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

被引:44
作者
FRAME, MDS
SARELIUS, IH
机构
[1] Department of Biophysics, University of Rochester, NY
[2] Department of Biophysics, Univ. of Rochester Medical Center, Rochester, NY 14642
关键词
CONDUCTED RESPONSE; GAP JUNCTION; VASCULAR COMMUNICATION; FLOW REGULATION;
D O I
10.1161/01.RES.77.4.695
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Our purpose was to determine whether L-arginine was involved in vascular communication between downstream and upstream locations within a defined microvascular region. Arteriolar diameter was measured for the branches along a transverse arteriole in the superfused cremaster of anesthetized (pentobarbital sodium, 70 mg/kg IF) hamsters (N=53). The upstream branch arterioles dilated significantly to locally applied L-arginine (100 mu mol/L pipette concentration) only if the downstream branches ( 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 exposure 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-arginine. Downstream-applied L-arginine also induced a conducted vasodilation (+17.8+/-2.8%; n=14) 13271+/-166 mu m upstream. This response was completely 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 site of L-arginine exposure and the upstream observation site. An acetylcholine-induced conducted vasodilation (+18.1+/- 2.6%, n=8) was also completely blocked by sucrose, halothane, or L-NNA. The change in responsivity upstream to locally applied L-arginine was not seen in the absence of a conducted vasodilation or when the conducted signal pathway was blocked after the conducted vasodilation was observed, and it could be triggered by a conducted response to acetylcholine as well as to L-arginine. Thus, the change in local responsivity upstream requires an ongoing conducted signal from downstream. Conducted signals likely play a dynamic role in the regulation of vascular responsivity within a defined microvascular region.
引用
收藏
页码:695 / 701
页数:7
相关论文
共 48 条
[21]   INTER-CELLULAR JUNCTIONS AND TRANSFER OF SMALL MOLECULES IN PRIMARY VASCULAR ENDOTHELIAL CULTURES [J].
LARSON, DM ;
SHERIDAN, JD .
JOURNAL OF CELL BIOLOGY, 1982, 92 (01) :183-191
[22]   VULNERABILITY OF CONDUCTED VASOMOTOR RESPONSE TO ISCHEMIA [J].
LIN, Y ;
DULING, BR .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1994, 267 (06) :H2363-H2370
[23]   MECHANISMS OF MYOGENIC ENHANCEMENT BY NOREPINEPHRINE [J].
LIU, J ;
HILL, MA ;
MEININGER, GA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 266 (02) :H440-H446
[24]   THE INFLUENCE OF THE SYMPATHETIC NERVOUS-SYSTEM ON INDIVIDUAL VESSELS OF THE MICRO-CIRCULATION OF SKELETAL-MUSCLE OF THE RAT [J].
MARSHALL, JM .
JOURNAL OF PHYSIOLOGY-LONDON, 1982, 332 (NOV) :169-+
[25]   THE L-ARGININE - NITRIC-OXIDE PATHWAY [J].
MONCADA, S .
ACTA PHYSIOLOGICA SCANDINAVICA, 1992, 145 (03) :201-227
[26]   L-ARGININE DILATES RAT PIAL ARTERIOLES BY NITRIC OXIDE-DEPENDENT MECHANISMS AND INCREASES BLOOD-FLOW DURING FOCAL CEREBRAL-ISCHEMIA [J].
MORIKAWA, E ;
ROSENBLATT, S ;
MOSKOWITZ, MA .
BRITISH JOURNAL OF PHARMACOLOGY, 1992, 107 (04) :905-907
[27]   ENDOTHELIUM-DEPENDENT HYPERPOLARIZATION CAUSED BY BRADYKININ IN HUMAN CORONARY-ARTERIES [J].
NAKASHIMA, M ;
MOMBOULI, JV ;
TAYLOR, AA ;
VANHOUTTE, PM .
JOURNAL OF CLINICAL INVESTIGATION, 1993, 92 (06) :2867-2871
[28]   MOLECULAR-CLONING AND CHARACTERIZATION OF THE CONSTITUTIVE BOVINE AORTIC ENDOTHELIAL-CELL NITRIC-OXIDE SYNTHASE [J].
NISHIDA, K ;
HARRISON, DG ;
NAVAS, JP ;
FISHER, AA ;
DOCKERY, SP ;
UEMATSU, M ;
NEREM, RM ;
ALEXANDER, RW ;
MURPHY, TJ .
JOURNAL OF CLINICAL INVESTIGATION, 1992, 90 (05) :2092-2096
[29]   SHEAR-STRESS ELEVATES ENDOTHELIAL CGMP - ROLE OF A POTASSIUM CHANNEL AND G-PROTEIN COUPLING [J].
OHNO, M ;
GIBBONS, GH ;
DZAU, VJ ;
COOKE, JP .
CIRCULATION, 1993, 88 (01) :193-197
[30]   HEMODYNAMIC SHEAR-STRESS ACTIVATES A K+ CURRENT IN VASCULAR ENDOTHELIAL-CELLS [J].
OLESEN, SP ;
CLAPHAM, DE ;
DAVIES, PF .
NATURE, 1988, 331 (6152) :168-170