Gender differences in the vasomotor effects of different steroid hormones in rat pulmonary and coronary arteries

被引:103
作者
English, KM
Jones, RD
Jones, TH
Morice, AH
Channer, KS
机构
[1] Royal Hallamshire Hosp, Dept Cardiol, Sheffield S10 2JF, S Yorkshire, England
[2] Univ Sheffield, Dept Human Metab & Clin Biochem, Sheffield, S Yorkshire, England
[3] Univ Hull, Acad Dept Med, Kingston Upon Hull HU6 7RX, N Humberside, England
关键词
vasoactive agents; arteries; hormones; vasodilatation; rat;
D O I
10.1055/s-2001-18689
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is well recognised that oestrogens possess vasodilatory properties, and similar responses to testosterone have been demonstrated. However, vasomotor effects of other steroid hormones have not been well described. Direct comparisons of the relative vasoactivity of different steroid hormones in different vascular beds in male and female genders have not been made. Coronary and pulmonary arteries from adult Wistar rats were mounted in a wire myograph, loaded to 100 and 17 mmHg respectively, maximally pre-contracted with 1 X 10(-4) M prostaglandin-F-2-alpha, and dose response curves to 1 X 10(-6) to 1 X 10(-3) or 3 X 10(-3) M of 17 beta -oestradiol, testosterone, progesterone, and cortisol dissolved in water were constructed. Addition of each steroid hormone caused acute, dose dependent dilatation in coronary and pulmonary vessels. In coronary arteries the order of activity was testosterone > progesterone > 17 beta -oestradiol > cortisol, p > 0.001. In pulmonary arteries, the order of activity was progesterone > testosterone > cortisol > 17 beta -oestradiol, p < 0.001. Pulmonary arteries from male animals were more sensitive to the effects of testosterone than those from female animals, p = 0.003, whereas coronary arteries from female animals were more sensitive to the effects of 17 beta -oestradiol than those from male animals, p < 0.001. We have demonstrated significant differences in the in vitro vasomotor effects of different steroid hormones in two distinct vascular beds. Gender differences in vasomotor responses to steroid hormones may play a role in the aetiology of vasospastic diseases.
引用
收藏
页码:645 / 652
页数:8
相关论文
共 27 条
[1]   Beneficial effect of treatment with transdermal estradiol-17-beta on exercise-induced angina and ST segment depression in syndrome X [J].
Albertsson, PA ;
Emanuelsson, H ;
Milsom, I .
INTERNATIONAL JOURNAL OF CARDIOLOGY, 1996, 54 (01) :13-20
[2]   THE EFFECTS OF SINGLE ORAL DOSES OF 17-BETA-ESTRADIOL AND PROGESTERONE ON FINGER SKIN CIRCULATION IN HEALTHY WOMEN AND IN WOMEN WITH PRIMARY RAYNAUDS-PHENOMENON [J].
BARTELINK, ML ;
WOLLERSHEIM, H ;
VEMER, H ;
THOMAS, CMG ;
DEBOO, T ;
THIEN, T .
EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY, 1994, 46 (06) :557-560
[3]  
BARTELINK ML, 1992, NETH J MED, V41, P149
[4]  
BRAY K, 1991, BRIT J PHARMACOL, V102, P85
[5]   Testosterone induces dilation of canine coronary conductance and resistance arteries in vivo [J].
Chou, TM ;
Sudhir, K ;
Hutchison, SJ ;
Ko, E ;
Amidon, TM ;
Collins, P ;
Chatterjee, K .
CIRCULATION, 1996, 94 (10) :2614-2619
[6]   PREGNANCY-RELATED AND GENDER-RELATED CHANGES IN PULMONARY VASCULAR REACTIVITY [J].
CUTAIA, M ;
FRIEDRICH, P ;
GRIMSON, R ;
PORCELLI, RJ .
EXPERIMENTAL LUNG RESEARCH, 1987, 13 (03) :343-357
[7]   PRIMARY PULMONARY-HYPERTENSION AND PREGNANCY [J].
DAWKINS, KD ;
BURKE, CM ;
BILLINGHAM, ME ;
JAMIESON, SW .
CHEST, 1986, 89 (03) :383-388
[8]   Low-dose transdermal testosterone therapy improves angina threshold in men with chronic stable angina - A randomized, double-blind, placebo-controlled study [J].
English, KM ;
Steeds, RP ;
Jones, TH ;
Diver, MJ ;
Channer, KS .
CIRCULATION, 2000, 102 (16) :1906-1911
[9]   Non-genomic effects of estrogen and the vessel wall [J].
Farhat, MY ;
AbiYounes, S ;
Ramwell, PW .
BIOCHEMICAL PHARMACOLOGY, 1996, 51 (05) :571-576
[10]   Effect of dehydroepiandrosterone on hypoxic pulmonary vasoconstriction:: A Ca2+-activated K+-channel opener [J].
Farrukh, IS ;
Peng, W ;
Orlinska, U ;
Hoidal, JR .
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, 1998, 274 (02) :L186-L195