A number of studies have emphasized that the sympathetic nervous system in vascular smooth muscle plays an important role in the regulation of vascular tension. Recently, however, it has been suggested that several factors produced in endothelial cells may affect this regulatory mechanism. We have previously reported that endothelin-1 (ET), a novel potent endothelium- derived vasoconstrictor peptide, increased the contraction of nasal vascular smooth muscle which was caused by administration of noradrenaline (NA) into the bath solution.
In this report, using canine nasal mucosa, we studied for additional effects of ET upon the vasoactivity of NA, and that of neuropeptide Y (NPY), which coexists with NA in the sympathetic nerve terminal. The results are as follows:
1) Pretreatment with α-adrenoceptor antagonists did not affect the vasoconstriction induced by ET.
2) With simultaneous administration of 10-
5M NA and 10-
9ET, the contraction peak was maintained for at least 2.5 hours.
3) Pretreatment with 10-
10M ET did not affect the contraction induced by 2.7×10-
7M NPY.
4) Pretreatment with 2.7×10-
8M NPY did not affect the contraction induced by 10-
9M ET.
These results suggest that ET may enhance and prolong the vasocontractile response mediated by α-adrenoceptors, but may not affect the response to NPY.
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