Regulation of phospholipid degradation and biosynthesis in the heart by isoprénaline: effect of mepacrine

Title:

Regulation of phospholipid degradation and biosynthesis in the heart by isoprénaline: effect of mepacrine

Creator:

Nováková, O., Drnková, J., Kubišta, V., and Novák, F.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:be450450-5844-4143-b5c9-ebf65f664e56
uuid:be450450-5844-4143-b5c9-ebf65f664e56

Subject:

phospholipids, mepacrine, isoprénaline, and heart

Type:

article, model:article, and TEXT

Description:

We investigated the effect of isoprénaline (IPRO), a /J-mimetic catecholamine, on incorporation of (32P)Pi into phospholipids of the mouse left ventricle in uiuo. All experimental groups of male mice received an injection of (32p)pi ^250 MBq x kg“1 b.w.) intraperitoneally two hours prior to sacrifice. A single dose of IPRO (5 mg x kg-1 b.w.) was injected one hour before killing. IPRO increased the specific radioactivity of phosphatidylcholine (PC) by a factor of 1.8, diphosphatidylglycerol (DPG) 2.1, sphingomyelin (SM) 3.5, phosphatidylinositol (PI) 1.7, phosphatidylserine (PS) 1.7, phosphatidylglycerol (PG) 1.7, phosphatidic acid (PA) 2.0 compared to control values. On the other hand, IPRO is also known to stimulate phospholipid degradation by activation of phospholipase A2. That is why we used mepacrine (50 mg x kg“1 b.w.), a phospholipase inhibitor, to find a possible link between biosynthesis and degradation of phospholipids. Pretreatment with mepacrine two hours prior to sacrifice suppressed IPRO stimulated incorporation of (32P)Pi into phospholipids nearly to control levels. Mepacrine itself did not significantly influence the specific radioactivity of phospholipids. We conclude that phospholipase A2 inhibitor, mepacrine, is able to prevent IPRO-stimulated ¡corporation into phospholipids, suggesting a feedback relation between their biosynthesis and degradation in the myocardium.

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 1994 Volume:43 | Number:3

Harvested from:

CDK

Metadata only:

false