renin–angiotensin–aldosterone system activity. After discontinuation, blood pressure–lowering effects are observed possibly through drug–tissue binding. We performed microdialysis evaluation of adipose tissue and skeletal muscle before and during an insulin-modified frequently sampled intravenous glucose tolerance test (IM-FSIGT). Aliskiren 300 mg (n = 8) or amlodipine 5 mg (n = 8) once daily were administered during a 12-week randomized treatment period. Aliskiren elicited variable changes in median interstitial angiotensin II (Ang II) in adipose (2.60–1.30 fmol/mL) and skeletal muscle (2.23–0.68 fmol/mL); amlodipine tended to increase adipose and skeletal muscle Ang II ( P = .066 for skeletal muscle treatment difference). Glucose/insulin increased median plasma Ang II 1 hour after glucose injection (1.04–2.50 fmol/mL; P = .001), which was markedly attenuated by aliskiren but not amlodipine. Aliskiren increased glucose disposition index ( P = .012) and tended to increase acute insulin response to glucose ( P = .067). Fasting adipose glycerol (−17%; P = .064) and fasting muscle glucose dialysate (−17%; P = .025) were decreased by aliskiren but not amlodipine. In summary, aliskiren decreased Ang II production in response to glucose/insulin stimulus and elicited metabolic effects in adipose and skeletal muscle suggestive of increased whole-body glucose utilization. [ABSTRACT FROM AUTHOR]

The article focuses on chronic deep brain stimulation decreases blood pressure and sympathetic nerve activity in a drug- and device-resistant hypertensive patient.

Supplemental Digital Content is available in the text. [ABSTRACT FROM AUTHOR]

Gut microorganisms may also modulate the risk of hypertension-related organ damage. 3 Pluznick JL, Protzko RJ, Gevorgyan H, Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation. Gut microbiota and serum metabolite differences in African Americans and White Americans with high blood pressure. [Extracted from the article]

The article presents a case study of a 56-year-old man with severe volatile treatment-resistant hypertension. Topics discussed include history of coronary 3-vessel disease and a myocardial infarction, treatment of the patient using angioplasty and stent implantation, diagnosis of hypercholesterolemia, and drugs used for the treatment such as Minoxidil and Molsidomine. Also discussed is the impact of using Valsalva maneuvers on the patient's blood pressure (BP).

Bilateral bipolar electric carotid sinus stimulation acutely reduced muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in patients with resistant arterial hypertension but is no longer available. The second-generation device uses a smaller unilateral unipolar disk electrode to reduce invasiveness while saving battery life. We hypothesized that the second-generation device acutely lowers BP and MSNA in treatment-resistant hypertensive patients. Eighteen treatment-resistant hypertensive patients (9 women/9 men; 53±11 years; 33±5 kg/m(2)) on stable medications have been included in the study. We monitored finger and brachial BP, heart rate, and MSNA. Without stimulation, BP was 165±31/91±18 mm Hg, heart rate was 75±17 bpm, and MSNA was 48±14 bursts per minute. Acute stimulation with intensities producing side effects that were tolerable in the short term elicited interindividually variable changes in systolic BP (-16.9±15.0 mm Hg; range, 0.0 to -40.8 mm Hg; P=0.002), heart rate (-3.6±3.6 bpm; P=0.004), and MSNA (-2.0±5.8 bursts per minute; P=0.375). Stimulation intensities had to be lowered in 12 patients to avoid side effects at the expense of efficacy (systolic BP, -6.3±7.0 mm Hg; range, 2.8 to -14.5 mm Hg; P=0.028 and heart rate, -1.5±2.3 bpm; P=0.078; comparison against responses with side effects). Reductions in diastolic BP and MSNA (total activity) were correlated (r(2)=0.329; P=0.025). In our patient cohort, unilateral unipolar electric baroreflex stimulation acutely lowered BP. However, side effects may limit efficacy. The approach should be tested in a controlled comparative study. [ABSTRACT FROM AUTHOR]

Patients with treatment-resistant arterial hypertension exhibited profound reductions in single sympathetic vasoconstrictor fiber firing rates after renal nerve ablation. In contrast, integrated multi-unit muscle sympathetic nerve activity (MSNA) changed little or not at all. We hypothesized that conventional MSNA analysis may have missed single fiber discharges, thus, obscuring sympathetic inhibition after renal denervation. We studied patients with difficult-to-control arterial hypertension (age 45–74 years) before, 6 (n = 11), and 12 months (n = 8) after renal nerve ablation. Electrocardiogram, respiration, brachial, and finger arterial blood pressure (BP), as well as the MSNA and raw MSNA signals were analyzed. We detected MSNA action-potential spikes using 2 stage kurtosis wavelet denoising techniques to assess mean, median, and maximum spike rates for each beat-to-beat interval. Supine heart rate and systolic BP did not change at 6 (ΔHR: −2 ± 3 bpm; ΔSBP: 2 ± 9 mm Hg) or at 12 months (ΔHR: −1 ± 3 mm Hg, ΔSBP: −1 ± 9 mm Hg) after renal nerve ablation. Mean burst frequency and mean spike frequency at baseline were 34 ± 3 bursts per minute and 8 ± 1 spikes per second. Both measurements did not change at 6 months (−1.4 ± 3.6 bursts/minute; −0.6 ± 1.4 spikes/second) or at 12 months (−2.5 ± 4.0 bursts/minute; −2.0 ± 1.6 spikes/second) after renal nerve ablation. After renal nerve ablation, BP decreased in 3 of 11 patients. BP and MSNA spike frequency changes were not correlated (slope = −0.06; P = .369). Spike rate analysis of multi-unit MSNA neurograms further suggests that profound sympathetic inhibition is not a consistent finding after renal nerve ablation. [ABSTRACT FROM AUTHOR]

Aortic pulse wave velocity (aPWV) can be measured with different methodologies, including applanation tonometry. These pilot study findings suggest that impedance cardiography combined with thigh oscillometry provides comparable results. Intra– and inter–observer variability was tested by two observers in two subjects. We instrumented 41 patients and 12 healthy normotensive controls for impedance cardiography and consecutive applanation tonometry and compared methods using the Bland–Altman method. Observer variability for the impedance–thigh cuff method (range, 3.61%–7.77%) was comparable with the tonometric method (range, 2.93%–7.37%). Comparison of the two methods based on the Bland–Altman plot revealed a good agreement between methods. The bias between impedance and tonometric measurements was −0.28 ± 0.37 m/s. Both measurements were significantly correlated (r 2 = 0.94; P < .0001; slope = 1.038).Impedance cardiography combined with thigh oscillometry is an easy to use approach which, in addition to providing hemodynamic information, yields aPWV measurements comparable to applanation tonometry. Following full validation according to current guidelines, the methodology could prove useful in cardiovascular risk stratification. [ABSTRACT FROM AUTHOR]

The article describes the case of a truly resistant hypertension in a 51-year-old woman who was normotensive until age 36 years. By age 43, she had received up to seven antihypertensive drugs and had developed five fainting episodes that could not be attributed to a cardiovascular cause. The results of physical and laboratory examinations performed on the patient are detailed. The authors suggest a more comprehensive definition of device-resistant hypertension.

The article discusses a study which tested the hypothesis that endovascular renal nerve ablation may attenuate central sympathetic outflow through decreased renal afferent nerve traffic. The hypothesis was tested by the researchers in 10 nonpreselected patient with difficult-to-control hypertension admitted for renal nerve ablation. It was found that the patients did not exhibit a consistent and clinically relevant muscle sympathetic nerve activity (MSNA) reduction after surgery.

This article discusses a study which tested the hypothesis that continuous-flow left ventricular devices impair baroreflex control of sympathetic nerve traffic. The study population included nine male heart failure patients implanted with a continuous-flow left ventricular assist devices. Researchers recorded echocardiography, respiration, finger blood pressure, brachial blood pressure and muscle sympathetic nerve activity.

The article presents a study which examines the impact of reduced-fat or reduced-carbohydrate hypocaloric diets on the left ventricular mass and function in overweight and obese subjects. The study conducted the diet intervention and obtained cardiac magnetic resonance imaging (MRI) and ambulatory blood pressure in 170 overweight subjects. The study found that reduced-carbohydrate diet led to significant decreases in left ventricular mass.

Summary: Reduced expression of the Indy (I''m Not Dead, Yet) gene in D. melanogaster and its homolog in C. elegans prolongs life span and in D. melanogaster augments mitochondrial biogenesis in a manner akin to caloric restriction. However, the cellular mechanism by which Indy does this is unknown. Here, we report on the knockout mouse model of the mammalian Indy (mIndy) homolog, SLC13A5. Deletion of mIndy in mice (mINDY −/− mice) reduces hepatocellular ATP/ADP ratio, activates hepatic AMPK, induces PGC-1α, inhibits ACC-2, and reduces SREBP-1c levels. This signaling network promotes hepatic mitochondrial biogenesis, lipid oxidation, and energy expenditure and attenuates hepatic de novo lipogenesis. Together, these traits protect mINDY−/− mice from the adiposity and insulin resistance that evolve with high-fat feeding and aging. Our studies demonstrate a profound effect of mIndy on mammalian energy metabolism and suggest that mINDY might be a therapeutic target for the treatment of obesity and type 2 diabetes. [Copyright &y& Elsevier]

Human subjects with impaired baroreflex function cannot buffer rises or falls in blood pressure (BP), thus allowing BP effects of endogenous or environmental stimuli that previously escaped detection to emerge dramatically. Studies in these patients led us to discover that water ingestion induced a robust increase in BP and vascular resistance. Here, using a mouse model of baroreflex impairment, we show that the increase in blood pressure after water ingestion is mediated through sympathetic nervous system activation and that the osmosensitive transient receptor potential vanilloid 4 channel (Trpv4) is an essential component of the response. Although portal osmolality decreases after water ingestion in both wild-type and Trpv4(-/-) mice, only the wild-type animals show a pressor response. The same volume of physiological saline does not elicit an increase in BP, suggesting osmolality as the stimulus. The osmopressor response to water, and Trpv4 thus represent new factors now implicated in the physiology of BP regulation. [ABSTRACT FROM AUTHOR]

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 > or =1 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 > or =6 minutes during the same experiment. Intra-arterial blood pressure was 193+/-9/94+/-5 mm Hg on medications. Acute electric baroreflex stimulation decreased systolic blood pressure by 32+/-10 mm Hg (range: +7 to -108 mm Hg; P=0.01). The depressor response was correlated with a muscle sympathetic nerve activity reduction (r(2)=0.42; P<0.05). 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 4.5+/-1.5 bpm with stimulation (P<0.05). Plasma renin concentration decreased 20+/-8% (P<0.05). 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. [ABSTRACT FROM AUTHOR]

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. Maximal apnea time was longer in divers (1.7+/-0.4 versus 3.9+/-1.1 minutes; P<0.0001), and it was accompanied by marked oxygen desaturation (97.6+/-0.7% versus 77.6+/-13.9%; P<0.0001). At the end of apnea, divers showed a >5-fold greater muscle sympathetic nerve activity increase (P<0.01) with a massively increased pressor response compared with control subjects (9+/-5 versus 32+/-15 mm Hg; P<0.001). Vascular resistance increased in both groups, but more so in divers (79+/-46% versus 140+/-82%; P<0.01). Heart rate did not change in either group. The rise in muscle sympathetic nerve activity correlated with oxygen desaturation (r(2)=0.26; P<0.01) and with the increase in mean arterial pressure (r(2)=0.40; P<0.0001). In elite divers, breath holds for several minutes result in an excessive chemoreflex activation of sympathetic vasoconstrictor activity. Extensive sympathetically mediated peripheral vasoconstriction may help to maintain adequate oxygen supply to vital organs under asphyxic conditions that untrained subjects are not able to tolerate voluntarily. Our results are relevant to conditions featuring periodic apnea. [ABSTRACT FROM AUTHOR]