ABSTRACT
In rat mesenteric and hepatic arteries the endothelium-dependent hyperpolarizations can be explained by the direct effects on smooth muscle of K + liberated from the endothelium. However, in other preparations in which there is a good EDHF-response, K + appears neither to hyperpolarize nor to relax the vascular smooth muscle. In these vessels, myo endothelial gap junctions might conduct endothelial cell hyperpolarization to the under lying smooth muscle or be the pathway through which any hyperpolarizing factor is transferred to these cells. In the present study, the effects of two gap junction inhibitors (Gap 27 and carbenoxolone) on the EDHF-responses in the guinea-pig internal carotid, the pig coronary and the rat hepatic and mesenteric arteries were investigated using micro electrode techniques. Using reverse transcriptase-polymerase chain reaction (RT-PCR) the presence of m R N A corresponding to all three vascular connexins, Cx37, Cx40 and Cx43 was detected in whole mesenteric and hepatic, pig coronary and guinea-pig internal carotid arteries. Gap junctions are formed from connexins and immunofluorescence staining of frozen sections of these blood vessels revealed the presence (and distribution) of Cx37, Cx40 and Cx43. Although the relative distribution of the connexins did not differ between pre parations with the exception of the guinea-pig internal carotid artery, the data indicates that gap junctions have only a minor, if any, role in the EDHF-response of the rat hepatic and mesenteric arteries. However, these structures may be important in the guinea-pig internal carotid and pig coronary arteries.
