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Combined inhibition of nitric oxide and vasodilating prostaglandins abolishes forearm vasodilatation to systemic hypoxia in healthy humans
Author(s) -
Markwald Rachel R.,
Kirby Brett S.,
Crecelius Anne R.,
Carlson Rick E.,
Voyles Wyatt F.,
Dinenno Frank A.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.205013
Subject(s) - vasodilation , nitric oxide , hypoxia (environmental) , forearm , medicine , cardiology , chemistry , pharmacology , endocrinology , anesthesia , oxygen , anatomy , organic chemistry
Non‐technical summary During hypoxia, there is less oxygen in the air we breathe and also in the blood being pumped away from the heart. Our blood vessels must relax in order to deliver more blood to match the resting oxygen demand of the muscles. The way in which multiple systems in the body coordinate this response is not well known. We examined the local response of the blood vessels to a hypoxic stimulus and show that two substances that the body produces, nitric oxide and prostaglandins, are necessary to cause relaxation of the blood vessels and increases in blood flow. These results help us better understand how oxygen delivery is regulated and may be especially important for populations that are unable to produce these substances that help increase blood flow, such as people with sleep apnoea, heart failure and diabetes.