Effects of menstrual cycle and race on peripheral vascular alpha-adrenergic responsiveness.
Gender differences in the incidence of many cardiovascular diseases may be due to the effects of sex hormones. Both alpha(1)- and alpha(2)-adrenergic receptors produce vasoconstriction in peripheral blood vessels and have demonstrated gender effects in previous studies. In addition, race has been shown to influence the effects of some alpha-adrenergic stimuli. We therefore sought to determine the effects of the menstrual cycle and race on peripheral blood flow responses to the intra-arterial infusion of phenylephrine (alpha(1)-agonist) and clonidine (alpha(2)-agonist). Ten white and 8 black women were studied during the early luteal phase and the follicular phase; these phases were verified in each woman through measurements of plasma estradiol and progesterone. Plasma norepinephrine was measured with HPLC. During phenylephrine infusion, there was significantly greater vasoconstriction in the luteal phase versus the follicular phase (P<0.05). There were no differences (P>0.8) between white and black women. During clonidine infusion, white women showed significantly more vasoconstriction in the follicular phase than during the luteal phase (P<0.006). For black women, the responses for both phases did not differ (P>0.9). Blood pressures were significantly higher in the black women (diastolic P<0.005, systolic P<0.05). The luteal-phase elevation of alpha(1)-adrenergic responses may be due to elevated levels of estradiol, progesterone, or both. The lack of luteal-phase reduction in alpha(2)-adrenergic vasoconstriction in black women may contribute to their increased pressor responses to adrenergic stimuli.
Freedman
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Departments of Psychiatry and Behavioral Neurosciences and Obstetrics and Gynecology and Internal Medicine (Pulmonary), Wayne State University School of Medicine, Detroit, MI, USA. aa2613@wayne.edu
Girgis
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D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage; D000328:Adult; D000959:Antihypertensive Agents / Q000008:administration & dosage; D044383:Black People; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D003000:Clonidine / Q000008:administration & dosage; D004730:Endothelium, Vascular / Q000737:chemistry / Q000502:physiology; D004958:Estradiol / Q000097:blood; D005260:Female; D005385:Fingers / Q000098:blood supply; D005498:Follicular Phase / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000208:ethnology / Q000503:physiopathology; D008183:Luteal Phase / Q000502:physiology*; D009638:Norepinephrine / Q000097:blood; D010656:Phenylephrine / Q000008:administration & dosage; D011374:Progesterone / Q000097:blood; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D018341:Receptors, Adrenergic, alpha-2 / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects; D044465:White People
D000316:Adrenergic alpha-Agonists; D000959:Antihypertensive Agents; D018340:Receptors, Adrenergic, alpha-1; D018341:Receptors, Adrenergic, alpha-2; D010656:Phenylephrine; D011374:Progesterone; D004958:Estradiol; D003000:Clonidine; D009638:Norepinephrine