Project: Research project

Project Details


Smoking is an important risk factor for cardiovascular disease,
in particular for acute cardiovascular events such as myocardial
infarction and sudden death. The mechanisms linking smoking to
acute cardiovascular events are not known. Sympathetic and
hemodynamic responses to cigarette smoking may be implicated.
Previous studies have demonstrated that smoking increases heart
rate and blood pressure and decreases muscle sympathetic nerve
activity (SNA) in healthy subjects. However, the baroreflex
response to the increased blood pressure during smoking may be
inhibiting muscle SNA and blunting the tachycardia during
smoking. Thus, in patients with baroreflex impairment (patients
with hypertension, coronary artery disease or heart failure),
smoking may trigger increases in muscle SNA and potentiated
increases in heart rate and blood pressure. It is not known
whether these populations, who are most vulnerable to acute
cardiovascular events, have a differential response to cigarette
smoking in comparison to healthy control subjects. We propose a
series of investigations that promise mechanistic insight into
the effects of cigarette smoking and the link between smoking and
acute cardiovascular events.

We will test the following specific hypotheses. 1) In young
healthy subjects, cigarette smoking increases baroreflex
independent skin SNA. Attenuation of the pressor effect of
cigarette smoking (using intravenous nitroprusside infusion) is
accompanied by increases in muscle SNA. 2) In patients with
baroreflex impairment (elderly subjects and patients with overt
cardiovascular disease), there is an increase in muscle SNA and
catecholamines and a potentiation of the pressor and heart rate
responses to smoking. 3) The effects of cigarette smoking on
skin SNA and muscle SNA are mediated by nicotine.

The integrity of the proposed hypotheses are supported by
exciting preliminary data. These studies build on our broad
experience in investigating both smoking and neural circulatory
control, and should contribute significantly to understanding the
mechanisms linking cigarette smoking to acute cardiovascular
Effective start/end date2/1/991/31/05


  • Medicine(all)