Vasodilation In Women Research Articles

Water immersion in preeclampsia

Preeclampsia is associated with profound vasoconstriction in most organ systems and reduced plasma volume. Because water immersion produces a marked central redistribution of blood volume and suppresses the renin-angiotensin system response and sympathetic activity, we hypothesized that water immersion might be useful in the treatment of preeclampsia. The effects of thermoneutral water immersion for 3 hours on central and peripheral hemodynamics were evaluated in 7 preeclamptic patients, 7 normal pregnant control patients, and 7 nonpregnant women. Finger plethysmography was used to determine hemodynamic measurements (cardiac output and total peripheral resistance), and forearm blood flow was measured by strain gauge plethysmography. Postischemic hyperemia was used to determine endothelium-dependent vasodilation. Analysis was by analysis of variance for repeated measurements. During water immersion cardiac output increased while diastolic blood pressure and heart rate decreased, although systolic blood pressure remained unchanged in each group. Forearm blood flow increased significantly in the normal pregnant and preeclamptic subjects. Total peripheral resistance decreased in all groups, but values in preeclamptic patients remained above those of normotensive pregnant women. Water immersion had no effect on endothelium-dependent vasodilation in the preeclamptic group, and most hemodynamic changes that were observed reversed to baseline within 2 hours of completion of the procedure. Although water immersion results in hemodynamic alterations in a manner that is theoretically therapeutic for women with preeclampsia, the effect was limited and short-lived. In addition water immersion had no effect on endothelium-dependent vasodilation in women with preeclampsia. The therapeutic potential for water immersion in preeclampsia appears to be limited.

Differences in the postexercise threshold for cutaneous active vasodilation between men and women

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at approximately 34 degrees C for 15 min. Mean skin temperature was then increased at a rate of 4.3 +/- 0.8 degrees C/h while local skin temperature was clamped at 34 degrees C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact alpha-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 +/- 0.08 degrees C and 37.58 +/- 0.04 degrees C for UT and BT, respectively) was greater than that measured in men (37.33 +/- 0.06 degrees C and 37.35 +/- 0.06 degrees C for UT and BT, respectively) (P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 +/- 4 beats/min) and women (87 +/- 6 beats/min) were elevated above baseline (61 +/- 3 and 68 +/- 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 +/- 3 mmHg) and women (79 +/- 3 mmHg) was reduced from baseline (93 +/- 3 and 93 +/- 4 mmHg for men and women, respectively) (P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women (P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 +/- 0.03 degrees C and 37.16 +/- 0.04 degrees C, respectively) and women (37.36 +/- 0.05 degrees C and 37.42 +/- 0.03 degrees C, respectively) were elevated above no exercise (36.94 +/- 0.07 degrees C and 36.97 +/- 0.05 degrees C for men and 36.99 +/- 0.09 degrees C and 37.03 +/- 0.11 degrees C for women for the UT and BT sites, respectively) (P < 0.05). A difference in the magnitude of the thresholds was measured between women and men (P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.

Raloxifene does not influence flow-mediated endothelium-dependent and endothelium-independent vasodilatation of osteopenic postmenopausal women

Objective: The study was undertaken to evaluate whether raloxifene influences endothelium-dependent and endothelium-independent vasodilatation in women. Study design: In a double-blind, placebo-controlled randomized study, 30 osteopenic but otherwise healthy postmenopausal women received either placebo (n = 15 with one dropout) or raloxifene (60 mg/d, n = 15). Brachial artery flow-mediated endothelium-dependent and endothelium-independent vasodilatation was evaluated by ultrasound before and after 6 months of treatment, along with lipid and glucose metabolism. Endothelium-dependent dilatation was evaluated after a 4-minute block of artery blood flow through a cuff insufflated at suprasystolic blood pressure. Endothelium-independent vasodilatation was evaluated after sublingual nitroglycerin administration (400 μg). Results: Placebo did not modify any vascular or metabolic parameter. Raloxifene significantly decreased low-density lipoprotein levels (4.60 ± 0.18 mmol/L vs 3.94 ± 0.30 mmol/L, P < .015) but did not modify endothelium-dependent (21.6% ± 4.6% vs 20.6% ± 3.8%) or endothelium-independent vasodilatation (26.3% ± 5.1% vs 32.0% ± 5.5%). Conclusion: Prolonged administration of raloxifene does not influence endothelium-dependent and endothelium-independent vasodilatation of osteopenic but otherwise healthy postmenopausal women. (Am J Obstet Gynecol 2003;188:313-7.)

Evidence that parenteral testosterone therapy may improve endothelium-dependent and -independent vasodilation in postmenopausal women already receiving estrogen.

The gender difference in cardiovascular disease has been partly attributed to higher androgenic hormone levels. Although testosterone in women may not affect lipids, it remains unknown whether it negates favorable estrogenic effects on endothelial function. We have investigated the effects of testosterone implant therapy on arterial reactivity encompassing endothelial-dependent and -independent vasodilation in women using hormone replacement therapy (HRT). B-mode ultrasound measurements of resting brachial artery diameter, following reactive hyperemia [endothelium-dependent flow- mediated dilation (FMD)] and following glyceryl trinitrate (GTN) (endothelium-independent dilation), were recorded in 33 postmenopausal women stabilized on HRT (>6 months), at baseline, and 6 weeks after a testosterone implant (50 mg), with 15 postmenopausal nonusers of HRT serving as controls. In the brachial artery, baseline resting diameter was similar (0.40 +/- 0.01 vs. 0.41 +/- 0.01 cm, P = 0.5). In the treated group, testosterone levels increased (0.99 +/- 0.08 to 4.99 +/- 0.3 nmol/L, P < 0.001), associated with a mean 42% increase in FMD (6.4% +/- 0.7 to 9.1% +/- 1.1, P = 0.03). The control group did not change (8.1% +/- 1.4 to 5.6% +/- 1.0, P = 0.4). ANOVA of repeated measures (P = 0.04) and mean change (P = 0.02) in FMD both demonstrated significantly greater improvement with testosterone compared with controls. GTN induced vasodilation increased with testosterone treatment (14.9% +/- 0.9 to 17.8% +/- 1.2, P = 0.03). Our preliminary data indicate that parenteral testosterone therapy improves both endothelial-dependent (flow-mediated) and endothelium-independent (GTN-mediated) brachial artery vasodilation in postmenopausal women using long-term estrogen therapy. The mechanisms underlying these potentially beneficial cardiovascular effects require further investigation.

Effect of long-term estrogen therapy on brachial arterial endothelium-dependent vasodilation in women with Raynaud’s phenomenon secondary to systemic sclerosis

Endothelium-dependent and endothelium-independent dilation were reduced in patients with Raynaud's phenomenon secondary to systemic sclerosis. Conjugated estrogen given for 4 weeks significantly improved endothelial function compared with placebo.

Gender Difference in Improvement of Endothelium-Dependent Vasodilation After Estrogen Supplementation

Objectives. We examined whether there is a gender difference in the improvement of endothelium-dependent vasodilation after estrogen supplementation.Background. Estrogen therapy reduces the risk of cardiovascular events in postmenopausal women, and the augmented release of endothelium-derived nitric oxide (NO) by estrogens has been suggested to be one of the mechanisms for the cardioprotective effects of estrogen.Methods. With ultrasound technique, we measured the diameter and blood flow of the brachial artery at rest, during reactive hyperemia after transient occlusion and after nitroglycerin administration before and after estradiol supplementation in 15 postmenopausal women (mean 63 years) and in 15 men matched for age and risk factors for atherosclerosis.Results. Estradiol supplementation augmented the flow-mediated vasodilation and serum level of nitrite/nitrate (metabolites of NO) in women (respectively, from a mean ± SEM of 8.0 ± 0.6% to 12.9 ± 0.6% [p < 0.01 by analysis of variance (ANOVA)] and from 64.9 ± 8.7 to 93.7 ± 9.4 μmol/liter [p < 0.05 by ANOVA]) but not in men (respectively, from 8.1 ± 0.6% to 8.3 ± 0.7% and from 57.8 ± 6.7 to 60.8 ± 5.4 μmol/liter). The increases in blood flow during reactive hyperemia and in diameter after nitroglycerin administration were not affected by estradiol supplementation in either men or women.Conclusions. Estradiol supplementation improves endothelium-dependent vasodilation in women, probably because of augmented NO production/release, but not in men. Thus, there may be gender differences in the effects of estrogen therapy on endothelial functions and NO production/release.