期刊
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
卷 279, 期 3, 页码 F544-F551出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.2000.279.3.F544
关键词
kidney; arachidonic acid metabolism; angiotensin II receptors; arteries; gas chromatography-mass spectroscopy
资金
- NHLBI NIH HHS [HL-25394, HL-34300] Funding Source: Medline
We studied hydroxyeicosatetraenoic acid (HETE) release in response to ANG II from preglomerular microvessels (PGMVs), the vascular segment governing changes in renal vascular resistance. PGMVs were isolated from Sprague-Dawley rats and incubated with NADPH and hormones at 37 degrees C. Eicosanoids were extracted, and cytochrome P-450 (CYP)-derived HETEs were purified and quantitated by negative chemical ionization gas chromatography-mass spectroscopy. PGMVs produced primarily 20- and 19-HETEs, namely, 7.9 +/- 1.7 and 2.2 +/- 0.5 ng/mg protein, respectively. ANG II (5 nM) increased CYP-HETE release by two- to threefold; bradykinin, phenylephrine, and Ca2+ ionophore were without effect. [Sar(1)]ANG II (0.1-100 mu M) dose dependently stimulated 19- and 20- HETEs, an effect blocked by the AT(2)-receptor antagonist PD-123319 as well as by U-73122, a phospholipase C inhibitor. Microvascular 20- HETE release was increased more than twofold by the third day in response to ANG II (120 ng.kg(-1).min(-1)) infused subcutaneously for 2 wk; it was not further enhanced after 14 days, although blood pressure continued to rise. Thus an AT(2)-phospholipse C effector unit is associated with synthesis of a vasoconstrictor product, 20- HETE, in a key renovascular segment.
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