Regulation of blood flow by prostaglandins

被引:16
作者
Boushel, R. [1 ]
Langberg, H. [2 ]
Risum, N. [2 ]
Kjaer, M. [2 ]
机构
[1] Concordia Univ, Dept Exercise Sci, Montreal, PQ H4B 1R6, Canada
[2] Bispebjerg Hosp, Sports Med Res Unit, Copenhagen Mescle Res Ctr, Dept Rheumatol, DK-2400 Copenhagen, Denmark
关键词
vasodilation; exercise; muscle; tendon;
D O I
10.2174/1570161043476410
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Prostaglandins (PGs) belong to the family of prostanoids together with thromboxanes and are produced mainly from arachadonic acid by the enzyme cyclooxygenase. PGs are known to stimulate platelet aggregation, mediate inflammation and edema, play a role in bone metabolism and in biological adaptation of connective tissues e. g. tendon. This review covers the role of PG for mediating tissue blood flow at rest and during increases in metabolic demand such as exercise and reactive hyperaemia. There is strong evidence that PGs contribute to elevate blood flow at rest and during reactive hyperaemia in a variety of tissues. Their role for regulating the large increases in muscle blood flow during exercise is less clear which may be explained by redundant mechanisms. Several interactions are known to exist between specific vasodilator substances, and therefore PGs can act in synergy with other substances and contribute to functional hyperaemia. Furthermore, there is evidence for differential, tissue-specific influences of PGs where their influence on blood flow during exercise may be profound.
引用
收藏
页码:191 / 197
页数:7
相关论文
共 66 条
[1]   INDOMETHACIN AND PROSTAGLANDIN HYPOTHESIS OF CORONARY BLOOD-FLOW REGULATION [J].
AFONSO, S ;
BANDOW, GT ;
ROWE, GG .
JOURNAL OF PHYSIOLOGY-LONDON, 1974, 241 (02) :299-308
[2]   REGULATION OF POSTOCCLUSIVE HYPEREMIA BY ENDOGENOUSLY SYNTHESIZED PROSTAGLANDINS IN DOG HEART [J].
ALEXANDER, RW ;
KENT, KM ;
PISANO, JJ ;
KEISER, HR ;
COOPER, T .
JOURNAL OF CLINICAL INVESTIGATION, 1975, 55 (06) :1174-1181
[3]  
ALMEKINDERS LC, 1993, MED SCI SPORT EXER, V25, P603
[4]   Reciprocal inhibition of nitric oxide and prostacyclin synthesis in human saphenous vein [J].
Barker, JE ;
Bakhle, YS ;
Anderson, J ;
Treasure, T ;
Piper, PJ .
BRITISH JOURNAL OF PHARMACOLOGY, 1996, 118 (03) :643-648
[5]   Nitric oxide attenuates the release of endothelium-derived hyperpolarizing factor [J].
Bauersachs, J ;
Popp, R ;
Hecker, M ;
Sauer, E ;
Fleming, I ;
Busse, R .
CIRCULATION, 1996, 94 (12) :3341-3347
[6]   CONTRIBUTION OF PROSTAGLANDINS TO MUSCLE BLOOD-FLOW IN ANESTHETIZED DOGS AT REST, DURING EXERCISE, AND FOLLOWING INFLOW OCCLUSION [J].
BEATY, O ;
DONALD, DE .
CIRCULATION RESEARCH, 1979, 44 (01) :67-75
[7]   MODIFICATION OF BASAL RELEASE OF PROSTAGLANDINS FROM RABBIT ISOLATED HEARTS [J].
BLOCK, AJ ;
POOLE, S ;
VANE, JR .
PROSTAGLANDINS & OTHER LIPID MEDIATORS, 1974, 7 (06) :473-486
[8]   Blood flow and oxygenation in peritendinous tissue and calf muscle during dynamic exercise in humans [J].
Boushel, R ;
Langberg, H ;
Green, S ;
Skovgaard, D ;
Bülow, J ;
Kjær, M .
JOURNAL OF PHYSIOLOGY-LONDON, 2000, 524 (01) :305-313
[9]   Combined inhibition of nitric oxide and prostaglandins reduces human skeletal muscle blood flow during exercise [J].
Boushel, R ;
Langberg, H ;
Gemmer, C ;
Olesen, J ;
Crameri, R ;
Scheede, C ;
Sander, M ;
Kjær, M .
JOURNAL OF PHYSIOLOGY-LONDON, 2002, 543 (02) :691-698
[10]   INHIBITION OF FUNCTIONAL VASODILATATION AND PROSTAGLANDIN FORMATION IN RABBIT ADIPOSE-TISSUE BY INDOMETHACIN AND ASPIRIN [J].
BOWERY, B ;
LEWIS, GP .
BRITISH JOURNAL OF PHARMACOLOGY, 1973, 47 (02) :305-314