Mechanisms of flow and ACh-induced dilation in rat soleus arterioles are altered by hindlimb unweighting

Journal of Applied Physiology

Volumn 92, Issue 3, 2002, Pages 901-911

  Schrage, William G ^a,b,d   Woodman, Christopher R ^b,c,d   Harold Laughlin, M ^a,b,c,d  

^a Department of Physiology ^*  (United States)

^b Biomedical Sciences   (United States)

^c UNIVERSITY OF MISSOURI   (United States)

^d UNIVERSITY OF MISSOURI   (United States)

Author keywords

Microcirculation; Physical inactivity; Reduced blood flow; Simulated microgravity; Skeletal muscle

Indexed keywords

ACETYLCHOLINE; ARGININE DERIVATIVE; INDOMETACIN; NITRIC OXIDE SYNTHASE INHIBITOR;

ANIMAL EXPERIMENT; ARTERIOLE; ARTERY BLOOD FLOW; ARTERY DILATATION; ARTICLE; CONTROLLED STUDY; HINDLIMB; IMMOBILIZATION; MALE; MICROCIRCULATION; MICROGRAVITY; NONHUMAN; PRIORITY JOURNAL; RAT; SKELETAL MUSCLE; SOLEUS MUSCLE;

EID: 0036092912     PISSN: 87507587     EISSN: None     Source Type: Journal    
DOI: 10.1152/japplphysiol.00642.2001     Document Type: Article

References (33)

1. Myogenic and vasoconstrictor responsiveness of skeletal muscle arterioles is diminished by hindlimb unloading
2. Structural and functional remodeling of skeletal muscle microvasculature is induced by simulated microgravity
3. Structural and functional responses to prolonged hindlimb suspension in rat muscle
4. Diameter changes in arteriolar networks of contracting skeletal muscle
5. 2 to acetylcholine in skeletal muscle venules
6. Flow effects on prostacyclin production by cultured human endothelial cells
7. In eNOS knockout mice skeletal muscle arteriolar dilation to acetylcholine is mediated by EDHF
8. Hindlimb unweighting decreases ecNOS gene expression and endothelium-dependent dilation in rat soleus feed arteries
9. Regulation of coronary blood flow: Coordination of heterogeneous control mechanisms in vascular microdomains
10. Flow-induced responses in skeletal muscle venules: Modulation by nitric oxide and prostaglandins
11. Endothelium regulates skeletal muscle microcirculation by a blood flow velocity-sensing mechanism
12. Interaction of pressure- and flow-induced responses in porcine coronary resistance vessels
13. Longitudinal gradients for endothelium-dependent and -independent vascular responses in the coronary microcirculation
14. Reductions in arterial diameter produced by chronic decreases in blood flow are endothelium-dependent
15. Maximal exercise performance after adaptations to microgravity
16. Hyperosmolality dilates rat skeletal muscle arterioles: Role of endothelial K(ATP) channels and daily exercise
17. Effect of hindlimb unweighting on tissue blood flow in the rat
18. Attenuated baroreflex control of sympathetic nerve activity after cardiovascular deconditioning in rats
19. Nitric oxide exerts feedback inhibition on EDHF-induced coronary arteriolar dilation in vivo
20. 2 max and regional blood flow responses to exercise
21. Coronary and systemic hemodynamic effects of sustained inhibition of nitric oxidesynthesis in conscious dogs. Evidence for cross talk between nitric oxide and cyclooxygenase in coronary vessels
22. Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling
23. Hindlimb unweighting alters endothelium-dependent dilation an ecNOS expression in soleus arterioles
24. Short-term daily exercise activity enhances endothelial NO synthesis in skeletal muscle arterioles of rats
25. Adaptation of flow-induced dilation of arterioles to daily exercise
26. Effects of spaceflight on human calf hemodynamics
27. Blood flow through terminal arterial vessels after denervation of the bat wing
28. Feed artery role in blood flow control to rat hindlimb skeletal muscles
29. Hindlimb unweighting decreases endothelium-dependent dilation and eNOS expression in soleus not gastrocnemius
30. 2 max of nontrained and trained rats
31. Influence of simulated microgravity on cardiac output and blood flow distribution during exercise
32. Effect of 29 days of simulated microgravity on maximal oxygen consumption and fat-free mass of rats
33. Gender-specific compensation for the lack of NO in the mediation of flow-induced arteriolar dilation