The effect of long term nicotine exposure on endothelial function in rats


MIZRAK S., Göksel Ülker S., Ercan G., Sönmez B.

Drug and Chemical Toxicology, vol.45, no.4, pp.1522-1527, 2022 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 45 Issue: 4
  • Publication Date: 2022
  • Doi Number: 10.1080/01480545.2020.1845714
  • Journal Name: Drug and Chemical Toxicology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, Environment Index, Food Science & Technology Abstracts, International Pharmaceutical Abstracts, MEDLINE, Veterinary Science Database
  • Page Numbers: pp.1522-1527
  • Keywords: endothelial function, NADPH oxidases, Nicotine, nitric oxide, nitric oxide synthase
  • Uşak University Affiliated: Yes

Abstract

Nicotine is one of the main chemicals in the cigarettes responsible for addiction formation. Many researches investigating the effects of nicotine on coronary heart disease and atherosclerosis have been published. The robustness of endothelial cells is very important in the development of atherosclerosis. The aim of this study is to evaluate the effect of nicotine exposure on the indicators of endothelial function either by examining the vascular reactivity of aorta taken from rats exposed to nicotine during prenatal (starting by the mating period) and postnatal periods (6 weeks after delivery), or by determining the protein expression of nitric oxide synthase (NOS) enzymes, NADPH oxidase (Nox) and nitrotyrosine. Chronic nicotine exposure at 6 mg/L in drinking water produced a significant decrease in phenylephrine contractility of thoracic aortic rings compared to control and low dose exposure group (0.4 mg/L, p < 0.001). Endothelium-dependent relaxations to acetylcholine increased dose-dependently while no changes were observed in endothelium-independent relaxations to sodium nitroprusside and protein expressions in rat thoracic aorta. It has been concluded that long term nicotine exposure does not have serious effects on endothelial vasodilator response directly and does not change protein expression of NOS or Nox enzymes. However, more studies should be done for the exact mechanisms responsible for the effect of nicotine on endothelial function.