[Acute effects of tobacco and vascular risk modulated by genetic factors]

Rev Port Cardiol. 2000 Dec;19(12):1279-83.
[Article in Portuguese]


Most studies regarding the acute effects of cigarette smoking refer to the higher sympathetic and adrenomedullary activity as a result of sympathetic ganglia and adrenal medulla nicotinic receptor activation. Although it is reasonable to suppose that the renin-angiotensin system might be activated, this possible effect of nicotine has not been studied. We have studied the effects of cigarette smoking on blood pressure, cardiac output, pulse pressure, renin-angiotensin system, kinins-NO, oxidative stress and insulin. Also, we have investigated if the variability of the biochemical parameters was dependent on genetic polymorphisms of the angiotensin converting enzyme and the acute phase protein haptoglobin. 39 normotensive individuals, 18 males and 21 females, of mean age 35.4 +/- 8.9 years were included in this study. Oxidative stress was dependent on the ACE I/D and Hp1/2 polymorphisms, with the ACE DD genotype and the Hp2-2 phenotype not showing variation in the anti-oxidant defense systems, and the ACE II-ID genotypes and Hp1-1 + 2-2 phenotypes showing a higher anti-oxidant response, hence a lower cardiovascular risk being predictable in the latter individuals.

Publication types

  • English Abstract

MeSH terms

  • Adult
  • Blood Pressure / drug effects*
  • Female
  • Haptoglobins / genetics
  • Heart Rate / drug effects*
  • Humans
  • Male
  • Nitric Oxide / blood
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic
  • Risk Factors
  • Smoking / adverse effects*
  • Vascular Diseases / epidemiology
  • Vascular Diseases / etiology
  • Vascular Diseases / genetics


  • Haptoglobins
  • Nitric Oxide
  • Peptidyl-Dipeptidase A