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离体兔心脏中激素选择性脂肪酶的激活

Hormone selective lipase activation in the isolated rabbit heart.

作者信息

Hsueh W, Isakson P C, Needleman P

出版信息

Prostaglandins. 1977 Jun;13(6):1073-91. doi: 10.1016/0090-6980(77)90135-6.

Abstract

The synthesis and release of PGs by the isolated perfused rabbit heart upon bradykinin stimulation results from lipase stimulation which liberates arachidonic acid for PG biosynthesis. The [14C]-labelled fatty acids, arachidonate, linoleate, and oleate, when infused into the heart preparation, were efficiently incorporated into the phospholipid pool in the heart mostly in the 2-position of phosphatidylcholine. On the other hand, [14C]-palmitate was esterified into both the 1- and the 2-position. Bradykinin released bioassayable PG when injected into the rabbit hearts, regardless of which fatty acid label was incorporated into the phospholipid pool. However, only [14C]-arachidonic acid (but not [14C]-linoleate, oleate or palmitate) was liberated from the variously labelled hearts upon hormone stimulation. This selective bradykinin effect on fatty acid release suggests that hormone stimulation either activates a specific lipase that distinguishes different fatty acids in the 2-position or activates lipase which is selectively compartmented with arachidonate-containing phospholipids. Ischemia, on the other hand, appeared to non-specifically stimulate tissue lipases, resulting in a non-selective release of oleic as well as arachidonic acid. A disproportionally large release of arachidonic acid was observed accompanying a relatively small PG (10:1 arachidonate: PG ratio) production during ischemia, as compared to bradykinin (3:1 ratio), suggesting distinct mechanisms for PG biosynthesis induced by bradykinin and ischemia.

摘要

缓激肽刺激下,离体灌注兔心脏中前列腺素(PGs)的合成与释放是由脂肪酶刺激引起的,脂肪酶刺激释放出花生四烯酸用于PG生物合成。将[14C]标记的脂肪酸、花生四烯酸、亚油酸和油酸注入心脏制剂后,它们大多在磷脂酰胆碱的2位被有效地掺入心脏的磷脂池中。另一方面,[14C]棕榈酸酯被酯化到1位和2位。无论磷脂池中掺入哪种脂肪酸标记,将缓激肽注入兔心脏时都会释放出可进行生物测定的PG。然而,在激素刺激下,只有[14C]花生四烯酸(而不是[14C]亚油酸、油酸或棕榈酸)从不同标记的心脏中释放出来。缓激肽对脂肪酸释放的这种选择性作用表明,激素刺激要么激活一种能区分2位不同脂肪酸的特异性脂肪酶,要么激活与含花生四烯酸的磷脂选择性分隔的脂肪酶。另一方面,缺血似乎非特异性地刺激组织脂肪酶,导致油酸和花生四烯酸的非选择性释放。与缓激肽刺激(3:1的比例)相比,缺血期间观察到花生四烯酸释放量相对较大,但PG生成量相对较小(花生四烯酸与PG的比例为10:1),这表明缓激肽和缺血诱导PG生物合成的机制不同。

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