AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol (May 9, 2002). doi:10.1152/ajpheart.00086.2002
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Articles in PresS, published online ahead of print May 7, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00086.2002
Submitted on February 2, 2002
Accepted on May 2, 2002

The neurotensin fragment, acetyl neurotensin (8-13), inhibits lowering of interstitial fluid pressure in rat trachea

Eli-Anne B. Gjerde1*, Edward T. Wei2, and Rolf K. Reed1

1 Department of Pysiology, University of Bergen, Bergen, Norway
2 School of Public Health, University of California, Berkeley, San Fransisco, CA, USA

* To whom correspondence should be addressed. E-mail: eli-anne.gjerde{at}fys.uib.no.

Injury to soft tissue results in lowering of interstitial fluid pressure (Pif), plasma protein extravasation and increased total tissue volume. In this study, the effects of AcNT (8-13), on Pif in rat trachea were examined after electrical stimulation (ES) of the n. vagus. Pif was measured with glass capillaries connected to a servocontrolled counter-pressure system. In pentobarbital anesthetized female Wistar rats, the Pif after i.v. saline was -1.8 ± 0.3 (SD) mmHg and decreased to -5.0 ± 0.6 mmHg (p<0.01, n=9) after ES. AcNT (8-13) 10 µg/kg blocked the fall in Pif after ES (-2.5 ± 2.3 mmHg, p<0.01, n=8). In tracheal tissue from animals pretreated with AcNT (8-13) at the same dose and immersed in phosphate-buffered saline (0.15 M, pH=7.4), the rate of fluid accumulation in excised tissues was significantly reduced after 2 h. The ability of AcNT (8-13) to modulate the fluid mechanics of tracheal interstitium after inflammation suggest that it may be a useful tool for studying cell adhesion and related factors that maintain structural integrity of connective tissue after injury.






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