EVIDENCE FOR K+ CHANNELS INVOLVEMENT IN CAPILLARY SENSING AND FOR BIDIRECTIONALITY IN CAPILLARY COMMUNICATION

Although the capillary sensing and communication phenomenon has been c haracterized, its mechanism is not clear. It has been hypothesized tha t capillary sensing involves a membrane potential change in the capill ary endothelium and/or pericyte and that communication represents an e lectrotonic spread of this change along the capillary. The goal of the present study was to address this hypothesis by examining the presenc e of Ki channels on the capillary and by determining bidirectionality of communication. Using intravital microscopy, we locally applied K+ ( 100 mM), acetylcholine (ACh; 3 mM), and norepinephrine (NE; 0.3 mM) on capillaries, 400-500 mu m downstream from the arteriole, at the surfa ce of the sartorius muscle in anesthetized frogs. Responses were measu red in terms of red blood cell velocity (V-RBC) changes in the stimula ted capillary (control prestimulation V-RBC ranged from 110 to 770 mu m/sec). K+ and ACh caused significant 19 and 38% increases in V-RBC, w hile NE caused a -46% decrease, respectively. The K+ response was bloc ked by local pretreatment with K+ channel blocker BaCl2 (1 mu M) and b y pretreatment with tetraethyl ammonium chloride (TEA; 5 mM). Response s to ACh and NE were attenuated by pretreatment with 1 mu M BaCl2 (to 1%) and with 50 mM TEA (to -25%), respectively. In a separate experime nt, NE (3 mM) application on the capillary 500 mu m away from the drai ning venule (capillary occluded) caused a 19% venular constriction (i. e., similar to a reported 21% arteriolar constriction caused by the NE stimulus). We concluded that (i) K+ channels were present on the capi llary and (ii) capillary communication was bidirectional. We interpret ed these results to be consistent with the above hypothesis of membran e potential change and electrotonic spread. (C) 1997 Academic Press.