Neuropeptide Y potentiates contraction and inhibits relaxation of rabbit coronary arteries

Chide Han, Peter W. Abel

Research output: Contribution to journalArticle

71 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)675-681
Number of pages7
JournalJournal of Cardiovascular Pharmacology
Volume9
Issue number6
StatePublished - 1987
Externally publishedYes

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Neuropeptide Y
Coronary Vessels
Rabbits
Norepinephrine
Vasodilator Agents
Adenosine
Histamine
Acetylcholine
Timolol
Phentolamine

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

Cite this

Neuropeptide Y potentiates contraction and inhibits relaxation of rabbit coronary arteries. / Han, Chide; Abel, Peter W.

In: Journal of Cardiovascular Pharmacology, Vol. 9, No. 6, 1987, p. 675-681.

Research output: Contribution to journalArticle

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AB - 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.

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