Mechanism and modification of bradykinin induced coronary vasodilation

P. Needleman; S. L. Key; S. E. Denny; P. C. Isakson; G. R. Marshall

doi:10.1073/pnas.72.6.2060

Mechanism and modification of bradykinin induced coronary vasodilation

P. Needleman, S. L. Key, S. E. Denny, P. C. Isakson, G. R. Marshall

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Abstract

In isolated perfused rabbit hearts, bradykinin produced a concentration dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin E like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ 20881) markedly enhanced both the coronary vasodilation and release of prostaglandin E like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.

Original language	English
Pages (from-to)	2060-2063
Number of pages	4
Journal	Proceedings of the National Academy of Sciences of the United States of America
Volume	72
Issue number	6
DOIs	https://doi.org/10.1073/pnas.72.6.2060
State	Published - 1975

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abstract = "In isolated perfused rabbit hearts, bradykinin produced a concentration dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin E like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ 20881) markedly enhanced both the coronary vasodilation and release of prostaglandin E like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.",

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AU - Needleman, P.

AU - Key, S. L.

AU - Denny, S. E.

AU - Isakson, P. C.

AU - Marshall, G. R.

PY - 1975

Y1 - 1975

N2 - In isolated perfused rabbit hearts, bradykinin produced a concentration dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin E like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ 20881) markedly enhanced both the coronary vasodilation and release of prostaglandin E like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.

AB - In isolated perfused rabbit hearts, bradykinin produced a concentration dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin E like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ 20881) markedly enhanced both the coronary vasodilation and release of prostaglandin E like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.

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JO - Proceedings of the National Academy of Sciences of the United States of America

JF - Proceedings of the National Academy of Sciences of the United States of America

SN - 0027-8424

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ER -

Mechanism and modification of bradykinin induced coronary vasodilation

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