Abstract
The interaction between the endothelium and purinergic perivascular nerves was investigated by measuring the changes in amplitude of
excitatory junction potential (EJP) of smooth muscle cells in hamster mesenteric arteries (100–350 Am). Uridin-5V-triphosphate (UTP) (100
AM) applied to endothelium-intact preparations evoked a hyperpolarization of 17.0F0.7 mV (n = 46). During this hyperpolarization, the
amplitude of electrically evoked EJPs was inhibited to about 50% of that of the control. In endothelium-denuded preparations, UTP (100 AM)
neither hyperpolarized the smooth muscle nor inhibited the amplitude of the EJP. Neither a nitric oxide (NO) synthase inhibitor, NN-nitro-Larginine
methyl ester (L-NAME) (100 AM), nor a cyclooxygenase inhibitor, indomethacin (1 AM), had an effect on the UTP-evoked
hyperpolarization and inhibition of the electrically evoked EJP. The UTP-evoked membrane hyperpolarization and inhibition of the EJP
amplitude was antagonized by the P2Y receptor antagonist, cibacron blue (100 AM). Endothelium-derived hyperpolarizing factor (EDHF)-
mediated hyperpolarization was inhibited by either adventitial or intimal application of apamin (0.1 AM) and charybdotoxin (0.1 AM).
However, the EJP inhibition was still present. In apamin- and charybdotoxin-treated preparations, focal application of adenosine 5Vtriphosphate
(ATP) (10 mM) evoked a depolarization of 15.5F1.3 mV (n = 15). This postjunctional response was not modified by UTP
(15.3F1.7 mV, n=4, P>0.05). These results suggest that exogenously applied UTP activates P2Y receptors of endothelium to release
endothelium-derived factors, which in turn inhibit ATP release from purinergic nerves. |
