Preservation of Adrenoceptor and Endothelin Receptor Mediated Vasoconstriction and of Endothelium-Dependent Relaxation after Cold Storage of Explanted Blood Vessels for ex vivo Analyses

Abstract

<b><i>Introduction:</i></b> Adrenoceptor and endothelin (ET) receptor-mediated vasoconstriction as well as endothelium-dependent vasodilation of human saphenous veins were compared before and after 20 h of cold storage. <b><i>Methods:</i></b> Contractile responses to potassium chloride (KCl), norepinephrine (NE), and ET-1 as well as vasodilator responses to acetylcholine (ACh) were evaluated. <b><i>Results:</i></b> Storage in HEPES-supplemented Dulbecco’s modified Eagle’s medium (HDMEM) diminished KCl induced contractile forces to 71% (<i>p</i> = 0.002) and NE induced contractions to 80% (<i>p</i> = 0.037), in contrast to HEPES-supplemented Krebs-Henseleit solution (HKH) and TiProtec solution. KCl-normalized NE contractions were not affected by storage. NE EC<sub>50</sub> values were slightly lower (7.1E−8 vs. 7.5E−8, <i>p</i> = 0.019) after storage in HKH, with no changes after storage in the other solutions. Endothelium-dependent responses to ACh were not affected by storage. ET-1 induced contractions were attenuated after storage in HDMEM (77%, <i>p</i> = 0.002), HKH (75%, <i>p</i> = 0.020), and TiProtec (73%, <i>p</i> = 0.010) with no changes in normalized constrictions. ET-1 EC<sub>50</sub> values were not affected by storage. <b><i>Conclusion:</i></b> Loss of contractility after storage in HDMEM may reflect the lower content of dextrose. There was no specific attenuation of adrenoceptor, ET-receptor, or ACh receptor mediated signal transduction after storage in any of the media. HKH or TiProtec are equally suitable cold storage solutions for ex vivo measurements.

The Role of Endothelin Receptors in the Regulation of Kidney Function and Blood Pressure

“…Преимущественно действия, опосредованные рецептором ETA, были связаны с артериальной гипертензией. К ним относятся опосредованное рецептором ETA повышение сосудистого сопротивления почек в исследованиях как на животных, так и на людях [43][44][45]. ET-1 также может способствовать образованию активных форм кислорода в почках [46], а повышенные уровни ET-1 сами по себе способствуют воспалению почек через активацию рецептора ETA [47].…”