L-ARGININE-INDUCED CONDUCTED SIGNALS ALTER UPSTREAM ARTERIOLAR RESPONSIVITY TO L-ARGININE

Citation
Mds. Frame et Ih. Sarelius, L-ARGININE-INDUCED CONDUCTED SIGNALS ALTER UPSTREAM ARTERIOLAR RESPONSIVITY TO L-ARGININE, Circulation research, 77(4), 1995, pp. 695-701
Citations number
48
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097330
Volume
77
Issue
4
Year of publication
1995
Pages
695 - 701
Database
ISI
SICI code
0009-7330(1995)77:4<695:LCSAUA>2.0.ZU;2-4
Abstract
Our purpose was to determine whether L-arginine was involved in vascul ar communication between downstream and upstream locations within a de fined microvascular region. Arteriolar diameter was measured for the b ranches along a transverse arteriole in the superfused cremaster of an esthetized (pentobarbital sodium, 70 mg/kg IF) hamsters (N=53). The up stream branch arterioles dilated significantly to locally applied L-ar ginine (100 mu mol/L pipette concentration) only if the downstream bra nches ( approximate to 1400 mu m away) were preexposed. With exposure order downstream to upstream, diameter change was last branch, -3.8+/- 1.5% (of baseline); third, +58.1+/-27%; first, +92+/-26% (n=5); with e xposure order upstream to downstream: first branch, -0.4+/-3%; third, +5+/-11%; last, -5.6+/-7.5% (n=4). Thus, downstream preex posure to L- arginine altered the responsivity upstream to locally applied L-argini ne. Downstream-applied L-arginine also induced a conducted vasodilatio n (+17.8+/-2.8%; n=14) 13271+/-166 mu m upstream. This response was co mpletely blocked Our by simultaneous sucrose (600 mOsm), halothane (0. 0345%), or N-omega-nitro-L-arginine (L-NNA, 100 mu mol/L) exposure to the feed vessel (second micropipette) midway between the downstream si te of L-arginine exposure and the upstream observation site. An acetyl choline-induced conducted vasodilation (+18.1+/- 2.6%, n=8) was also c ompletely blocked by sucrose, halothane, or L-NNA. The change in respo nsivity upstream to locally applied L-arginine was not seen in the abs ence of a conducted vasodilation or when the conducted signal pathway was blocked after the conducted vasodilation was observed, and it coul d be triggered by a conducted response to acetylcholine as well as to L-arginine. Thus, the change in local responsivity upstream requires a n ongoing conducted signal from downstream. Conducted signals likely p lay a dynamic role in the regulation of vascular responsivity within a defined microvascular region.