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Perinatal development influences mechanisms of bradykinin-induced relaxations in pulmonary resistance and conduit arteries differently



Perinatal development influences mechanisms of bradykinin-induced relaxations in pulmonary resistance and conduit arteries differently



Cardiovascular Research 51(1): 140-150



Objective: As bradykinin (BYK) relaxes conduit (EPA) and resistance (RPA) pulmonary arteries from both perinatal and adult lungs, we investigated whether this vasodilator's relaxation-mechanisms were altered during perinatal development, differed between EPA and RPA and differed with other endothelium-dependent vasodilators, acetyicholine (ACH) and substance P (SP). Methods: Arteries from mature foetal (5 days), neonatal (apprxeq5 min), newborn (60-84 h) and adult pigs: (gtoreq6 months) were isolated, mounted for in vitro isometric force recording, activated with PGF2alpha (30 mumol/l) and relaxed with BYK (10 pmol/l-1 mumol/l), SP (10 pmol/1-0.1 mumol/l) or ACH (1 nmol/l-1 mmol/l). Results: (i) BYK: L-NAME (100 mumol/l) attenuated relaxations in foetal EPA (apprxeq55%) but nearly abolished them in the adult (apprxeq80%). In RPA, L-NAME nearly abolished (apprxeq90%) relaxations in the foetus and this effect diminished progressively with age to apprxeq20% in the adult. Indomethacin (IND, mumol/l) attenuated relaxations in neonatal (apprxeq25%), new-born and adult EPA (both apprxeq45%). Together, L-NAME and IND abolished relaxations in all EPA and in neonatal RPA but not in older RPA. SKF525a (100 mumol/l) attenuated relaxations in foetal RPA (apprxeq4%), diminishing in the adult RPA to apprxeq10%. Together, SKF52Sa and L-NAME largely abolished relaxations in postnatal RPA (apprxeq80%). Activation with K+=125 mmol/l attenuated relaxations in adult EPA (apprxeq80%), foetal RPA (apprxeq45%) and neonatal RPA (apprxeq75%) and abolished relaxations in RPA from older ages. (ii) ACH: L-NAME abolished relaxations in new-born EPA and RPA. In adult EPA, combined L-NAME and IND moderately attenuated relaxations. (iii) SP: Combined application of L-NAME and IND attenuated relaxations to a similar degree in new-born and adult EPA and RPA. Conclusions: In postnatal EPA, BYK-relaxations depend completely on prostaglandin- and NO-synthesis whereas those to SP (at all ages) and ACH (in the adult) do not. In RPA, BYK-relaxations develop from being completely dependant on the sole release of NO (foetus) to being almost completely independent of it (adult), a situation mimicked partially by SP but not by ACH, which, in new-born RPA is completely dependent on NO. BYK-relaxations in postnatal RPA depend on the release of a hyperpolarising factor generated through an SKF525a-sensitive pathway in conjunction with NO. The mechanisms of endothelium-dependent BYK-relaxations in the pulmonary vascular bed undergo diverging alterations, depending on the stage of development and arterial size/function. These changes are specific for BYK as they differ from those obtained from ACH or SP.

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Accession: 011130546

Download citation: RISBibTeXText

PMID: 11399256

DOI: 10.1016/s0008-6363(01)00275-9


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