Nowa wersja platformy, zawierająca wyłącznie zasoby pełnotekstowe, jest już dostępna.
Przejdź na https://bibliotekanauki.pl
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 3

Liczba wyników na stronie
first rewind previous Strona / 1 next fast forward last
Wyniki wyszukiwania
help Sortuj według:

help Ogranicz wyniki do:
first rewind previous Strona / 1 next fast forward last
EN
The aim of our study was to examine whether non ß1-/ß2-adrenoceptors participate in the relaxation of the human pulmonary artery. For this purpose the vasodilatory effect of the non-conventional partial ß-adrenoceptor agonist cyanopindolol was examined. Cyanopindolol (1 - 300 µM), studied in the presence of the ß1-/ß2-adrenoceptor antagonist propranolol, relaxed the human pulmonary artery preconstricted with serotonin 1 µM in a concentration-dependent manner (maximally by about 80%). This effect was diminished by bupranolol 10 µM (an antagonist of ß1-ß3-adrenoceptors and the low affinity state of the ß1-adrenoceptor) and CGP 20712 10 µM (known to antagonize the low-affinity state of the ß1-adrenoceptor at high concentrations). In further experiments, the effect of ß-adrenoceptor ligands on the serotonin-induced vasoconstriction was examined. The concentration-response curve for serotonin was not affected by cyanopindolol 30 µM, bupranolol 10 µM and CGP 20712 10 µM but shifted to the right by cyanopindolol 100 and 300 µM; the serotonin 5-HT2A receptor antagonist ketanserin 0.3 µM abolished the maximum contraction elicited by serotonin. In conclusion, the present study reveals that the vasodilatory effect of cyanopindolol in the human pulmonary artery consists of two components, i.e. activation of a propranolol-insensitive atypical ß-adrenoceptor and antagonism against 5-HT2A receptors.
first rewind previous Strona / 1 next fast forward last
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.