Differential inhibitory effect of neomycin on contractile responses of various canine arteries

The influence of neomycin on vascular smooth muscle contractile responses was examined in different isolated arterial preparations of the dog. Prior exposure (5 minutes) to 7 mM neomycin decreased contractile responses elicited with norepinephrine (NE, 0.6 muM) or KC1 (K-+, 80 nM) in helical strips of canine aortae (Ao) and femoral (F), carotid (Cd), renal (R), superior mesenteric (Sm), terminal mesenteric (Tm) and coronary (Cr) arteries. Addition of neomycin subsequent to NE-induced contractile responses depressed tension responses of the F, Cd, R, Sm and Tm arteries but had little or no effect on the Ao. However, after contractions had been elicited with K-+, neomycin had no effect on tension responses of the Ao, F, Cd, R or Sm arteries but depressed contractions of the Cr and Tm arterial strips. Preincubation with neomycin (0.7-3.5 mM) produced a concentration-related inhibition of contractile responses elicited in Tm arterial strips by addition of calcium ions (Ca-++; 1.6 mM) to a Ca-++-free depolarizing solution; conversely, subsequent addition of neomycin had no effect on maintained Ca-++ contractures. In constant flow-perfused terminal mesenteric arterial branches, neomycin (0.5-4.0 mM) produced a concentration-related antagonism of pressor responses elicited with NE (1-8 mug) or K-+ (40 mM). The inhibitory action of neomycin on K-+-induced pressor responses was inversely related to the Ca-++ concentration of the perfusion fluid. However, inhibition of NE pressor responses by neomycin did not appear to be related to the Ca-++ concentration. The differential inhibitory action of neomycin on contractions induced by NE and K-+ in various canine arteries suggests that different vascular beds vary in the manner in which Ca-++ is bound and subsequently utilized by stimulatory agents to elicit tension changes.