| 7540111 |
Wilson LB, Wall PT, Matsukawa K: Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn. Cardiovasc Res. 1995 Mar;29(3):379-84.
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. |
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