Prostatic ischemia induces ventral prostatic hyperplasia in the SHR; possible mechanism of development of BPH.
In the light of increasing evidence that benign prostatic hyperplasia is associated with cardiovascular disease, we have investigated the relationship between prostatic blood flow and prostatic hyperplasia in the spontaneously-hypertensive-rat (SHR). Twelve-week-old male SHRs were treated with nicorandil for six weeks. Wistar-Kyoto rats were used as controls. Six weeks after nicorandil treatment, blood pressure and the prostatic blood flow were estimated, and tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, dihydrotestosterone, and α-SMA were measured. SHRs showed significant increases in blood pressure, tissue levels of malondialdehyde, HIF-1α, TGF-β1, bFGF, α-SMA and a significant decrease in the prostatic blood flow. Although treatment with nicorandil failed to alter the blood-pressure and α-SMA, it significantly ameliorated the increased levels of malondialdehyde, HIF-1α, TGF-β1, and bFGF. There were no significant differences in tissue levels of dihydrotestosterone among any groups. These data indicate that development of prostatic hyperplasia may be associated with prostatic hypoxia, which nicorandil prevents via its effect to increase the blood flow.
Department of Pharmacology, Kochi University School of Medicine, Nankoku, 783-8505, Japan.
Motoaki
M
Saito
1] Division of Urology, Tottori University School of Medicine, 36-1 Nishi-cho, Yonago, 683-8503, Japan [2] Division of Molecular Pharmacology, Tottori University School of Medicine, 86 Nishi-cho, Yonago, 683-8503, Japan.
Panagiota
P
Tsounapi
Division of Molecular Pharmacology, Tottori University School of Medicine, 86 Nishi-cho, Yonago, 683-8503, Japan.
Ryo
R
Oikawa
Division of Molecular Pharmacology, Tottori University School of Medicine, 86 Nishi-cho, Yonago, 683-8503, Japan.
Shogo
S
Shimizu
Division of Urology, Tottori University School of Medicine, 36-1 Nishi-cho, Yonago, 683-8503, Japan.
Masashi
M
Honda
Division of Urology, Tottori University School of Medicine, 36-1 Nishi-cho, Yonago, 683-8503, Japan.
Takehiro
T
Sejima
Division of Molecular Pharmacology, Tottori University School of Medicine, 86 Nishi-cho, Yonago, 683-8503, Japan.
Yukako
Y
Kinoshita
Division of Molecular Pharmacology, Tottori University School of Medicine, 86 Nishi-cho, Yonago, 683-8503, Japan.
Shuhei
S
Tomita
D000199:Actins / Q000378:metabolism; D000818:Animals; D015415:Biomarkers / Q000378:metabolism*; D001794:Blood Pressure; D013196:Dihydrotestosterone / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006973:Hypertension / Q000150:complications*; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007511:Ischemia / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress; D011467:Prostate / Q000378:metabolism / Q000473:pathology*; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000473:pathology; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D012039:Regional Blood Flow; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
D000199:Actins; D015415:Biomarkers; D013196:Dihydrotestosterone; D016222:Fibroblast Growth Factor 2; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D008315:Malondialdehyde; D053773:Transforming Growth Factor beta1; C497444:Hif1a protein, rat; C498862:Acta2 protein, rat