In vivo transfer of antisense oligonucleotide against urinary kininase blunts deoxycorticosterone acetate-salt hypertension in rats
作者： Izumi Hayashi , Masataka Majima , Tomoe Fujita , Toshiaki Okumura , Yuji Kumagai
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摘要: We have previously reported that the renal kallikrein-kinin system suppressed development of deoxycorticosterone acetate (DOCA)-salt hypertension. Kinins were degraded in kidney mainly by carboxypeptidase Y (CPY)-like kininase. Blockade kinin degradation may reduce hypertension developmental stage. constructed an antisense oligonucleotide against rat CPY homologue (5'-CAT-CTC-TGC-TTC-CTT-GTG-TC-3', AS) and its randomized control (5'-TCC-TTC-CTG-CTT-GAG-TTC-CT-3', RC), prepared HVJ-liposome complex prolongs increases effectiveness oligonucleotide. Antisense was transfected (25 nmole rat(-1), terms nucleotide) into from artery. Blood pressure measured through a catheter inserted abdominal aorta. Mean blood (MBP) DOCA-salt treated (for 2 weeks) Sprague Dawley strain rats 130+/-3 mmHg (n=11), reduced significantly (P<0.05) more AS transfection (122+/-4 mmHg, n=6) than RC treatment (137+/-6 n=5) 4 days after transfection. This reduction MBP accompanied increased urinary sodium excretion (AS, 8.4+/-1.5 mmole day(-1); RC, 4.6+/-0.5 day(-1), P<0.05) CPY-like kininase activity. Ebelactone B (5 mg kg(-1), twice day, p.o.), inhibitor for kininase, also induced natriuresis to same degree as AS. Lisinopril, angiotensin converting enzyme (ACE) failed elevated MBP. These results suggest contribution ACE degrade kidney, knockdown partly prevent
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