The effects of neuropeptide Y (NPY) on contraction and relaxation of isolated rabbit coronary arteries were studied. NPY alone caused a weak contraction of coronary arteries with a mean EC50 value of 29 ± 2.0 nM. Following exposure of coronary arteries to 30 nM NPY, the potencies of norepinephrine (in the presence of 3 μM timolol) and histamine in causing contraction were increased twofold, with no change in maximal contraction. After half-maximal contraction of coronary arteries with histamine and addition of 30 nM NPY, relaxation produced by norepinephrine (in the presence of 3 fiM phentolamine), adenosine, and acetylcholine was inhibited. Concentration-response curves for all vasodilators were shifted to the right 10-22-fold by 30 nM NPY. Maximal relaxation caused by adenosine and norepinephrine was not changed by NPY, whereas the maximal response to acetylcholine was 37% less in the presence of NPY. Correlation of the tension produced by NPY with the shift in agonist contraction or relaxation concentration-response curves indicated that NPY-induced increases in baseline tone had no effect on the degree of shift in agonist concentration-response curves. These results show that NPY causes a modest potentiation of agonist-induced contraction and a dramatic blockade of vasodilator-induced relaxation of rabbit coronary arteries.
|Number of pages||7|
|Journal||Journal of Cardiovascular Pharmacology|
|Publication status||Published - 1987|
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine