title: Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn.
abstract: OBJECTIVE
  The aim was to determine if the coadministration of antagonists to substance P and somatostatin into the L7 dorsal horn blunts the reflex cardiovascular responses to static contraction to a greater extent than each antagonist alone. The possibility that this attenuation is mediated by blunting the contraction evoked increases in sympathetic outflow was also tested.
  
  
  METHODS
  Using alpha chloralose anaesthetised cats (n = 8), static contraction and stretch of the triceps surae muscle were performed before and after microinjecting (1 microliter) 250 ng of the substance P antagonist, D-Pro2-D-Phe7-D-Trp9-substance P, and the somatostatin antagonist, cyclo(7-amino-heptanoyl-phenylalanyl-D-tryptophyl-lysyl-threonyl-[ benzyl]). The muscle was contracted by electrically stimulating the peripheral end of the cut L7 ventral root.
  
  
  RESULTS
  Before injecting the antagonists, static muscle contraction increased mean arterial blood pressure by 40(SEM 6) mm Hg, heart rate by 13(2) beats.min-1, and renal sympathetic nerve activity (RSNA) by 41(7)%. These changes were blunted by the antagonists since the increases in blood pressure, heart rate, and RSNA were reduced to 21(3) mm Hg, 8(1) beats.min-1, and 23(5)%, respectively. In contrast, antagonist administration did not affect the pressor [33(5) v 31(5) mm Hg], heart rate [9(2) v 10(2) beats.min-1], or RSNA [23(4)% v 25(5)%] responses to muscle stretch. Microinjection of 2% lignocaine into the dorsal horn virtually abolished the reflex changes elicited by muscle stretch.
  
  
  CONCLUSIONS
  The release of substance P and somatostatin in the spinal cord plays a role in mediating the cardiovascular changes caused by static contraction, but the release of other neurotransmitters/neuromodulators is also involved. The attenuation produced by these antagonists is mediated, at least in part, by reducing sympathetic outflow.
authors.affiliation: Moss Heart Center, UT Southwestern Medical Center, Dallas, TX 75235-9040, USA.
authors.forename: L B
authors.initials: LB
authors.lastname: Wilson
authors.forename: P T
authors.initials: PT
authors.lastname: Wall
authors.forename: K
authors.initials: K
authors.lastname: Matsukawa
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002415:Cats; D004558:Electric Stimulation; D006339:Heart Rate / Q000187:drug effects; D007668:Kidney / Q000294:innervation; D008012:Lidocaine / Q000494:pharmacology; D009119:Muscle Contraction; D011311:Pressoreceptors / Q000187:drug effects; D012018:Reflex / Q000187:drug effects*; D013004:Somatostatin / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects; D013373:Substance P / Q000031:analogs & derivatives* / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000187:drug effects; D013997:Time Factors
chemical_list: D013373:Substance P; D013004:Somatostatin; C041817:substance P, Pro(2)-Phe(7)-Trp(9)-; C043820:cyclo(7-aminoheptanoylphenylalanyl-tryptophyl-lysyl-benzylthreonyl); D008012:Lidocaine