Attenuation of reflex pressor and ventilatory responses to static contraction by an NK-1 receptor antagonist

J. M. Hill, J. G. Pickar, Marc P Kaufman

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The chemical messengers released onto second-order dorsal horn neurons from the spinal terminals of contraction-activated group III and IV muscle afferents have not been identified. One candidate is the tachykinin substance P. Related to substance P are two other tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which, like substance P, have been isolated in the dorsal horn of the spinal cord and have receptors there. Whether NKA or NKB plays a transmitter/modulator role in the spinal processing of the exercise pressor reflex is unknown. Therefore, we tested the following hypotheses. After the intrathecal injection of a highly selective NK-1 (substance P) receptor antagonist onto the lumbrosacral spinal cord, the reflex pressor and ventilatory responses to static muscular contraction will be attenuated. Likewise, after the intrathecal injection either of an NK-2 (NKA) receptor antagonist or an NK-3 (NKB) receptor antagonist onto the lumbosacral spinal cord, the reflex pressor and ventilatory responses to static contraction will be attenuated. We found that, 10 min after the intrathecal injection of 100 μg of the NK-1 receptor antagonist, the pressor and ventilatory responses to contraction were significantly (P < 0.05) attenuated. Mean arterial pressure was attenuated by 13 ± 3 mmHg (48%) and minute volume of ventilation by 120 ± 38 ml/min (34%). The cardiovascular and ventilatory responses to contraction before either 100 μg of the NK-2 receptor antagonist or 100 μg of the NK-3 receptor antagonist were not different (P > 0.05) from those after the NK-2 or the NK-3 receptor antagonists. We were unable to demonstrate a role for NK-2 (NKA) and NK-3 (NKB) receptors in the spinal processing of the exercise pressor reflex. Our results provide evidence that substance P, acting via the NK-1 receptor, is involved in the transmission of contraction-activated afferent input to the dorsal horn of the spinal cord.

Original languageEnglish (US)
Pages (from-to)1389-1395
Number of pages7
JournalJournal of Applied Physiology
Volume73
Issue number4
StatePublished - 1992

Fingerprint

Neurokinin-1 Receptors
Neurokinin-3 Receptors
Substance P
Neurokinin A
Spinal Injections
Reflex
Neurokinin B
Tachykinins
Spinal Cord
Neurokinin-2 Receptors
Neurokinin-1 Receptor Antagonists
Posterior Horn Cells
Muscle Contraction
Muscles
NK 2
Spinal Cord Dorsal Horn

Keywords

  • cats
  • control of circulation
  • CP 96,345
  • exercise
  • peptides
  • substance P
  • tachykinins

ASJC Scopus subject areas

  • Endocrinology
  • Physiology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Attenuation of reflex pressor and ventilatory responses to static contraction by an NK-1 receptor antagonist. / Hill, J. M.; Pickar, J. G.; Kaufman, Marc P.

In: Journal of Applied Physiology, Vol. 73, No. 4, 1992, p. 1389-1395.

Research output: Contribution to journalArticle

@article{f89a964b06b3489da949aa41da8c578c,
title = "Attenuation of reflex pressor and ventilatory responses to static contraction by an NK-1 receptor antagonist",
abstract = "The chemical messengers released onto second-order dorsal horn neurons from the spinal terminals of contraction-activated group III and IV muscle afferents have not been identified. One candidate is the tachykinin substance P. Related to substance P are two other tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which, like substance P, have been isolated in the dorsal horn of the spinal cord and have receptors there. Whether NKA or NKB plays a transmitter/modulator role in the spinal processing of the exercise pressor reflex is unknown. Therefore, we tested the following hypotheses. After the intrathecal injection of a highly selective NK-1 (substance P) receptor antagonist onto the lumbrosacral spinal cord, the reflex pressor and ventilatory responses to static muscular contraction will be attenuated. Likewise, after the intrathecal injection either of an NK-2 (NKA) receptor antagonist or an NK-3 (NKB) receptor antagonist onto the lumbosacral spinal cord, the reflex pressor and ventilatory responses to static contraction will be attenuated. We found that, 10 min after the intrathecal injection of 100 μg of the NK-1 receptor antagonist, the pressor and ventilatory responses to contraction were significantly (P < 0.05) attenuated. Mean arterial pressure was attenuated by 13 ± 3 mmHg (48{\%}) and minute volume of ventilation by 120 ± 38 ml/min (34{\%}). The cardiovascular and ventilatory responses to contraction before either 100 μg of the NK-2 receptor antagonist or 100 μg of the NK-3 receptor antagonist were not different (P > 0.05) from those after the NK-2 or the NK-3 receptor antagonists. We were unable to demonstrate a role for NK-2 (NKA) and NK-3 (NKB) receptors in the spinal processing of the exercise pressor reflex. Our results provide evidence that substance P, acting via the NK-1 receptor, is involved in the transmission of contraction-activated afferent input to the dorsal horn of the spinal cord.",
keywords = "cats, control of circulation, CP 96,345, exercise, peptides, substance P, tachykinins",
author = "Hill, {J. M.} and Pickar, {J. G.} and Kaufman, {Marc P}",
year = "1992",
language = "English (US)",
volume = "73",
pages = "1389--1395",
journal = "Journal of Applied Physiology",
issn = "8750-7587",
publisher = "American Physiological Society",
number = "4",

}

TY - JOUR

T1 - Attenuation of reflex pressor and ventilatory responses to static contraction by an NK-1 receptor antagonist

AU - Hill, J. M.

AU - Pickar, J. G.

AU - Kaufman, Marc P

PY - 1992

Y1 - 1992

N2 - The chemical messengers released onto second-order dorsal horn neurons from the spinal terminals of contraction-activated group III and IV muscle afferents have not been identified. One candidate is the tachykinin substance P. Related to substance P are two other tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which, like substance P, have been isolated in the dorsal horn of the spinal cord and have receptors there. Whether NKA or NKB plays a transmitter/modulator role in the spinal processing of the exercise pressor reflex is unknown. Therefore, we tested the following hypotheses. After the intrathecal injection of a highly selective NK-1 (substance P) receptor antagonist onto the lumbrosacral spinal cord, the reflex pressor and ventilatory responses to static muscular contraction will be attenuated. Likewise, after the intrathecal injection either of an NK-2 (NKA) receptor antagonist or an NK-3 (NKB) receptor antagonist onto the lumbosacral spinal cord, the reflex pressor and ventilatory responses to static contraction will be attenuated. We found that, 10 min after the intrathecal injection of 100 μg of the NK-1 receptor antagonist, the pressor and ventilatory responses to contraction were significantly (P < 0.05) attenuated. Mean arterial pressure was attenuated by 13 ± 3 mmHg (48%) and minute volume of ventilation by 120 ± 38 ml/min (34%). The cardiovascular and ventilatory responses to contraction before either 100 μg of the NK-2 receptor antagonist or 100 μg of the NK-3 receptor antagonist were not different (P > 0.05) from those after the NK-2 or the NK-3 receptor antagonists. We were unable to demonstrate a role for NK-2 (NKA) and NK-3 (NKB) receptors in the spinal processing of the exercise pressor reflex. Our results provide evidence that substance P, acting via the NK-1 receptor, is involved in the transmission of contraction-activated afferent input to the dorsal horn of the spinal cord.

AB - The chemical messengers released onto second-order dorsal horn neurons from the spinal terminals of contraction-activated group III and IV muscle afferents have not been identified. One candidate is the tachykinin substance P. Related to substance P are two other tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which, like substance P, have been isolated in the dorsal horn of the spinal cord and have receptors there. Whether NKA or NKB plays a transmitter/modulator role in the spinal processing of the exercise pressor reflex is unknown. Therefore, we tested the following hypotheses. After the intrathecal injection of a highly selective NK-1 (substance P) receptor antagonist onto the lumbrosacral spinal cord, the reflex pressor and ventilatory responses to static muscular contraction will be attenuated. Likewise, after the intrathecal injection either of an NK-2 (NKA) receptor antagonist or an NK-3 (NKB) receptor antagonist onto the lumbosacral spinal cord, the reflex pressor and ventilatory responses to static contraction will be attenuated. We found that, 10 min after the intrathecal injection of 100 μg of the NK-1 receptor antagonist, the pressor and ventilatory responses to contraction were significantly (P < 0.05) attenuated. Mean arterial pressure was attenuated by 13 ± 3 mmHg (48%) and minute volume of ventilation by 120 ± 38 ml/min (34%). The cardiovascular and ventilatory responses to contraction before either 100 μg of the NK-2 receptor antagonist or 100 μg of the NK-3 receptor antagonist were not different (P > 0.05) from those after the NK-2 or the NK-3 receptor antagonists. We were unable to demonstrate a role for NK-2 (NKA) and NK-3 (NKB) receptors in the spinal processing of the exercise pressor reflex. Our results provide evidence that substance P, acting via the NK-1 receptor, is involved in the transmission of contraction-activated afferent input to the dorsal horn of the spinal cord.

KW - cats

KW - control of circulation

KW - CP 96,345

KW - exercise

KW - peptides

KW - substance P

KW - tachykinins

UR - http://www.scopus.com/inward/record.url?scp=0026644821&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026644821&partnerID=8YFLogxK

M3 - Article

C2 - 1332931

AN - SCOPUS:0026644821

VL - 73

SP - 1389

EP - 1395

JO - Journal of Applied Physiology

JF - Journal of Applied Physiology

SN - 8750-7587

IS - 4

ER -