Effect of Age on Blood Pressure Response to Cigarette Smoking

Kurihara, Shigemitsu

doi:10.1159/000176848

Cited by 9 publications

(2 citation statements)

References 18 publications

(21 reference statements)

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“…Nicotine in cigarettes causes an increase in serum catecholamines, increasing BP and heart rate [27]. This has a more pronounced effect with aging.…”

Section: Smokingmentioning

confidence: 99%

The secondary prevention of coronary artery disease in older persons

Thomas

Foody²

2007

Curr Cardio Risk Rep

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Coronary artery disease (CAD) is the leading cause of morbidity and mortality in older persons and has considerable health care costs. Older persons are a unique socioeconomic group that is underrepresented in clinical trials. They have atypical clinical presentations and vary in response to medications. This review discusses the risk factors of CAD and the secondary prevention of CAD, with a specific focus on the older age group. This article briefly reviews the paradox of care and the quality of care in the older population.

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“…Nicotine in cigarettes causes an increase in serum catecholamines, increasing BP and heart rate [27]. This has a more pronounced effect with aging.…”

Section: Smokingmentioning

confidence: 99%

The secondary prevention of coronary artery disease in older persons

Thomas

Foody²

2007

Curr Cardio Risk Rep

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“…In addition, tissue repair processes diminish with age. Older people who smoke are more susceptible to vascular disease (19) and lung diseases including lung cancer (20) than age‐matched nonsmokers. However, little is known about the actions of nicotine on the immune system of aged individuals, especially those who may already have a diminished immunologic potential.…”

mentioning

confidence: 99%

Differential Effects of Nicotine and Aging on Splenocyte Proliferation and the Production of Th1‐ Versus Th2‐Type Cytokines

Hallquist¹,

Hakki²,

Wecker

et al. 2000

Proc Soc Exp Biol Med

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Abstract. Nicotine has a multitude of biological actions in the central and peripheral nervous systems where nicotinic acetylcholine receptors are found. Nicotinic acetylcholine receptors have also been identified on immune cells, but the effects of nicotine on immune responses are not well characterized. These studies tested the hypotheses that nicotine has an effect on both T‐lymphocyte proliferation and the production of cytokines by activated T cells, processes that are necessary for effective T‐cell–mediated immune responses. In addition, the effects of nicotine on these immune responses in aging animals and the effects of nicotine exposure prior to immunostimulation were investigated. Murine splenocytes were exposed to nicotine and stimulated with concanavalin A (ConA). The highest concentration of nicotine (128 μg/ml) significantly depressed proliferation of T cells both when nicotine and ConA were added concurrently and when nicotine was added 3 hr prior to ConA. Nicotine, added concurrently with ConA at concentrations between 0.25 and 64 μg/ml, significantly inhibited the production of IL‐10 by splenocytes from young adult mice, whereas the inhibition of production of IL‐10 by splenocytes from old mice was significantly inhibited, but the response was more variable, depending on the nicotine concentration. In contrast, the production of IFN‐γ by splenocytes from either young adult or old mice was not affected when nicotine (0.016–64 μg/ml) was added concurrently with ConA. Pre‐exposure to 1 μg/ml of nicotine for 3 hr significantly enhanced the production of IFN‐γ by splenocytes from young adult mice, whereas pre‐exposure to 0.016 μg/ml of nicotine tended to but did not significantly enhance IFN‐γ production. Nicotine is now being used as an over‐the‐counter drug by people who differ in age and general immunocompetence. Therefore, the effects of nicotine on immune responses, independent from the effects of the other chemicals found in tobacco, need to be investigated.

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