Effects of long-term @entity172 replacement therapy versus combined hormone replacement therapy on XXXX -dependent vasomotor function.

@entity172 @entity1 @entity2691 @entity1507 @entity2692 @entity7707 @entity842
Postmenopausal hormone replacement therapy (HRT) with @entity172 may increase production of the predominant endothelium-derived vasodilator @entity842 (NO) and consequently improve vascular reactivity. In contrast, concurrent progestin therapy may oppose this beneficial effect. We studied the effect of long-term @entity172 HRT and combined HRT on vasomotor function and on plasma @entity1507 , which reflects the amount of NO in the circulation. As lipid peroxidation affects NO production and impairs endothelial function, we also measured the amount of the in vivo lipid peroxidation marker urinary 8-iso-prostaglandin F(2 alpha). The study group comprised 15 @entity1 receiving @entity2691 HRT (mean age, 56 yr; treatment duration, 10.5 yr) and 15 @entity1 receiving combined HRT with @entity2691 and @entity2692 (mean age, 58 yr; treatment duration, 11.3 yr). The peak flow velocity (PFV) and pulsatility index of the common carotid and internal carotid artery and the abdominal aorta were measured by ultrasonography after long-term HRT (baseline), after a 4-wk pause and again 3 wk after reintroducing HRT. A statistically significant interaction between the groups and time points was observed in the PFV of the internal carotid artery (P = 0.011). In @entity1 taking @entity2691 , the PFV values decreased significantly after withdrawal of HRT (P = 0.007) and increased again to the baseline level after reintroduction of therapy (P < 0.001). In @entity1 receiving combined HRT, the PFV remained stable over all study periods. At baseline, the PFV of @entity1 taking @entity2691 correlated with the plasma @entity1507 concentration in the common carotid artery (r = 0.646; P = 0.009) and in the abdominal aorta (r = 0.579; P = 0.024). For pulsatility index and urinary @entity7707 excretion, there were no significant differences between the groups. Our results suggest that the favorable effects of long-term @entity172 treatment on blood flow are at least partly mediated through NO. The addition of levonorgestrel to the treatment regimen appears to abolish this effect.
