Faculdade de Odontologia de Bauru - Universidade de São Paulo - Ciências Biológicas - Farmacologia, Bauru, SP - Brazil.
Programa Conjunto de Pós-Graduação em Ciências Fisiológicas - Departamento de Educação Física - Faculdade de Ciências - Universidade Estadual de São Paulo, Bauru, SP - Brazil.
Arq Bras Cardiol. 2020 Feb;114(2):295-303. doi: 10.36660/abc.20180433.
Cigarette smoking is usually associated with hypertension and may modify vasoconstrictor response.
The present study aimed to analyze and compare the interaction of passive cigarette smoking and hypertension on epinephrine and felypressin blood pressure effects after intravascular injection.
45-day male Wistar rats had the main left renal artery partially constricted and the right kidney removed (1K1C model). Rats were placed in the chamber for exposition to passive cigarette smoking (10 cigarettes) during 10 min (6 days a week). Hypertensive rats received atenolol (90 mg/kg/day) by gavage for two weeks. Hypotensive and hypertensive response, response duration and heart rate were recorded from direct blood pressure values. The significance level was 5%.
Passive cigarette smoking increased maximal hypertensive response to epinephrine in normotensive and 1K1C-atenolol treated rats and to felypressin only in 1K1C-atenolol treated rats; it also reduced epinephrine hypotensive response. Epinephrine increased heart rate in normotensive and hypertensive passive smokers or non-smoker rats. Comparing the two vasoconstrictors, epinephrine showed greater hypertensive response in normotensive smokers, 1K1C-atenolol treated smokers and non-smokers. However, in normotensive-nonsmoker rats, felypressin showed a greater and longer hypertensive effect.
Our results suggest that passive cigarette smoking may reduce epinephrine vasodilation and increase hypertensive response when compared to felypressin. Therefore, felypressin may be safe for hypertensive patients to avoid tachycardia and atenolol interaction, but for normotensive and non-smoker patients, epinephrine may be safer than felypressin.
吸烟通常与高血压有关,并可能改变血管收缩反应。
本研究旨在分析和比较被动吸烟与高血压对血管内注射后肾上腺素和菲莱普辛血压效应的相互作用。
45 天雄性 Wistar 大鼠部分结扎左肾动脉并切除右肾(1K1C 模型)。大鼠被放置在室内暴露于被动吸烟(10 支香烟)10 分钟(每周 6 天)。高血压大鼠给予阿替洛尔(90mg/kg/天)灌胃 2 周。通过直接血压值记录低血压和高血压反应、反应持续时间和心率。显著性水平为 5%。
被动吸烟增加了正常血压和 1K1C-阿替洛尔治疗大鼠对肾上腺素的最大高血压反应,以及仅在 1K1C-阿替洛尔治疗大鼠中对菲莱普辛的高血压反应;它还降低了肾上腺素的降压反应。肾上腺素增加了正常血压和高血压吸烟者或非吸烟者的心率。比较两种血管收缩剂,肾上腺素在正常血压吸烟者、1K1C-阿替洛尔治疗的吸烟者和非吸烟者中显示出更大的高血压反应。然而,在正常血压非吸烟者的大鼠中,菲莱普辛显示出更大和更长的高血压作用。
我们的结果表明,与菲莱普辛相比,被动吸烟可能会减少肾上腺素的血管扩张作用并增加高血压反应。因此,菲莱普辛可能对高血压患者是安全的,以避免心动过速和阿替洛尔的相互作用,但对于正常血压和非吸烟者,肾上腺素可能比菲莱普辛更安全。