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

Smoking tobacco contributes to and exacerbates many chronic diseases of aging, including hypertension, stroke, COPD, heart disease, and atherosclerosis. It is also associated with an increased risk of peptic ulcers and of cancers of the lungs and oral cavity. Older patients generally continue to smoke because of physiologic and psychological addiction to nicotine. Nicotine administration through gum or patch eases the symptoms of nicotine withdrawal for highly-tolerant patients. Detecting and treating alcohol abuse, depression, or life stress may then make it easier to motivate the patient to quit smoking. Physician advice combined with follow-up visits and phone calls has been shown to be one of most effective methods of getting patients to stop smoking.
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PMID:Smoking cessation: clinical steps to improve compliance. 838 53

We examined whether a histamine (H3)-agonist, (R) alpha-methylhistamine, [(R) alpha-MeHA] reduced the pressor responses induced by nicotine in urethane-anesthetized guinea pigs treated by atropine. Nicotine dose-dependently increased the basal mean arterial pressure (MAP) and the heart rate (HR) of the preparation. Both effects were due to stimulation of sympathetic ganglia, since muscarinic receptors were blocked. Adrenalectomy did not affect either the hypertension or the tachycardia to nicotine. Nicotine (7 micrograms kg-1) evoked a transient hypertension of approximately 30 mm Hg and a tachycardia by approximately 20 beats/min. (R) alpha-MeHA dose-dependently inhibited the increase in mean arterial pressure and the increase in HR to nicotine but not those produced by exogenous norepinephrine (NE). The inhibitory effects of (R) alpha-MeHA were dose-dependently antagonized by the H3-antagonist thioperamide, but not by combined mepyramine/cimetidine. They were also suppressed by a nitric oxide (NO)-synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME); this suppression was reversed by L-arginine. Histamine in the presence of mepyramine and cimetidine induced a similar inhibition of the hypertension to nicotine but a less potent inhibition of the tachycardia. These findings indicate that postganglionic noradrenergic nerve fibers are endowed with presynaptic H3-receptors, the stimulation of which inhibits NE release through an NO mechanism.
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PMID:Reduction of the pressor response to nicotine in the guinea pigs by a histamine (H3) agonist is attenuated by an inhibitor of nitric oxide synthesis. 884 81

The significance of smoking in the hypertensive patient may be unappreciated. The risk of hypertension may be tripled in such patients. Tobacco addiction may also compromise the treatment of hypertensives. The importance of smoking cessation for hypertensive smokers cannot be overemphasized and should be seen as fundamental. Nicotine replacement therapy (NRT), when used appropriately, can enhance the likelihood of cessation. All smokers, but particularly hypertensive smokers, should be advised to quit and offered specific and ongoing assistance in this respect.
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PMID:Tobacco addiction and hypertension. 886 38

Nicotine is absorbed in substantial quantities from smokeless tobacco and could contribute to the adverse consequences of smokeless tobacco use. Chronic systemic exposure to nicotine could contribute to accelerated coronary artery disease, acute cardiac ischemic events, and hypertension. Systemic absorption of sodium and mutagenic chemicals from smokeless tobacco could aggravate hypertension or cardiac failure, or contribute to cancer, respectively. Information concerning the potential hazards of nicotine and other systemically absorbed toxins may be incorporated into educational programs to discourage the use of smokeless tobacco.
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PMID:Systemic absorption and effects of nicotine from smokeless tobacco. 952 34

1. Nicotine is involved in many cardio-respiratory diseases, including hypertension and sudden infant death syndrome (SIDS), which is the most common cause of death in infants between 1 month and 1 year of age. While the aetiology of SIDS remains largely unknown, recent clinical studies suggest maternal cigarette smoking is a major risk factor in SIDS and an abnormality of cardio-respiratory control, particularly a centrally mediated slowing of the heart that precedes or accompanies apnoea, is involved. 2. Because the sites, mechanisms of action and diverse receptor types of nicotine within the central nervous system are controversial and poorly understood, in the present study we examined the effects of nicotine on specific brainstem neurons that control heart rate. Cardiac vagal neurons were identified in an in vitro slice preparation using a retrograde fluorescent tracer and were studied using both whole-cell and perforated patch-clamp electrophysiological techniques. 3. We have found there are different pre- and post-synaptic nicotinic receptors that have dramatic effects on glutamatergic neurotransmission as well as directly activating vagal cardio-inhibitory neurons.
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PMID:Nicotine excites cardiac vagal neurons via three sites of action. 967 23

Cardiovascular complications are the main cause of death in hypertensive patients. They occur more often in tobacco smokers. The effect of nicotine activity is insulin resistance leading to lipid disorders which are risk factor for atherosclerosis. Smoking and hypertension intensify the atherogenic effect of each other. The risk of ischaemic heart disease in a hypertensive smoker is almost 3.5 times greater than in a non-smoker with normal blood pressure at the same serum cholesterol concentration. Nicotine multiplies the risk of cardiovascular complications caused by left ventricular hypertrophy in arterial hypertension. Strokes (ischaemic strokes and subarachnoid haemorrhages) are more common in smokers. Smokers also develop accelerated malignant hypertension more frequently than non-smokers. Smoking is also a risk factor for renal artery stenosis, both atheromatous and fibromuscular.
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PMID:[Nicotine and cardiovascular complications of chronic hypertensive disease]. 969 47

Smoking and arterial hypertension are highly prevalent at the community level. While the coexistence of both risk factors is less frequent, the potentiation of cardiovascular risk when both are present makes the association highly relevant in terms of a preventive approach. There are many interrelationships between smoking and high blood pressure at the clinical, epidemiological and pathophysiological levels. Those demonstrable links compel us to review the usual explanation of the influence of smoking on blood pressure. Pharmacological treatment of the hypertensive patient who smokes must be adapted to the patient's risk profile, using the most efficacious antihypertensive agents. With the exception of nonselective beta-blockers, all the available antihypertensive drugs can be prescribed. Minimal intervention and nicotine replacement constitute the most well tested interventions in helping smokers to quit their habit. Nicotine replacement is currently a well tolerated intervention, even in patients with cardiovascular disease.
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PMID:Management of the hypertensive patient who smokes. 971 43

Although peripheral cholinergic neurotransmission has long been known to play a pivotal role in the control of heart rate and blood pressure, recent evidence has suggested that central cholinergic mechanisms may be involved in the genesis of hypertension, anxiety, cardiorespiratory control, and, in particular, the respiratory modulation of heart rate. Yet, the sites, mechanisms, and receptor subtypes involved in the action of nicotine within the central nervous system are controversial. The present study demonstrates that nicotine has at least 3 sites of action to increase the activity of vagal cardiac neurons. Nicotine, but not muscarinic agonists, activates postsynaptic receptors and a depolarizing inward current in vagal cardiac neurons studied with the perforated patch-clamp technique in a visualized brain stem slice. In addition, nicotine acts at different presynaptic and postsynaptic sites to facilitate glutamatergic neurotransmission. Presynaptic nicotinic receptors increase the frequency of transmitter release and are sensitive to block by alpha-bungarotoxin. Nicotine also elicits a previously undescribed augmentation of postsynaptic non-NMDA currents. The presynaptic and postsynaptic receptors may prove to be future targets in the search for agonists to increase vagal cardiac activity and reduce the fatality associated with cardiac hyperexcitability and for antagonists to reduce cardiac vagal activity in pathological conditions associated with abnormally low heart rates and cardiac function such as sudden infant death syndrome.
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PMID:Nicotine enhances presynaptic and postsynaptic glutamatergic neurotransmission to activate cardiac parasympathetic neurons. 985 41

Intake of nicotine has been related in many cases to acute or chronic hypertension. Using the patch-clamp technique the effect of nicotine on voltage-dependent K+ channel currents in rat tail artery smooth muscle cells was studied. Nicotine at concentrations of 1-100 microM or 0.3-3 mM increased or decreased, respectively, the amplitude of the tetraethylammonium-sensitive K+ currents. Pretreatment of cells with 10 microM dihydro-beta-erythroidine hydrobromide, a nicotinic receptor antagonist, abolished the excitatory effect (n=6), but not the inhibitory effect (n=10), of nicotine on K+ channel currents. The activation of nicotinic receptors with 100 microM 1,1-dimethyl-4-phenylpiperazinium iodide increased K+ channel currents by 27.4+/-3.8% (n=13, P < 0.01). Our results indicate that the excitatory and inhibitory effects of nicotine on K+ channels are respectively mediated by a nicotinic receptor-dependent mechanism and by a direct interaction of nicotine with K+ channels.
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PMID:Effects of nicotine on K+ channel currents in vascular smooth muscle cells from rat tail arteries. 993 30

Nicotine, a rapid-acting poison, is present in environmental tobacco smoke and has been used as a greenhouse insecticide. Due to its toxicity, several health hazard evaluations (HHE) have resulted from potential nicotine exposures to casino workers, airline flight attendants, and greenhouse employees. Exposure to nicotine can occur by inhalation, skin adsorption, and ingestion, resulting in such adverse health effects as nausea, vomiting, headache, dizziness, tachycardia, hypertension, convulsions, and cardiac arrhythmia. The development of an improved sampling and analytical methodology for nicotine was required to accommodate the broad concentration of nicotine levels and varying sampling scenarios presented by the differing HHE requests. A XAD-4 sorbent tube was selected for the collection of airborne nicotine. Analytical methodology for the separation, identification, and quantitation of nicotine by both gas chromatography-flame ionization detection and gas chromatography-nitrogen/ phosphorous detection is described. The limit of detection for nicotine was 0.013 microg/sample. The desorption efficiency for nicotine was determined over the range of study and ranged from 90.9% (0.096 microg) to 93.7% (24.0 microg). Nicotine exhibited storage stability for 30 days at 5 degrees C and for 14 days at ambient temperature. Based on the results of this research study, the new method for nicotine was published in the NIOSH Manual of Analytical Methods (NMAM 2551).
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PMID:Development of a versatile method for the detection of nicotine in air. 1176 27


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