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Biomedical subjects

K Narkiewicz

Publications and source records attributed to K Narkiewicz.

At least 37 records · Page 2Linked to original sources
PubMed1999

Nocturnal continuous positive airway pressure decreases daytime sympathetic traffic in obstructive sleep apnea.

BACKGROUND: Patients with obstructive sleep apnea (OSA) have high levels of muscle sympathetic nerve activity (MSNA). We tested the hypothesis that long-term continuous positive airway pressure (CPAP) treatment will decrease MSNA in OSA patients. METHODS AND RESULTS: We measured blood pressure, heart rate, and MSNA in 11 normotensive, otherwise healthy patients with OSA who were treated with CPAP. The measurements were obtained at baseline and after 1 month, 6 months, and 1 year of CPAP treatment. These measurements were compared with those recorded in 9 otherwise healthy OSA patients who were not treated with CPAP for 1 year. In both untreated and treated patients, blood pressure and heart rate did not change over time. MSNA was similar during repeated measurements in the untreated group. By contrast, MSNA decreased significantly over time in patients treated with CPAP. This decrease was evident after both 6 months and 1 year of CPAP treatment (P=0.02 for both). CONCLUSIONS: CPAP treatment decreases muscle sympathetic traffic in patients with OSA. This effect of CPAP is evident only after an extended duration of therapy.

Adult↗
PubMed1999

Enhanced sympathetic and ventilatory responses to central chemoreflex activation in heart failure.

BACKGROUND: Sympathetic activation and respiratory abnormalities may each be implicated in the pathophysiology of congestive heart failure (CHF). Chemoreflexes are an important mechanism regulating both sympathetic drive and breathing. We therefore tested the hypothesis that chemoreflex function is altered in CHF. METHODS AND RESULTS: We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 9 patients with CHF and 9 control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with CHF compared with control subjects (47+/-8 versus 23+/-3 bursts per minute, P<0.01). During hypercapnia, patients with CHF had greater increases in minute ventilation (6.7+/-1.4 versus 2.7+/-0.9 L/min, P=0.03) and heart rate (7.0+/-2.1 versus 0.6+/-1.2 bpm, P=0.02). Despite higher ventilation, which inhibits sympathetic activity, the MSNA increase in patients with CHF was also greater than that in control subjects (58+/-12% versus 21+/-9%, P=0.03). Ventilatory, autonomic, and blood pressure responses to hypoxia and the cold pressor test in CHF patients were not different from those in control subjects. CONCLUSIONS: Chronic heart failure is characterized by a selective potentiation of ventilatory and sympathetic responses to central chemoreceptor activation by hypercapnia.

Adult↗
PubMed1999

Sympathetic rhythmicity in cardiac transplant recipients.

BACKGROUND: Variability of R-R interval and muscle sympathetic nerve activity (MSNA) occurs predominantly at a low frequency (LF, +/-0.1 Hz) and a high frequency (HF, +/-0.25 Hz) in normal humans. Increased sympathetic drive in normal humans is associated with an increased LF component of the R-R interval and MSNA. Patients with severe heart failure have high sympathetic activity but decreased or absent LF power of both R-R and MSNA. We tested the hypothesis that this dysfunction in autonomic modulation in heart failure can be reversed by heart transplantation. METHODS AND RESULTS: We performed spectral analysis of resting MSNA, R-R interval, and respiration in 9 patients with heart transplants, 9 chronic heart failure patients, and 9 normal control subjects, all closely matched for age, sex, and body mass index. MSNA (bursts per minute) was higher in patients with heart transplants (74+/-3) than either patients with heart failure (56+/-6) or normal subjects (40+/-4) (P<0.001). LF variability in the R-R interval was reduced in both heart transplant recipients and heart failure patients compared with the control subjects (P<0.01). The LF variability in MSNA was also nearly absent in the heart failure patients (P<0.01). However, the LF and HF oscillations in MSNA in patients with heart transplants were comparable to those evident in the control subjects. CONCLUSIONS: Cardiac transplantation does not reduce MSNA. However, LF oscillations in sympathetic activity are restored after transplantation such that the MSNA oscillatory profile is similar to that observed in normal subjects.

Female↗
PubMed1999

Selective potentiation of peripheral chemoreflex sensitivity in obstructive sleep apnea.

BACKGROUND: The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Abnormalities in chemoreflex mechanisms may be implicated in increased cardiovascular stress in patients with obstructive sleep apnea (OSA). We tested the hypothesis that chemoreflex function is altered in patients with OSA. METHODS AND RESULTS: We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypoxia, hypercapnia, and the cold pressor test in 16 untreated normotensive patients with OSA and 12 normal control subjects matched for age and body mass index. Baseline muscle sympathetic nerve activity (MSNA) was higher in the patients with OSA than in the control subjects (43+/-4 versus 21+/-3 bursts per minute; P<0. 001). During hypoxia, patients with OSA had greater increases in minute ventilation (5.8+/-0.8 versus 3.2+/-0.7 L/min; P=0.02), heart rate (10+/-1 versus 7+/-1 bpm; P=0.03), and mean arterial pressure (7+/-2 versus 0+/-2 mm Hg; P=0.001) than control subjects. Despite higher ventilation and blood pressure (both of which inhibit sympathetic activity) in OSA patients, the MSNA increase during hypoxia was similar in OSA patients and control subjects. When the sympathetic-inhibitory influence of breathing was eliminated by apnea during hypoxia, the increase in MSNA in OSA patients (106+/-20%) was greater than in control subjects (52+/-23%; P=0.04). Prolongation of R-R interval with apnea during hypoxia was also greater in OSA patients (24+/-6%) than in control subjects (7+/-5%) (P=0.04). Autonomic, ventilatory, and blood pressure responses to hypercapnia and the cold pressor test in OSA patients were not different from those observed in control subjects. CONCLUSIONS: OSA is associated with a selective potentiation of autonomic, hemodynamic, and ventilatory responses to peripheral chemoreceptor activation by hypoxia.

Adult↗
PubMed1999

Theophylline therapy for near-fatal Cheyne-Stokes respiration. A case report.

BACKGROUND: Cheyne-Stokes respiration is characterized by periodic breathing that alternates with hypopnea or apnea. OBJECTIVE: To describe the effect of theophylline on near-fatal Cheyne-Stokes respiration. DESIGN: Case report. SETTING: Tertiary referral center. PATIENT: A 48-year-old diabetic woman with a history of three cardiorespiratory arrests, a normal coronary arteriogram, normal left ventricular function, and severe Cheyne-Stokes respiration. MEASUREMENTS: Oxygen saturation, intra-arterial blood pressure, central venous pressure, chest wall movement, electrocardiography, electromyography, electroencephalography, electro-oculography, minute ventilation, arterial blood gases, and serum theophylline levels. RESULTS: After intravenous administration of 1.2 mg of theophylline at 0.6 mg/kg per hour (serum level, 5.6 microg/mL), both Cheyne-Stokes respiration and oxygen desaturation were markedly attenuated. After infusion of 2.4 mg of theophylline (serum level, 11.6 microg/mL), Cheyne-Stokes respiration resolved completely. No change was seen with placebo. Cheyne-Stokes respiration did not recur during outpatient treatment with oral theophylline. CONCLUSION: Theophylline may be a rapid and effective therapy for life-threatening Cheyne-Stokes respiration.

Blood Pressure↗
PubMed1999

Obstructive sleep apnea as a cause of neurogenic hypertension.

Abnormalities in neural circulatory control may contribute importantly to the hypertensive state. The sympathetic nervous system in particular is a key mechanism for increasing blood pressure. Patients with obstructive sleep apnea have increased sympathetic activity. Obesity or other coexisting disease states do not explain the heightened sympathetic drive. This review examines the evidence linking sleep apnea with hypertension and the possible role of excessive sympathetic drive as a mediator of higher blood pressure in sleep apnea. Abnormalities in reflex circulatory control that could act to increase sympathetic activity in sleep apnea are also discussed.

Heart↗
PubMed1999

Heritability of plasma leptin levels: a twin study.

OBJECTIVE: To examine the influence of genetic factors on plasma leptin levels. SUBJECTS AND METHODS: We measured plasma leptin levels, body mass index and body fat distribution in healthy young female monozygotic (n = 19) and dizygotic (n = 14) twins. The twin zygosity was verified by determination of short tandem repeat and amplified fragment length polymorphism systems. The genetic analysis included analysis of variance-based and maximum likelihood-based methods. RESULTS: Plasma leptin levels were correlated significantly with body mass index (r = 0.59, P < 0.001), waist circumference (r = 0.54, P < 0.001) and hip circumference (r = 0.63, P < 0.001), but not with age (r = -0.17) or the waist:hip ratio (r = 0.02). The heritability estimates derived from intraclass correlations were significant for body mass index (P = 0.001), waist circumference (P = 0.004), hip circumference (P = 0.01) and plasma leptin levels (P = 0.005), but not for the waist:hip ratio (P = 0.22). In the maximum likelihood-based path analysis, heritability was estimated at 79% for body mass index and at 73% for plasma leptin levels. After adjustment for body mass index, the heritability estimate for leptin levels from the model-fitting approach was 55%. CONCLUSIONS: Genetic factors are major determinants of plasma leptin levels in humans and may account for as much as half of the variance in leptin levels.

Adipose Tissue↗
PubMed1999

Effects of obstructive sleep apnea on endothelin-1 and blood pressure.

OBJECTIVE: To evaluate blood pressure and humoral vasoconstrictor responses to recurrent episodes of obstructive sleep apnea and the effects of therapy by means of continuous positive airway pressure. PATIENTS AND METHODS: We prospectively evaluated overnight changes in hemodynamics, oxygen saturation, the apnea-hypopnea index, circulating endothelin-1, norepinephrine and plasma renin activity in 22 patients with severe obstructive sleep apnea before and after successful therapy using continuous positive airway pressure therapy (three measurements). Measurements of endothelin-1 and blood pressure were also obtained on three occasions, at similar times, in 12 healthy control subjects without sleep disturbances. RESULTS: Mean arterial pressure and endothelin-1 concentrations increased significantly after 4 h of untreated obstructive sleep apnea, and decreased after 5 h of continuous positive airway pressure. Changes in endothelin-1 levels were correlated with changes in mean arterial pressure (r = 0.44, P < 0.02) and with changes in oxygen saturation (r = 0.37, P < 0.05). Norepinephrine levels and plasma renin activity did not change significantly in patients with obstructive sleep apnea, and were not correlated with changes in blood pressure or oxygen saturation. In controls, blood pressure measurements at similar times during the night showed changes directionally opposite to that seen in obstructive sleep apnea, while endothelin-1 levels remained unchanged. CONCLUSIONS: Sleep apnea elicits increases in blood pressure and endothelin-1, with reductions in both after treatment. Vasoconstrictor and mitogenic effects of endothelin-1 may be implicated in increased cardiovascular risk in patients with obstructive sleep apnea.

Angiotensin I↗
PubMed1999

An independent relationship between plasma leptin and heart rate in untreated patients with essential hypertension.

OBJECTIVE: To test the hypothesis that hemodynamic measurements in patients with essential hypertension are related independently to plasma leptin levels. PATIENTS AND METHODS: We measured plasma leptin, insulin, office and ambulatory blood pressure and heart rate in 60 men with untreated mild hypertension. RESULTS: Plasma leptin correlated significantly with body mass index (r = 0.43, P = 0.001), 24 h heart rate (r = 0.35, P = 0.006) and 24 h diastolic blood pressure (r = 0.27, P = 0.04) but not with age (r = 0.03; P = 0.85) or 24 h systolic blood pressure (r = -0.08, P = 0.56). Plasma leptin levels adjusted for body mass index correlated significantly with 24 h heart rate (r = 0.36, P = 0.005) but not with 24 h diastolic blood pressure (r = 0.19, P = 0.15). We divided the patient population into tertiles of body mass index-adjusted plasma leptin levels. Age, plasma insulin, blood pressure, smoking status and physical activity habits were similar across the adjusted leptin tertiles. Patients from the third tertile of adjusted plasma leptin distribution (those with leptin levels higher than would be expected on the basis of body mass index) had significantly faster ambulatory heart rates than subjects from both the first and the second tertiles. The difference in heart rate across the three tertiles was most pronounced for the night-time values. CONCLUSIONS: In patients with essential hypertension, heart rate is faster in those patients with higher plasma leptin levels. This relationship is independent of age, body mass index, insulin levels, blood pressure level, smoking status and physical activity.

Adipose Tissue↗
PubMed1999

Genetic determinants of plasma ACE and renin activity in young normotensive twins.

OBJECTIVE: We investigated the determinants of plasma renin activity (PRA) and plasma levels of angiotensin-converting enzyme (pACE), including the effect of the D/I polymorphism of the angiotensin-converting enzyme (ACE) gene, in monozygotic (MZ) and dizygotic (DZ) twins. METHODS: Sixty-nine pairs of twins underwent measurements of blood pressure, pACE and ACE D/I genotyping. In addition, in 30 pairs ambulatory blood pressure (ABP) monitoring was carried out. To ascertain twin's zygosity, some highly discriminating variable number of tandem repeats micro- and mini-satellite systems were analysed by polymerase chain reaction (PCR) followed by polyacrylamide gel electrophoresis and silver staining. The D/I polymorphism was assessed by PCR; pACE was measured in triplicate with a colorimetric assay, and PRA by a commercial kit. In DZ twins, identity by descent of the D/I alleles was examined by PCR amplification of a highly polymorphic simple sequence repeat at the human growth hormone gene. RESULTS: pACE levels were significantly (P < 0.01) higher in DD (9.27 +/- 2.60 IU/l, mean +/-SD) than in II (6.68 +/- 3.0), with DI having intermediate levels (7.93 +/- 2.7). No difference of PRA between different D/I genotypes was found. Twin data analysis showed a statistically significant heritability of pACE, but not of PRA. No differences between MZ and DZ twins in PRA, pACE and the relationship of the D/I genotype with pACE was found. Besides showing that the D/I genotype was the most important predictor of pACE, a multivariate analysis demonstrated that identity by descent of the D/I allele, as assessed by growth hormone (GH) genotyping, also significantly affected pACE. CONCLUSIONS: In this study of normotensive twins, pACE and not PRA showed significant heritability, the former being tightly associated with the D/I ACE gene polymorphism, and/or with a quantitative trait locus in linkage disequilibrium with it.

Adult↗
PubMed1999

Recent weight gain in patients with newly diagnosed obstructive sleep apnea.

OBJECTIVE: Patients with obstructive sleep apnea are often obese. Obesity may contribute to both sleep apnea itself and to the cardiovascular risk associated with sleep apnea. Weight loss in obese patients with sleep apnea may alleviate symptoms and decrease the severity of sleep apnea. Whether patients with obstructive sleep apnea are indeed predisposed to recent weight gain, as compared with similarly obese subjects without sleep apnea, is not known. PATIENTS AND METHODS: We compared 1-year weight histories in 53 male and female patients newly diagnosed with obstructive sleep apnea, compared with 24 controls matched for gender, age, body mass index, and percent body fat. Sleep apnea patients had never been treated. Control subjects were proven to be free of sleep-disordered breathing by overnight polysomnography. RESULTS: Patients with obstructive sleep apnea (n = 53) had a significant recent weight gain of 7.4 +/- 1.5 kg compared with a weight loss of 0.5 +/- 1.7 kg (P = 0.001) in similarly obese controls (n = 24). Male patients with obstructive sleep apnea (n = 28) had a history of significant weight gain (6.8 +/- 2.3 kg) over the year preceding the study compared with male control subjects (n = 13), in whom average weight fell by 0.58 +/- 2.4 kg (P = 0.03). Female patients (n = 25) with obstructive sleep apnea had an 8.0 +/- 1.9 kg weight gain compared with female controls (n = 11) who had a history of weight loss of 0.46 +/- 2.6 kg (P = 0.02). CONCLUSION: These findings support the concept that patients with obstructive sleep apnea may be susceptible to increasing obesity in the period preceding the diagnosis of obstructive sleep apnea.

Adipose Tissue↗
PubMed1999

The effects of short-term passive smoke exposure on endothelium-dependent and independent vasodilation.

OBJECTIVE: There is limited information on the mechanisms mediating the deleterious effects of passive smoke exposure. Cross-sectional studies indicate that nonsmokers exposed chronically to passive smoke have impaired endothelium mediated vasodilation. We tested the hypothesis that acute exposure to sidestream (passive) smoke impairs endothelium-dependent vasodilation in healthy nonsmokers. METHODS AND RESULTS: We studied 12 healthy nonsmokers (aged 27 +/- 5 years, nine men and three women). We obtained measurements of blood pressure, heart rate, and bilateral forearm blood flow (FBF). Each individual was studied twice, following a randomized, placebo-controlled design. The effects of passive smoke were studied on one day and the effects of vehicle (room air) on a separate day. Acetylcholine (ACh) and sodium nitroprusside (SNP) were infused into the left brachial artery before and after 15 min of exposure to either passive smoke (carbon monoxide concentration between 20 and 40 p.p.m.) or vehicle (room air). The order of ACh and SNP, and smoke or vehicle, was randomized between individuals. Smoke exposure increased carboxyhemoglobin from 0.5 +/- 0.1 % to 0.8 +/- 0.1% (P= 0.002). Neither passive smoke nor vehicle changed baseline measurements of heart rate, blood pressure and forearm vascular resistance (FVR). The vasodilatory responses to ACh and SNP were very similar, both before and after exposure to passive smoke and before and after vehicle. CONCLUSION: Our data demonstrate that acute exposure to passive smoke does not alter either endothelium-dependent or independent vasodilatory responses in healthy nonsmoking individuals. Hence, impaired endothelial vasodilatory responses in nonsmokers chronically exposed to passive smoke most likely reflect chronic functional and/or structural changes in responses to cigarette smoke, rather than the acute effects of cigarette smoke toxicity on endothelial function.

Acetylcholine↗
PubMed1999

Human obesity is characterized by a selective potentiation of central chemoreflex sensitivity.

The chemoreflexes are an important mechanism for regulation of both breathing and autonomic cardiovascular function. Obesity is associated with an increased risk of alveolar hypoventilation and carbon dioxide retention, suggesting that abnormalities in chemoreflex control mechanisms may be implicated. We tested the hypothesis that chemoreflex function is altered in obesity. We compared ventilatory, sympathetic, heart rate, and blood pressure responses to hypercapnia, hypoxia, and the cold pressor test in 14 obese subjects and 14 normal-weight subjects matched for age and gender. During hypercapnia, the increase in minute ventilation was significantly greater in obese subjects (7.0+/-0.3 L/min) than in normal-weight subjects (3.3+/-1.1 L/min; P=0.03). Despite higher minute ventilation during hypercapnia in obese subjects, the increase in muscle sympathetic nerve activity was similar in obese and normal-weight subjects. When the inhibitory influence of breathing during hypercapnia was eliminated by apnea, the increase in sympathetic nerve activity in obese subjects (99+/-16%) was greater than in normal-weight subjects (44+/-16%; P=0.02). The magnitude of the ventilatory and autonomic responses to hypoxia and the cold pressor test was similar in obese and normal-weight subjects. We conclude that chemoreflex responses to hypercapnia are potentiated in eucapnic obese subjects. In contrast, responses to hypoxia and to the excitatory cold pressor stimulus in obese subjects are similar to those in normal-weight subjects. Thus, obesity is characterized by selective potentiation of central chemoreflex sensitivity.

Adult↗
PubMed1998

Central vagotonic effects of atropine modulate spectral oscillations of sympathetic nerve activity.

BACKGROUND: Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. METHODS AND RESULTS: Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 microgram/kg IV) and high (15 microgram/kg IV) doses of atropine. After low-dose atropine, RR increased by 9+/-1% (P<0.0001), the low-frequency (LF) component (in normalized units, NU) of RR variability decreased by -32+/-8%, and the high-frequency (HF)NU component increased (+74+/-19%); hence, LF/HF of RR variability fell by 52+/-10% (all P<0.01). Although overall MSNA did not change, LFNU of MSNA decreased (-15+/-5%), HFNU of MSNA increased (+31+/-3%), and LF/HF of MSNA fell (-41+/-8%) (all P<0.01). After high-dose atropine, LFNU of MSNA decreased (-17+/-12%), HFNU of MSNA increased (+22+/-3%), and LF/HF of MSNA fell (-51+/-21%) (all P<0.02). CONCLUSIONS: Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.

Adult↗
PubMed1998

Altered cardiovascular variability in obstructive sleep apnea.

BACKGROUND: Altered cardiovascular variability is a prognostic indicator for cardiovascular events. Patients with obstructive sleep apnea (OSA) are at an increased risk for cardiovascular disease. We tested the hypothesis that OSA is accompanied by alterations in cardiovascular variability, even in the absence of overt cardiovascular disease. METHODS AND RESULTS: Spectral analysis of variability of muscle sympathetic nerve activity, RR interval, and blood pressure were obtained during undisturbed supine rest in 15 patients with moderate-to-severe OSA, 18 patients with mild OSA, and 16 healthy control subjects in whom sleep disordered breathing was excluded by complete overnight polysomnography. Patients with OSA were newly diagnosed, never treated for OSA, and free of any other known diseases. Patients with moderate-to-severe OSA had shorter RR intervals (793+/-27 ms) and increased sympathetic burst frequency (49+/-4 bursts/min) compared with control subjects (947+/-42 ms; 24+/-3 bursts/min; P=0.008 and P<0.001, respectively). In these patients, total variance of RR was reduced (P=0.01) and spectral analysis of RR variability showed an increase in low frequency normalized units, a decrease in high frequency normalized units, and an increase in the ratio of low to high frequency (all P<0.05). Even though blood pressure was similar to that of the control subjects, blood pressure variance in patients with moderate-to-severe OSA was more than double the variance in control subjects (P=0.01). Patients with mild OSA also had a reduction in RR variance (P=0.02) in the absence of any significant difference in absolute RR interval. For all patients with OSA, linear regression showed a positive correlation (r=0.40; P=0.02) between sleep apnea severity and blood pressure variance. CONCLUSIONS: Cardiovascular variability is altered in patients with OSA. This alteration is evident even in the absence of hypertension, heart failure, or other disease states and may be linked to the severity of OSA. Abnormalities in cardiovascular variability may be implicated in the subsequent development of overt cardiovascular disease in patients with OSA.

Adult↗
PubMed1998

Sympathetic activity in obese subjects with and without obstructive sleep apnea.

BACKGROUND: Obese humans are reported to have increased muscle sympathetic nerve activity (MSNA). Obstructive sleep apnea (OSA) may also be accompanied by increased MSNA. Because there is a high prevalence of OSA in obese humans, it is possible that high MSNA reported in obese subjects may in fact reflect the presence of OSA in these subjects. We tested the hypothesis that obesity, per se, in the absence of OSA, is not accompanied by increased MSNA. METHODS AND RESULTS: We measured MSNA in 25 healthy normal-weight subjects and 30 healthy sedentary obese subjects. All subjects were screened by history and examination to exclude subjects with OSA or hypertension. OSA was further excluded by overnight polysomnographic studies. Despite careful screening, polysomnography revealed that 1 of 25 normal-weight subjects and 9 of 30 obese subjects had occult OSA (P=0.015). MSNA was similar in normal-weight subjects (41+/-3 bursts per 100 heartbeats) and obese subjects without sleep apnea (42+/-3 bursts per 100 heartbeats, P=0.99). MSNA in the 9 obese subjects with occult OSA was 61+/-8 bursts per 100 heartbeats, which was higher than MSNA in normal-weight subjects without sleep apnea (P=0.02) and higher than MSNA in obese subjects without sleep apnea (P=0.02). CONCLUSIONS: Obesity alone, in the absence of OSA, is not accompanied by increased sympathetic activity to muscle blood vessels.

Adult↗
PubMed1998

Cigarette smoking increases sympathetic outflow in humans.

BACKGROUND: It is generally accepted that smoking increases blood pressure and inhibits muscle sympathetic nerve activity (SNA). The decrease in muscle SNA with cigarette smoking might be secondary to baroreflex responses to the pressor effect of smoking, thus obscuring a sympathetic excitatory effect of smoking. We tested the hypothesis that smoking increases sympathetic outflow. METHODS AND RESULTS: We examined the effects of sham smoking, cigarette smoking, and cigarette smoking in combination with nitroprusside on muscle (baroreflex-dependent) SNA in 10 healthy habitual smokers. The 3 sessions were performed in random order, each study on a separate day. In an additional study, we also investigated the effects of sham smoking and cigarette smoking on skin (baroreflex-independent) SNA in 9 subjects. Compared with sham smoking, cigarette smoking alone increased blood pressure and decreased muscle SNA. When the blood pressure increase in response to smoking was blunted by nitroprusside infusion, there was a striking increase in muscle SNA. Muscle SNA increased up to 3-fold the levels seen before smoking (P<0.001), accompanied by an increase in heart rate of up to 37+/-4 bpm. Cigarette smoking also induced a 102+/-22% increase in skin SNA (P=0.03). CONCLUSIONS: These data provide the first direct evidence that cigarette smoking increases sympathetic outflow.

Adult↗