THE EXERCISE PRESSER REFLEX IS ATTENUATED BY INTRATHECAL OXYTOCIN

We tested the hypothesis that oxytocin (Oxt) acts in the lumbar spinal cord to attenuate reflex presser (mean arterial pressure, MAP) and he art rate (HR) responses to static hindlimb contraction (i.e., the exer cise presser reflex). Thus we compared MAP and HR responses to electri cally stimulated hindlimb static contraction in the anesthetized cat b efore and after intrathecal injection of Oxt (30 pmol, n = 3; 300 pmol , n = 6; or 3 nmol, n = 6). The 300-pmol dose was most effective; it a ttenuated the presser response to static contraction by 39 +/- 10% but had no effect on HR. In three other cats, contraction-induced increas es in MAP and HR were monitored before and after intrathecal injection of 300 pmol of Oxt + 300 nmol of the selective Oxt receptor antagonis t [d(CH2)5(1),O-Me-Tyr(2),Thr(4),Tyr(9) Orn(8)]vasotocin. Pretreatment with the antagonist eliminated the effect of Oxt on MAP. In an additi onal 10 cats, increases in these same variables in response to static contraction were compared before and after intrathecal injection of th e Oxt antagonist (30 nmol, n = 3 or 300 nmol, n = 7) into the lumbar s pinal cord (L(1)-L(7)). Whereas 30 nmol of the Oxt antagonist had no e ffect, the 300-nmol dose augmented the contraction-induced presser and HR responses by 28 +/- 7 and 32 +/- 17%, respectively. These data imp ly that endogenous Oxt modulates the exercise presser reflex by its ac tion on Oxt receptors in the lumbar spinal cord that can attenuate sen sory nerve transmission from skeletal muscle.