Chronic femoral artery occlusion augments exercise pressor reflex in decerebrated rats.

Hirotsugu Tsuchimochi, Jennifer L McCord, Shawn G Hayes, Satoshi Koba, Marc P Kaufman
Author Information
  1. Hirotsugu Tsuchimochi: Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, 500 University Drive, Hershey Medical Center, Hershey, PA 17033, USA.

Abstract

In decerebrated rats, we determined the pressor and cardioaccelerator reflex responses to static contraction of hindlimb muscles whose femoral arteries were either occluded 72 h before contraction, occluded 3 min before contraction, or freely perfused. We found that the pressor reflex arising from the limb whose femoral artery was occluded for 72 h before contraction (32 +/- 5 mmHg, n = 16) was significantly higher than the pressor reflex arising from the contralateral freely perfused limb (15 +/- 3 mmHg, n = 16, P < 0.001) or than that arising from the contralateral limb whose femoral artery was occluded for only 3 min (17 +/- 4 mmHg, n = 16, P < 0.001). Moreover, the pressor reflex arising from the limb whose femoral artery was occluded for 3 min before the start of contraction was not significantly different than that arising from the contralateral freely perfused limb (n = 16, P = 0.819). The pressor component of the reflex arising from the limb whose femoral artery was occluded for 72 h was not changed by transient receptor potential vanilloid (TRPV) 1 receptor blockade with iodo-resiniferatoxin (n = 15, P = 0.272), although the cardioaccelerator component was significantly reduced (P = 0.005). In addition, the pressor response evoked by capsaicin injection in the femoral artery of the 72-h occluded limb was more than double that evoked from the freely perfused limb (P = 0.026). We conclude that chronic (i.e., 72 h) but not acute (3 min), femoral arterial occlusion augments pressor reflex arising from contraction of hindlimb muscles and that TRPV1 receptors play little role in this augmentation.

References

  1. J Physiol. 1971 Jul;215(3):789-804 [PMID: 5090995]
  2. Neuropharmacology. 1981 Feb;20(2):191-8 [PMID: 7207713]
  3. Am J Physiol Heart Circ Physiol. 2000 Jun;278(6):H1966-73 [PMID: 10843895]
  4. J Physiol. 1972 Jul;224(1):173-86 [PMID: 5039977]
  5. Am J Physiol Heart Circ Physiol. 2008 Oct;295(4):H1429-38 [PMID: 18641268]
  6. Circulation. 2002 Oct 22;106(17):2257-62 [PMID: 12390957]
  7. J Appl Physiol (1985). 1988 Jun;64(6):2306-13 [PMID: 3136123]
  8. Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H1262-H1269 [PMID: 18660449]
  9. J Physiol. 2008 Mar 15;586(6):1649-67 [PMID: 18218679]
  10. Am J Physiol. 1991 Nov;261(5 Pt 2):R1307-12 [PMID: 1951780]
  11. J Appl Physiol (1985). 1990 Mar;68(3):861-7 [PMID: 2111312]
  12. Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H1017-H1024 [PMID: 18599594]
  13. J Appl Physiol (1985). 1989 Mar;66(3):1046-53 [PMID: 2496081]
  14. Am J Physiol Heart Circ Physiol. 2004 Dec;287(6):H2434-47 [PMID: 15271665]
  15. J Appl Physiol (1985). 2004 Nov;97(5):1709-14 [PMID: 15220301]
  16. Circ Res. 1977 Sep;41(3):332-41 [PMID: 196781]
  17. J Appl Physiol Respir Environ Exerc Physiol. 1978 Nov;45(5):762-7 [PMID: 730573]
  18. J Appl Physiol (1985). 1990 Oct;69(4):1225-30 [PMID: 2124582]
  19. Circulation. 2005 Oct 11;112(15):2293-300 [PMID: 16216976]
  20. Eur J Vasc Endovasc Surg. 2007 Jan;33(1):20-5 [PMID: 16934498]
  21. J Physiol. 2006 Dec 15;577(Pt 3):1009-20 [PMID: 17023501]
  22. Angiology. 1999 May;50(5):361-74 [PMID: 10348424]
  23. Annu Rev Physiol. 1983;45:229-42 [PMID: 6342515]
  24. Circulation. 2003 Sep 2;108(9):1126-32 [PMID: 12925464]
  25. J Appl Physiol (1985). 1985 Aug;59(2):459-67 [PMID: 4030598]
  26. Am J Physiol. 1981 Mar;240(3):H315-9 [PMID: 7212075]
  27. Neurosci Lett. 1983 Sep 19;40(1):19-22 [PMID: 6633963]
  28. Circ Res. 1982 Jan;50(1):133-9 [PMID: 7053873]
  29. J Physiol. 1989 Oct;417:13-24 [PMID: 2621589]
  30. J Appl Physiol Respir Environ Exerc Physiol. 1983 Jul;55(1 Pt 1):105-12 [PMID: 6309712]
  31. J Neurophysiol. 1993 Apr;69(4):1053-9 [PMID: 8492148]
  32. Brain Res. 1981 Nov 23;225(1):95-105 [PMID: 6271342]
  33. J Physiol. 1937 Jun 3;89(4):372-83 [PMID: 16994867]
  34. J Physiol. 1988 Apr;398:49-63 [PMID: 3392680]
  35. J Physiol. 2001 Dec 15;537(Pt 3):961-70 [PMID: 11744768]
  36. Anat Rec. 1986 May;215(1):71-81 [PMID: 3706794]
  37. J Appl Physiol Respir Environ Exerc Physiol. 1984 Sep;57(3):644-50 [PMID: 6092310]
  38. J Appl Physiol (1985). 1989 Jun;66(6):2721-4 [PMID: 2501290]

Grants

  1. HL-30710/NHLBI NIH HHS

MeSH Term

Animals
Arterial Occlusive Diseases
Baroreflex
Blood Pressure
Capsaicin
Chronic Disease
Constriction, Pathologic
Decerebrate State
Disease Models, Animal
Diterpenes
Femoral Artery
Heart Rate
Hindlimb
Ischemia
Ligation
Male
Muscle Contraction
Muscle, Skeletal
Physical Exertion
Rats
Rats, Sprague-Dawley
Regional Blood Flow
Sensory System Agents
TRPV Cation Channels
Time Factors

Chemicals

Diterpenes
Sensory System Agents
TRPV Cation Channels
Trpv1 protein, rat
iodoresiniferatoxin
Capsaicin

Word Cloud

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