Estrogen induces angiogenesis of the female rabbit bladder

Abstract

Postmenopausal bladder dysfunction has been speculated to involve decreased circulating estrogen levels. It is our hypothesis that estrogen induces bladder dysfunctions by modulating blood flow to the bladder, i.e. low estrogen reduces blood flow to the bladder, whereas high estrogen increases blood flow. Our previous studies have demonstrated that estrogen administration in female rabbits induces a 'functional hypertrophy' of the urinary bladder smooth muscle represented by increased smooth muscle mass, which corresponds to increased contractile responses to all forms of stimulation. The present study investigates the effect of estrogen on vasculature density and distribution. Twentyfour female New Zealand white rabbits were separated into six groups of four rabbits each. Group 1 served as controls. Groups 2-6 were ovariectomized. Two weeks after ovariectomy (Ovx), groups 3-6 were given 17-b estradiol(1 mg/kg per day) by s.c. implant for 1, 3, 7, and 14 days respectively. Blood vessel density and distribution were evaluated by immunohistochemistry and quantitative image analyses. Ovx resulted in significant vascular degeneration and decreased density, whereas estradiol administration mediated a significant angiogenic effect characterized by increased vascular density, and distribution of new vasculature within the smooth muscle bundles of the detrusor. Estradiol-induced vasculogenesis corresponds with our previously demonstrated increase in blood flow to the bladder and increased contractility. The most interesting aspect of these studies is the increased vascularization localized within the muscle bundles rather than between the muscle bundles, which may be important in the link between estrogen and increased incidence of cancers.

Comparison of urodynamic effects of phytoestrogens equol, puerarin and genistein with these of estradiol 17β in ovariectomized rats

“…2 vP and uP in ovx control animals are considerably lower than in E2 treated animals which confirms our previous observation. The increased bladder and urethral pressure are most likely due to increased muscular activity as a higher muscle mass of the detrusor and sphincter and higher blood supply was reported in ovx-E2 in comparison to untreated animals (Aikawa et al, 2003;Lin et al, 2006a;Lin et al, 2006b;Lin et al, 2006c). It appears that the 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 6 phytoestrogens have similar, though weaker effects in the detrusor than in the sphincter apparatus.…”

Combined usage of estrogen and melatonin restores bladder contractility and reduces kidney and bladder damage in ovariectomized and pinealectomized rat

“…Also, previous studies suggested that Ovx can cause a decreased of blood fl ow around the bladder neck and urethra, mucosal and smooth muscle atrophy, increased collagen synthesis and distribution, and decreased contractility. Estrogen replacement reduced the effects of Ovx and resulted in smooth muscle hypertrophy and enhanced contractility (27). Also it has been reported that estrogen mediates angiogenesis accounting for the increased vascular density and increased blood fl ow.…”

The immediate effect of nitric oxide on the rabbit bladder after ovariectomy

“…Estrogen is essential for the mainenance of physiological function of the female urogenital tract. Previous studies have shown that bladder blood flow is regulated, in part, by estrogen [1]. In previous reports, ovariectomy resulted in decreased blood flow and hypoxia to the bladder mucosa and a mildly decreased blood flow to the smooth muscle as early as post-ovariectomy day 1.…”