Effects of clonidine on the reflex cardiovascular responses and release of substance P during muscle contraction

Ahmmed Ally, André F. Meintjes, Jere H. Mitchell, L. Britt Wilson

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48±6 mm Hg, 18±2 beats per minute, and 66±5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51±6 mm Hg, 17±2 beats per minute, and 50±3%, respectively. Microdialysis of clonidine (380 μmol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19±4 mm Hg, 7±1 beats per minute, and 24±5%, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22±4 mm Hg; HR, 6±1 beats per minute; and RSNA, 15±4%). This attenuation by clonidine was dose dependent (3.8 μmol/L, 38 μmol/L, 380 μmol/L, and 3.8 mmol/L). Preadministration of the α2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 μmol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 μmol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380±0.018 fmol/100 μL; after clonidine, 0.356±0.012 fmol/100 μL). These results demonstrate that stimulation of α2-adrenergic receptors in the L-7 dorsal horn attenuates the cardiovascular responses and RSNA changes to static contraction and passive stretch. This attenuation by clonidine appears not to be mediated through presynaptic inhibition of SP release.

Original languageEnglish (US)
Pages (from-to)567-575
Number of pages9
JournalCirculation Research
Volume75
Issue number3
StatePublished - Sep 1994

Fingerprint

Clonidine
Substance P
Muscle Contraction
Reflex
Kidney
Arterial Pressure
Heart Rate
Microdialysis
Muscles
Adrenergic Antagonists
Yohimbine
Spinal Nerve Roots
Adrenergic Receptors
Spinal Cord
Cats
Spinal Cord Dorsal Horn

Keywords

  • α- adrenergic receptor
  • exercise pressor reflex
  • passive stretch
  • sympathetic nerve activity
  • yohimbine

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Effects of clonidine on the reflex cardiovascular responses and release of substance P during muscle contraction. / Ally, Ahmmed; Meintjes, André F.; Mitchell, Jere H.; Wilson, L. Britt.

In: Circulation Research, Vol. 75, No. 3, 09.1994, p. 567-575.

Research output: Contribution to journalArticle

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abstract = "The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48±6 mm Hg, 18±2 beats per minute, and 66±5{\%}, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51±6 mm Hg, 17±2 beats per minute, and 50±3{\%}, respectively. Microdialysis of clonidine (380 μmol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19±4 mm Hg, 7±1 beats per minute, and 24±5{\%}, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22±4 mm Hg; HR, 6±1 beats per minute; and RSNA, 15±4{\%}). This attenuation by clonidine was dose dependent (3.8 μmol/L, 38 μmol/L, 380 μmol/L, and 3.8 mmol/L). Preadministration of the α2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 μmol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 μmol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380±0.018 fmol/100 μL; after clonidine, 0.356±0.012 fmol/100 μL). These results demonstrate that stimulation of α2-adrenergic receptors in the L-7 dorsal horn attenuates the cardiovascular responses and RSNA changes to static contraction and passive stretch. This attenuation by clonidine appears not to be mediated through presynaptic inhibition of SP release.",
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N2 - The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48±6 mm Hg, 18±2 beats per minute, and 66±5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51±6 mm Hg, 17±2 beats per minute, and 50±3%, respectively. Microdialysis of clonidine (380 μmol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19±4 mm Hg, 7±1 beats per minute, and 24±5%, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22±4 mm Hg; HR, 6±1 beats per minute; and RSNA, 15±4%). This attenuation by clonidine was dose dependent (3.8 μmol/L, 38 μmol/L, 380 μmol/L, and 3.8 mmol/L). Preadministration of the α2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 μmol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 μmol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380±0.018 fmol/100 μL; after clonidine, 0.356±0.012 fmol/100 μL). These results demonstrate that stimulation of α2-adrenergic receptors in the L-7 dorsal horn attenuates the cardiovascular responses and RSNA changes to static contraction and passive stretch. This attenuation by clonidine appears not to be mediated through presynaptic inhibition of SP release.

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