Apv. Dantas et al., Influence of female sex hormones on endothelium-derived vasoconstrictor prostanoid generation in microvessels of spontaneously hypertensive rats, HYPERTENSIO, 34(4), 1999, pp. 914-919
Citations number
30
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Although female sex hormones may attenuate endothelial dysfunction in spont
aneously hypertensive rats (SHR) by increasing endothelium-derived relaxing
factors (EDRFs), the influence of ovarian hormones on the generation of en
dothelium-derived contracting factors (EDCFs) remains unknown. The aim of t
his study was to evaluate the effect of estrogen and progesterone on the ge
neration of vasoconstrictor prostanoids and superoxide anion (O-2(-)) by mi
crovessels from SHR. Vascular reactivity to norepinephrine (NE), acetylchol
ine (ACh), and sodium nitroprusside (SNP) were evaluated in the mesenteric
arteriolar bed from estrous (OE) and ovariectomized (OVX) SHR. OVX-SHR were
treated for 24 hours or 15 days with estradiol and for 15 days with estrad
iol + progesterone. The vascular reactivity was evaluated in the absence or
presence of indomethacin (INDO, 10 mu mol/L) and sodium diclofenac (DIC, 1
0 mu mol/L), ridogrel (RID, 50 mu mol/L), dazoxiben (DAZ, 10 mu mol/L), or
superoxide dismutase (SOD, 100 U/mL). Prostanoid levels in the arteriolar p
erfusate of mesenteries with or without endothelium were measured by enzyme
immunoassay. An increased reactivity to NE and reduced sensitivity to ACh
were observed in microvessels from OVX-SHR compared with OE-SHR. There were
no differences in the responses to SNP. Treatments with estradiol and estr
adiol + progesterone similarly restored these altered responses. INDO, DIC,
RID, and SOD also restored the NE and ACh responses in OVX-SHR. DAZ had no
effect on the vascular reactivities. The release of PGF(2 alpha), but not
of TXB2 and 6-keto-PGF(1 alpha), was greater in OVX-SHR than in OE-SHR micr
ovessels with endothelium when stimulated by NE. This response was normaliz
ed by hormonal treatments. Neither NE nor ACh stimulated prostanoid product
ion by microvessels without endothelium. These results suggest that estroge
n may protect female SHR against severe hypertension partly by decreasing t
he synthesis of EDCFs such as PGH(2)/PGF(2 alpha) and O-2(-).