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Smoking and hypertension

Norman M Kaplan, MD
Section Editors
George L Bakris, MD
James K Stoller, MD, MS
Deputy Editor
John P Forman, MD, MSc


Tobacco use is the most common cause of avoidable cardiovascular mortality worldwide [1]. There are now 1.3 billion cigarette smokers, 82 percent in developing countries, and if current practices continue, there will be an estimated one billion tobacco-related deaths during the 21st century. The immediate noxious effects of smoking are related to sympathetic nervous overactivity, which increases myocardial oxygen consumption through a rise in blood pressure, heart rate, and myocardial contractility [2].

Chronically, cigarette smoking induces arterial stiffness which may persist for a decade after smoking cessation [3]. The incidence of hypertension is increased among those who smoke 15 or more cigarettes per day [4], and the coexistence of hypertension and smoking decreases left ventricular function in asymptomatic people [5].

With each cigarette, the blood pressure rises transiently and the pressor effect may be missed if the blood pressure is measured 30 minutes after the last smoke. The transient rise in blood pressure may be most prominent with the first cigarette of the day even in habitual smokers. In one study of normotensive smokers, there was an average elevation in systolic pressure of 20 mmHg after the first cigarette (figure 1) [6]. Furthermore, ambulatory blood pressure monitoring suggests an interactive effect between smoking and coffee drinking in patients with mild primary hypertension (formerly called "essential" hypertension), resulting in a mean elevation in daytime systolic pressure of approximately 6 mmHg [7].

However, habitual smokers generally have lower blood pressures than nonsmokers as observed in most [8,9], but not all [10], studies. The mild reduction in blood pressure in smokers is related to decreased body weight [11]. Support for this observation is the higher body weight and increased blood pressure among former smokers versus that observed among never-smokers [12]. A vasodilator effect of cotinine, the major metabolite of nicotine, also may contribute to the lower blood pressure [13].

Despite these observations, smoking should be avoided in any hypertensive patient because it can markedly increase the risk of secondary cardiovascular complications and enhance the progression of renal insufficiency [14,15]. An example of the latter effect was observed in one prospective study (with a mean follow-up of 35 months) that examined the factors associated with alterations in renal function among 53 hypertensive patients in whom the serum creatinine concentration rose from 1.5 to 1.9 mg/dL (133 to 168 µmol/L) despite a significant reduction in the target mean blood pressure (127 to 97 mmHg) [14]. Smoking was the most significant independent factor underlying progressive renal disease (serum creatinine 1.5 and 2.1 mg/dL [133 and 186 µmol/L] at the beginning and end of the study for smokers, respectively, versus 1.25 and 1.32 mg/dL [110 and 117 µmol/L] for nonsmokers, respectively). The mechanism underlying this adverse effect is unclear but may be related to the transient increase in systemic blood pressure with smoking being transmitted to the glomerulus, resulting in glomerular hypertension.


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Literature review current through: Sep 2016. | This topic last updated: Dec 2, 2015.
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