Why does smoking raise my blood pressure?

Smoking has been shown to lead to acute increases in blood pressure (BP) within minutes of the first inhalation, but BP returns to pre-smoking levels about an hour after cessation of smoking.¹ Systolic blood pressure has been reported to increase 10 – 25 mm Hg and diastolic 6 – 12 mm Hg depending on the nicotine content of the cigarette. Nicotine has been shown to cause the release of norepinephrine through a cascade of events in the sympathetic nervous system.² The increase in BP is attributed to the effects of nicotine on the sympathetic nervous system, which increases total peripheral resistance and cardiac output.¹  

However, the long-term effects of smoking are not as clear. Evidence from multiple studies on chronic smokers compared to non-smokers reveal much smaller and variable effects of smoking on BP.^3-8 The differences in BP of smokers compared to non-smokers seem to be influenced more by body mass index and alcohol intake than by smoking.⁸ When examined more closely, the chronic effects of smoking are better demonstrated by the high prevalence of renovascular hypertension (renal artery stenosis [RAS]) and malignant hypertension (systolic BP ≥ 180 mm Hg or diastolic BP  ≥ 110 mm Hg) in smokers due to the development of atherosclerosis.^9-14 In a study of patients with RAS (n=63) and a control group of age (±3 years) and sex matched hypertensive patients, there were significantly more smokers among patients with RAS (53/63, 84%) than in the control group (29/63, 46%) (p<0.001).¹² Another study compared smoking habits in 48 consecutive cases of malignant hypertension to 92 consecutive patients without malignant hypertension at a blood pressure clinic.¹⁰ Patients with malignant hypertension were more likely to be smokers than those without malignant hypertension (69% vs 37%, p<0.001).

There are a few proposed mechanisms by which cigarette smoking induces atherogenesis.¹⁵ One mechanism involves the increased adhesion and aggregation of platelets due to reduced availability of platelet-derived nitric oxide and decreased platelet sensitivity to nitric oxide.¹⁶ Another is the alteration on thrombotic factors such as increased levels of fibrinogen and tissue factor that increase atherosclerosis.^17-20

^References 

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4. Verberk WJ, Kessels AG, de Leeuw PW. Prevalence, causes, and consequences of masked hypertension: a meta-analysis. Am J Hypertens. 2008;21(9):969-975.
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13. Plus M. Renovascular hypertension. https://medlineplus.gov/ency/article/000204.htm. Accessed 12 December, 2017.
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15. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731-1737.
16. Ichiki K, Ikeda H, Haramaki N, Ueno T, Imaizumi T. Long-term smoking impairs platelet-derived nitric oxide release. Circulation. 1996;94(12):3109-3114.
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20. Kannel WB, D'Agostino RB, Belanger AJ. Fibrinogen, cigarette smoking, and risk of cardiovascular disease: insights from the Framingham Study. Am Heart J. 1987;113(4):1006-1010.