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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Either excitatory or inhibitory cardio-respiratory responses induced by nicotine have been reported. We evaluated the joint and separate contributions of peripheral arterial chemoreceptors and pulmonary vagal afferences to nicotine-induced cardio-respiratory responses in 11 pentobarbitone-anaesthetized cats. Nicotine, given i.v. in doses of from 1 to 200 microg/kg, evoked dose-dependent transient increases in tidal volume (VT) and arterial blood pressure (BP), but the highest doses evoked brief apnoea, immediately followed by intense hyperventilation, as well as discrete early hypotension followed by late hypertension. Bilateral section of the aortic and carotid nerves abolished all hyperventilatory responses to nicotine, giving way to apnoea followed by few cycles of reduced VT and profound hypotension followed by slight hypertension in response to intermediate doses (50-100 microg/kg). Subsequent bilateral vagotomy (BV) suppressed apnoeic and hypotensive responses. In other cats initially subjected to BV, only increases in VT and BP were observed in response to nicotine, effects which were no longer observed after additional carotid and aortic deafferentation. These data suggest that excitatory effects of nicotine on respiration and BP are reflexes evoked by stimulation of peripheral arterial chemoreceptors, while inhibitory effects are also reflex responses but evoked from stimulation of pulmonary vagal afferences.
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PMID:Acute ventilatory and circulatory reactions evoked by nicotine: are they excitatory or depressant? 1242 66

Vietnamese populations in Vietnam and the United States have a high prevalence of smoking. The associations among behavioral risk factors, acculturation, and smoking among the Vietnamese population living in the United States are not well documented. The present study aimed to identify the factors associated with smoking behavior among Vietnamese men living in Santa Clara County, California. A cross-sectional random-digit-dialed telephone survey was conducted. The sampling frame consisted of 27 Vietnamese surnames from the Santa Clara County telephone directory. A total of 660 adult respondents were interviewed to collect information on general health status, alcohol and tobacco use, HIV/AIDS, sexual behavior, injury control, hypertension, cholesterol screening, and acculturation. Of the 660 adults interviewed, 364 (55.2%) were male and 296 (44.8%) were female. Among males, 31.9% were current smokers, and among females, only one woman reported smoking. Univariate analyses revealed that having less than a college education, having poor English language skills, using Vietnamese at home and with friends, being less acculturated, not having a routine physical or blood cholesterol check, and being a binge drinker were significantly associated with an increased likelihood of smoking. Multivariate analysis revealed two independently associated factors: Respondents who were more acculturated were less likely to smoke (OR = 0.38, 95% CI = 0.18-0.83), and those not having cholesterol checked were more likely to smoke (OR = 2.48, 95% CI = 1.30-4.71). Acculturation level was inversely associated with smoking among Vietnamese adult men in Santa Clara County. Other health risk behaviors coexisted with smoking behavior and should be considered in prevention programs.
Nicotine Tob Res 2005 Feb
PMID:Prevalence and predictors of smoking behavior among Vietnamese men living in California. 1580 82

Nicotine, a component of cigarette smoke, has been implicated in the pathogenesis of cardiovascular disease. We examined whether nicotine regulates angiotensin-converting enzyme (ACE), an enzyme that plays an important role in the pathophysiology of atherosclerosis and hypertension. Human umbilical cord vein endothelial cells were treated with nicotine (0.1-1 microM) alone or in combination with vascular endothelial growth factor (VEGF; 0.5 nM) or GF-109203X (GFX; 2.5 microM). The amount of ACE in intact endothelial cells was measured by an inhibitor-binding assay method, and ACE mRNA levels were quantified using LightCycler technology. Phosphorylated PKC levels were measured by Western immunoblotting. Nicotine did not modulate basal ACE production but significantly potentiated VEGF-induced ACE upregulation. Treatment of endothelial cells with the PKC inhibitor GFX totally blocked VEGF- and nicotine-induced ACE upregulation. VEGF induced PKC phosphorylation, which was potentiated by cotreatment with nicotine. We conclude that nicotine significantly potentiated VEGF-induced ACE upregulation. This effect was probably mediated by PKC phosphorylation. The interaction of nicotine with VEGF in ACE induction may contribute to the pathogenesis of smoking-related cardiovascular disease.
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PMID:Regulation of angiotensin-converting enzyme production by nicotine in human endothelial cells. 1596 16

The present study evaluated nicotine plasma levels achieved following 1 day's regular use of four commonly used brands of Swedish portion snus and 2-mg Nicorette chewing gum. The study also estimated the amount of sodium chloride extracted from each snus sachet to identify potential risks for exacerbation of heart failure and hypertension with the use of Swedish snus. Extracted dose of nicotine, area under the venous plasma concentration-time curve (AUC), maximum plasma nicotine concentration (Cmax) of the last (12th) dosing interval, and the Cmax and AUC ratios versus Nicorette were calculated. Relative bioavailable dose was calculated using AUC of 2-mg Nicorette gum as the reference. The mean extracted nicotine doses were 2.74+/-0.80, 1.55+/-0.68, 2.00+/-0.56, and 1.08+/-0.94 mg/sachet for General, Catch Licorice, Catch Mini, and Catch Dry Mini snus, respectively. The approximate bioavailable dose of nicotine from snus was 40%-60% of the extracted dose. The steady-state nicotine plasma concentration-time curve for the weakest brand, Catch Dry Mini portion snus, did not differ significantly from that of the 2-mg Nicorette gum. The AUC and Cmax for Catch Licorice 1 g and Catch Mini 0.5 g portion snus were twice those for the 2-mg Nicorette gum; for the strongest brand, General, these values were 2(1/2) times those for Nicorette gum. The differences in AUC and Cmax versus the 2-mg Nicorette gum were statistically significant (p=.020). Nicotine plasma levels with General portion snus were sustained at higher levels than current nicotine replacement therapy products, peaking at 29.0+/-8.5 ng/ml, and more closely mimicking cigarette smokers' nicotine plasma levels. The risks of aggravation of heart failure and hypertension with respect to increased salt load from the use of snus appeared to be negligible.
Nicotine Tob Res 2005 Jun
PMID:Steady-state nicotine plasma levels following use of four different types of Swedish snus compared with 2-mg Nicorette chewing gum: a crossover study. 1608 7

Smoking is a leading cause of cardiovascular disease, hypertension, myocardial infarction, and stroke. Nicotine is one of the components of cigarette smoke. Nicotine effects on the cardiovascular system reflect the activity of the nicotine receptors centrally and on peripheral autonomic ganglia. It has been found that cigarette smoke extract-induced contraction of porcine coronary arteries is related to superoxide anion-mediated degradation of nitric oxide. Treatment of rabbit aortas with an oxygen free radicals scavenger attenuated cigarette smoke impairment of arterial relaxation. Treatment of smokers with vitamin C, an antioxidant, improved impaired endothelium-dependent reactivity of large peripheral arteries. Thus it appears that chronic smoking and acute exposure to cigarette smoke extract may alter endothelium-dependent reactivity via the production of oxygen derived free radicals. This review discusses the effects of nicotine on resistance arterioles, compliance arteries, smooth muscle cells, and ion channels in the cardiovascular system. We discuss studies performed on humans, nicotine-exposed animals, and cell cultures yielding varying and inconsistent results that may be due to differences in experimental design, species, and the dose of exposure. Nicotine exposure appears to induce a combination of free radical production, vascular wall adhesion, and a reduction of fibrinolytic activity in the plasma.
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PMID:Nicotine effect on cardiovascular system and ion channels. 1663 75

Sympathetic overactivity is implicated in the increased cardiovascular risk of cigarette smokers. Excitatory nicotinic receptors are present on peripheral chemoreceptor cells. Chemoreceptors located in the carotid and aortic bodies increase ventilation (Ve), blood pressure (BP), heart rate (HR), and sympathetic nerve activity to muscle circulation (MSNA) in response to hypoxia. We tested the hypothesis that nicotine replacement therapy (NRT) increases MSNA and chemoreceptor sensitivity to hypoxia. Sixteen young healthy smokers were included in the study (8 women). After a randomized and blinded sublingual administration of a 4-mg tablet of nicotine or placebo, we measured minute Ve, HR, mean BP, and MSNA during normoxia and 5 minutes of isocapnic hypoxia. Maximal voluntary end-expiratory apneas were performed at baseline and at the end of the fifth minute of hypoxia. Nicotine increased HR by 7+/-3 bpm, mean BP by 5+/-2 mm Hg, and MSNA by 4+/-1 bursts/min, whereas subjects breathed room air (all P<0.05). During hypoxia, nicotine also raised HR by 8+/-2 bpm, mean BP by 2+/-1 mm Hg, and MSNA by 7+/-2 bursts/min (all P<0.05). Nicotine increased MSNA during the apneas performed in normoxia and hypoxia (P<0.05). Nicotine also raised the product of systolic BP and HR, a marker of cardiac oxygen consumption, during normoxia, hypoxia, and the apneas (P<0.05). Ve, apnea duration, and O2 saturation during hypoxia and the apneas remained unaffected. In conclusion, sympathoexcitatory effects of NRT are not because of an increased chemoreflex sensitivity to hypoxia. NRT increases myocardial oxygen consumption in periods of reduced oxygen availability.
Hypertension 2006 Jun
PMID:Acute cardiovascular and sympathetic effects of nicotine replacement therapy. 1665 63

Smoking is related to 30% of cancer deaths. It is a risk factor for respiratory tract, esophagus, stomach, pancreas, uterine cervix, kidney and bladder carcinomas. Nicotine induces tolerance and addiction by acting on the central dopaminergic pathways, thus leading to pleasure and reward sensations within the limbic system. It stimulates the central nervous system (CNS), enhances alertness and reduces the appetite. A 50% reduction of nicotine consumption may trigger withdrawal symptoms in addicted individuals: anxiety, anger, sleep disorders, hunger, cognitive dysfunction and cigarette craving. Medical advice is the cornerstone of smoking cessation. Pharmacotherapy of nicotine addiction comprises first-line (bupropion and nicotine replacement therapy) and second-line (clonidine and nortriptyline) drugs. Bupropion is a non-tricyclic antidepressant that inhibits dopamine uptake, whose contraindications are: epilepsy, eating disorders, uncontrolled hypertension, recent alcohol abstinence and current therapy with MAO inhibitors. Nicotine replacement therapy can be done with patches or gums. Counseling groups and behavioral interventions are efficacious. The effects of acupuncture on smoking cessation are not fully elucidated. Prompt smoking cessation or gradual reduction strategies have similar success rates.
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PMID:Methods for smoking cessation and treatment of nicotine dependence. 1687 54

We studied phenotypic and clinical outcome data in an observational, multicenter cohort study of 1001 Western European white women and their singleton babies, with stringently defined moderate-to-severe preeclampsia. Ninety women admitted to being current smokers; 71 had stopped smoking before entry to the study. Across the categories of never-smoker, stopped, and current smoker there were significant increases in the proportion of women delivering before 34 weeks' gestation (P=0.011), delivering a baby below the third birth weight centile (P<0.001), or delivering a baby with any adverse outcome (P=0.011). By comparison with never-smokers, smoking during pregnancy was associated with a doubling of risk of being delivered before 34 weeks' (odds ratio: 1.98; 95% CI: 1.24 to 3.16; P=0.004), of delivering babies below the third centile of corrected birth weight (odds ratio: 2.20; 95% CI 1.41 to 3.44; P<0.0001), or for their babies to have any adverse outcome (odds ratio: 1.87; 95% CI: 1.19 to 2.95; P<0.006). Worryingly, the risk of developing eclampsia was increased 5-fold (odds ratio: 4.88; 95% CI: 1.44 to 16.61; P=0.005). The proportion of smokers in these preeclamptic women was lower than in our pregnant population generally. However, preeclampsia still carries significant perinatal morbidity, and cigarette smoking in preeclamptic pregnancies exacerbates this. Stopping smoking decreases the risks. Smoking in young women should be a particular target for advice by general practitioners before pregnancy, with active encouragement after conception to enroll in such trials as the current Smoking, Nicotine and Pregnancy Trial to support cessation.
Hypertension 2008 Apr
PMID:Smoking in moderate/severe preeclampsia worsens pregnancy outcome, but smoking cessation limits the damage. 1825 22

Epidemiological studies suggest that maternal cigarette smoking is associated with an increased risk of elevated blood pressure (BP) in postnatal life. The present study tested the hypothesis that prenatal nicotine exposure causes an increase in BP response to angiotensin II (Ang II) in adult offspring. Nicotine was administered to pregnant rats via subcutaneous osmotic minipumps throughout the gestation. BP and vascular responses to Ang II were measured in 5-month-old adult offspring. Prenatal nicotine had no effect on baseline BP but significantly increased Ang II-stimulated BP in male but not female offspring. The baroreflex sensitivity was significantly decreased in both male and female offspring. Prenatal nicotine significantly increased arterial media thickness in male but not female offspring. In male offspring, nicotine exposure significantly increased Ang II-induced contractions of aortas and mesenteric arteries. These responses were not affected by inhibition of endothelial NO synthase activity. Losartan blocked Ang II-induced contractions in both control and nicotine-treated animals. In contrast, PD123319 had no effect on Ang II-induced contractions in control but inhibited them in nicotine-treated animals. Nicotine significantly increased Ang II type 1 receptor but decreased Ang II type 2 receptor protein levels, resulting in a significant increase in the ratio of Ang II type 1 receptor/Ang II type 2 receptor in the aorta. Furthermore, the increased contractions of mesenteric arteries were mediated by increases in intracellular Ca(2+) concentrations and Ca(2+) sensitivity. These results suggest that prenatal nicotine exposure alters vascular function via changes in Ang II receptor-mediated signaling pathways in adult offspring in a gender-specific manner, which may lead to an increased risk of hypertension in male offspring.
Hypertension 2008 Apr
PMID:Prenatal gender-related nicotine exposure increases blood pressure response to angiotensin II in adult offspring. 1825 24

Since 2000, the Genetics of Coronary Artery Disease in Alaska Natives (GOCADAN) study has been collecting information on cardiovascular disease (CVD) and its risk factors from 1,214 Alaska Natives of the Norton Sound region, a population with increasing rates of heart disease and stroke. Because smoking was reported in a large proportion of the participants, this analysis was undertaken to evaluate smoking patterns and their relation to other risk factors and to CVD. The relationships among smoking habits and demographic factors, body mass index, plasma fibrinogen, prevalent hypertension, and carotid plaque were evaluated. Eighty percent of participants had smoked 100+ cigarettes in their lifetime. Fifty-seven percent of women and 63% of men (p = .12) were current smokers: one in four smokers had quit. Current smokers (OR = 2.1; 95% CI = 1.1-3.8) and those who had quit <5 years ago (OR = 1.6; 95% CI = 1.1-2.2) were more likely than non-smokers to have carotid plaque. Pack-years smoked also were correlated with carotid plaque. The high prevalence of smoking and low rates of cessation in this population demonstrate an urgent need for smoking prevention and cessation programs among Alaskan Eskimos of the Norton Sound region and other Alaska Native groups.
Nicotine Tob Res 2008 Mar
PMID:Prevalence of smoking and its relationship with carotid atherosclerosis in Alaskan Eskimos of the Norton Sound region: the GOCADAN study. 1832 67


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