Linked Life Data

7515323

Source:http://linkedlifedata.com/resource/pubmed/id/7515323

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pubmed-article:7515323pubmed:abstractTextWe studied whether primary cultured porcine brain capillary endothelial cells (PBCEC) respond to bradykinin with an enhanced intracellular cytosolic calcium concentration [Ca2+]i with subsequent formation of nitric oxide (NO) and prostacyclin (PGI2). In addition we examined whether these cells synthetize and release kinins that may accumulate during angiotensin-converting enzyme (ACE) inhibition. [Ca2+]i was assessed by the fluorescent dye Fura-2, NO formation by determination of intracellular cyclic GMP and PGI2 by a specific radioimmunoassay for 6-ketoprostaglandin F1 alpha. Bradykinin and the ACE inhibitor ramiprilat concentration-dependently increased the formation of cyclic GMP which was completely prevented by the stereospecific inhibitor of NO synthase, NG-nitro-L-arginine. Also the specific B2-kinin receptor antagonist icatibant (Hoe 140) abolished the increase in cyclic GMP as well as the ramiprilat-induced increase in PGI2 formation. The data demonstrate the existence of B2-kinin receptors and ACE activity in PBCEC. Moreover PBCEC are capable of producing and releasing kinins in amounts that lead via stimulation of B2-kinin receptors to an enhanced [Ca2+]i as well as NO and PGI2 synthesis and release, provided that degradation of kinins is prevented by inhibition of endothelial ACE activity.lld:pubmed
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pubmed-article:7515323pubmed:articleTitleEnhancement of cytosolic calcium, prostacyclin and nitric oxide by bradykinin and the ACE inhibitor ramiprilat in porcine brain capillary endothelial cells.lld:pubmed
pubmed-article:7515323pubmed:affiliationHoechst AG, SBU Cardiovascular Agents, Frankfurt/Main, Germany.lld:pubmed
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