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Spinal vasopressin modulates the reflex cardiovascular response to static contraction
C L Stebbins1, A Ortiz-Acevedo, J M Hill
1Department of Internal Medicine, University of California, Davis 95616.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 1, 1992
Summary
Arginine vasopressin (AVP) in the spinal cord reduces cardiovascular responses to muscle contraction, primarily through V1 receptors. This modulation impacts sensory nerve transmission from contracting muscles.
Area of Science:
- Neuroscience
- Cardiovascular Physiology
- Pain Research
Background:
- Arginine vasopressin (AVP) is implicated in modulating spinal cord activity.
- Nociceptors (group III and IV afferents) transmit signals related to muscle contraction and pain.
- Spinal AVP may influence cardiovascular reflexes originating from contracting muscles.
Purpose of the Study:
- To investigate the role of spinal arginine vasopressin (AVP) in mediating reflex cardiovascular responses to static muscle contraction.
- To determine the specific vasopressin receptor subtypes (V1 or V2) involved in this modulation.
Main Methods:
- Electrically induced static hindlimb muscle contraction in cats.
- Intrathecal (IT) administration of AVP, V1 receptor antagonist, V2 receptor antagonist, and V2 receptor agonist.
- Measurement of mean arterial pressure (MAP), myocardial contractility (dP/dt), and heart rate (HR).
Main Results:
- IT AVP injection attenuated pressor and contractile responses to muscle contraction.
- V1 receptor blockade enhanced contraction-induced increases in MAP and dP/dt.
- V2 receptor blockade had no effect, while V2 stimulation attenuated dP/dt and HR responses.
Conclusions:
- Spinal AVP attenuates reflex cardiovascular responses to muscle contraction.
- This effect is primarily mediated via V1 receptors in the lumbar spinal cord.
- AVP modulates sensory nerve transmission from contracting muscles.