Why does nicotine increase blood pressure

Bolinder G , de Faire U : Ambulatory h blood pressure monitoring in healthy, middle-aged smokeless tobacco users, smokers, and nontobacco users. Am J Hypertens ; 11 : — J Hypertens ; 13 : — Am J Hypertens ; 14 : — J Pharmacol Exp Ther ; : — Oxford University Press is a department of the University of Oxford.

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Oxford Academic. Cite Cite Neal L. Select Format Select format. Permissions Icon Permissions. Coronary heart disease: Epidemiology of smoking and intervention studies of smoking. Exercise also seems to lower high blood pressure.

Salt can raise blood pressure in some people. Most people who have high blood pressure should get no more than 2, mg of salt each day from their food and drinks. This is about one teaspoon plus one fourth of a teaspoon. Your doctor may tell you to limit your salt even more than this. Do not add salt to your food at the table. Check the labels on your drinks and canned and frozen foods to see how much salt or sodium they have in them.

While some foods, such as potato chips, obviously have a lot of salt in them, you may be surprised to see how much salt is in foods like bread or cheese. Alcohol can raise blood pressure in some people.

If you drink alcohol, do not have more than one or two drinks a day. One drink is one can of beer, one glass of wine, or one jigger of hard liquor. If your blood pressure goes up when you drink alcohol, it is best not to drink it. Stress may make your blood pressure go up. To fight the effects of stress, try relaxation or biofeedback techniques. These things work best when you do them at least once every day. Ask your doctor for help with stress.

Many different kinds of medicine can be used to treat high blood pressure see the box below. These are called antihypertensive medicines. The goal is to get your blood pressure to a normal level with medicine that is easy to take and has few, if any, side effects. Some people have to take this medicine for the rest of their lives. These medicines help your body get rid of extra salt and water so that your blood vessels do not have to hold so much fluid.

Beta blockers. These medicines block the effects of a hormone in your body called adrenaline. ACE inhibitors. These medicines keep your blood vessels from getting narrow. Calcium channel blockers. These medicines keep your blood vessels from getting narrow by keeping too much calcium from going into your cells. These medicines combine at least two of the above medicines for treating your high blood pressure. Some examples include an ACE inhibitor with a calcium channel blocker, an ACE inhibitor with a diuretic, or a beta blocker with a diuretic.

Medicines affect everyone differently. Because blood pressure may increase after cessation of smoking, a smoke quitting program should not postpone initiation of antihypertensive treatment in patients otherwise in need of such treatment. Abstract The addictive effects of smoking are only partly known, but it is likely that hemodynamic effects of tobacco smoking may contribute to the habituation. Findings identify an increase in BP of active smokers or non-smokers exposed to passive smoking, while a lot of others refer a lowering of BP due to smoking.

This discrepancy could be explained as follows. Initially, a vasoconstriction mediated by nicotine causes acute but transient increase in systolic BP. This phase is followed by a decrease in BP as a consequence of depressant effects played chronically by nicotine itself.

Simultaneously, carbon monoxide is acting directly on the arterial wall causing, in the long run, structurally irreversible alterations. At this time, there is a change in BP that increases again, and often constantly, its levels following chronic exposure. Changes in response to antihypertensive drugs have been observed in hypertensive smokers since smoking influences metabolic steps of the drugs.

Tobacco smoke is a term indicating cigarette smoking, cigar smoking, and pipe smoking. Usually, the main reports concerning the relationship between smoking and cardiovascular alterations are attributed to cigarette smoking since systematic studies on the harm caused by pipe and cigars are yet lacking.

There are a lot of reports that identify cardiovascular system as one of the major target organs for smoking [ 1 — 12 ]. Either active or passive exposure to smoking causes damage to the heart and blood vessels although pathological mechanisms of damage may differ with regards to the type of action but not for that is concerning chemical toxics responsible of the alterations [ 13 — 30 ]. In spite of the great number of observations which show the certainty of cardiovascular damage from smoking, the opinions are not yet unanimous.

On the contrary, experimental findings conducted on both animals and humans give evidence of exactly reproducible results of cardiovascular alterations. Adverse effects on the heart and vessels are mediated by many chemical compounds that are usually concentrated and condensed into tobacco mixtures [ 23 ]. Chemical compounds of smoking cause both structural and functional alterations of heart and blood vessels, although with different results which are depending on several factors related to the type of smoking, environment, and subject exposed.

Worldwide, more than 3 million people currently die each year from smoking, half of them before the age of 70, an enormous human cost, and more than one and third have cardiovascular events that often determine permanent disability of affected subjects [ 24 , 25 ]. Main cardiovascular diseases related to cigarette smoking are listed in Table 1.

Among cardiovascular parameters, blood pressure BP is adversely influenced by tobacco smoke with a high rate by a mechanism yet under discussion.

In addition, it is not clear if smoking exposure causes a rise or reduction of blood pressure and, otherwise, also if the occurrence of hypertension in smokers is a consequence of the greatest number of hypertensive people independently from smoking, or smoking actively contributes to changes in BP.

The purpose of this paper is to discuss those results that have been reached by the analysis on the relationship between smoking and BP in both smokers and nonsmokers who were passively exposed. The possible interference of smoking on the effects of the most used antihypertensive drugs is also treated. Active smokers can display BP values which vary widely according to a great number of individual, racial, and lifestyle factors.

Moreover, changes in BP have been documented in the same smoker while he is smoking a cigarette or not. While a smoker is actively smoking, transiently sympathetic responses, which acutely raise BP levels, usually occur. Reports emphasize that hypertension or hypotension can be associated with cigarette smoking in active smokers but there is no evidence on the BP measures whether smoking was lacking.

Some findings [ 31 , 32 ] identified that cigarette smoking in males was inversely related to systolic BP with a reduction of 1. There was no clear relation with diastolic blood pressure. This finding was conducted in an oriental population enrolled in the study, but also in Western countries blood pressure reduction was observed primarily in young smokers [ 32 ].

In addition, epidemiologic surveys [ 33 — 41 ], although not all, demonstrated that individuals who smoked a different number of cigarettes had lower blood pressure than that of non-smokers. Such a characteristic occurred in males, females, adolescents, adults, and different races. However, this observation was attributed primarily to chronic smoking. Associated loss in body weight of active smokers contributes to lowering BP.

Such data contrast strongly with the results obtained in active smokers while they are smoking a cigarette as well as in dated chronic smokers [ 32 , 42 — 45 ]. These individuals display an evident increase in blood pressure that seems to be clearly related to the toxic effects of nicotine and carbon monoxide of acute type but, particularly for that concerns carbon monoxide, also of chronic type with structural arterial lesions associated.

Structural alterations, in the run, tend to change the behaviour of BP that becomes irreversibly elevated although it was starting from increased levels initially responsive to smoking cessation. Nowadays, there is evidence that changes in vascular wall begin as early as a smoker begins with smoking but they are of no estimation because of masked damage, as that will be described ahead. Passive smokers display different levels of BP depending on the type and duration of exposure to environmental tobacco smoke.

Increased levels of BP, particularly systolic BP, usually follow acute but transient exposure [ 46 ]. Occasionally, there is evidence of hypotension followed, however, by stable hypertension in those individuals exposed for long time to passive smoking even if exposure occurs irregularly. An obvious consideration is that acute but transient exposure to passive smoking of a non-smoker individual makes him susceptible of main smoking compounds, primarily nicotine but also carbon monoxide, which have, initially, hypertensive effects directly or indirectly throughout adrenergic and sympathetic stimulation on arterial bed.

Similarly, increased heart rate can, usually, be identified. Prolonging the exposure, these parameters [ 1 — 3 , 5 , 17 , 18 ] meet some changes which depend on a large number of factors related to cardiovascular parameters. They influence differently BP levels at the end of isolated acute exposure. Physiology, biochemical characteristics and lifestyle interfere with BP in exposed individuals.

Table 2 shows the main cardiovascular parameters involved. Baseline levels usually tend to be reached after the exposure in a variable but short time and adrenergic and sympathetic profile of the individual also contributes to that. Finally, lifestyle is a strong positive or adverse factor to restore cardiovascular parameters, particularly systolic blood pressure, according to respectively regular physical exercise performed by the individual or lacking that.

BP is a clinical parameter of easy assessment and often linked to endothelial dysfunction. Such a statement is particularly true for the essential hypertension [ 47 , 48 ]. Moreover, smoking and endothelial dysfunction are closely related in passive smokers [ 19 ]. The acute response of BP to environmental tobacco smoke would seem to determine an increase in systolic BP levels in some reports [ 49 , 50 ], whereas others [ 51 ] did not conclude for this statement.

The possible hypothesis by which smoking compounds influence BP could be explained as follows. Initially, a vasoconstriction mechanism mediated by nicotine causes acute but transient increase in systolic BP. This phase is followed by a decrease in BP as a consequence of depressant effects played chronically by nicotine.

At this time, there is a change in BP that increases again, and often constantly, its levels [ 29 ]. Such a hypothesis explains BP changes following chronic exposure. On the contrary, acute exposure to passive smoking determines a transient increase in systolic BP due to a combined effect of nicotine that acts by endothelial dysfunction and sympathetic stimulation, and carbon monoxide which exerts its toxic effects directly [ 52 — 55 ].

Increased systolic BP after acute exposure to passive smoking was found also by Mahmud and Feely [ 56 ], whereas Leone and Corsini [ 57 ] documented a decrease in BP following repeated acute exposure to passive smoking. Decrease in BP was proportional to the increase in carboxyhemoglobin concentrations.

Diastolic BP would seem to be affected weakly by environmental tobacco smoke exposure. These observations identify no uniform course of blood pressure in both active smokers and non-smokers exposed and that concept needs to be clarified by the hypothesis of masked cardiovascular damage.

The phenomenon of masked hypertension from smoking was, firstly, described by Leone et al. In the time, that phenomenon has found scientific support. From up to here discussed data, a significant observation emerges: a different response characterizes BP in actively or passively exposed smokers due to the fact that the parameter is assessed immediately after an acute exposure to environmental tobacco smoke or after a chronic and prolonged exposure.

Acute exposure is followed by a transient but significant increase in systolic BP, whereas chronic exposure may be followed by reduced or increased BP depending on the presence of reversible or irreversible alterations of the arterial wall caused by smoking compounds, particularly carbon monoxide. These alterations are, for a variable time, masked by the paralyzing action exerted by nicotine on ganglionic ends that follows initial stimulation.

Acute exposure to passive smoking influences adversely either blood vessel dilation since there is a reduced release of nitric oxide, or arterial stiffness. Consequently, an increase in BP [ 33 , 45 , 47 , 48 ] is observed. These changes on arterial stiffness, and then, BP usually occur before they are clinically manifested [ 16 ] and are greater than those seen when a smoker smokes a single cigarette.

Although this type of changes affecting BP is, usually, proven lately, there is evidence, however, that it begins acutely while an individual smokes [ 14 ].

In conclusion, even if assessing systolic BP immediately after environmental smoking exposure may be difficult unless in experimental findings, one cannot deny its increase and, consequently, its interpretation as a marker of smoking exposure. As already described, nicotine may mask the effects of carbon monoxide on arterial wall for a long time.