Vasopressin inhibits sympathetic ganglionic transmission but potentiates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

K. P. Patel, P. G. Schmid

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

To determine whether vasopressin (AVP) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or i.a. norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1-8 Hz), or administration of NE (50-200 ng), in the isolated constant-flow perfused hind limb of chloralose-anesthetized rabbits (n = 7), before and after i.a. infusion of AVP (0.65 mU/kg/min). AVP significantly potentiated responses to LSNS (relative potency (RP) = 1.59) and to NE (RP = 5.17). The potentiation of LSNS and NE by AVP infusion was abolished by the AVP V1 antagonist, d(CH2)5[Tyr(Me)2]AVP, 400 ng, total dose (n = 6). Because there was a significant difference between the RP of LSNS (stimulation of both preganglionic and postganglionic nerves) and NE (direct effect on the vascular smooth muscle), we verified whether this difference might represent disparate actions of AVP on the ganglia and/or sympathetic neuroeffector sites. To evaluate responses to stimulating only the postganglionic sympathetic nerves, we repeated the above study in animals pretreated with a supramaximal dose of the ganglionic blocking agent hexamethonium (25 mg/kg i.v.). After ganglionic blockade the responses to LSNS were reduced to 22% of control. In the presence of ganglionic blockade, AVP potentiated responses to LSNS (RP = 4.09) (n = 6). Potentiation was now no different between postganglionic LSNS and NE. We draw the following conclusions from these data: 1) AVP potentiates vasoconstrictor responses to both LSNS and NE; 2) AVP-mediated potentiation of vasoconstrictor responses to these stimuli is mediated via V1 receptors; and 3) AVP seems to have disparate actions, i.e., inhibition of neurotransmission at the sympathetic ganglia and potentiation at the neuroeffector site.

Original languageEnglish (US)
Pages (from-to)779-785
Number of pages7
JournalJournal of Pharmacology and Experimental Therapeutics
Volume245
Issue number3
StatePublished - Jan 1 1988

Fingerprint

Hindlimb
Vasopressins
Norepinephrine
Rabbits
Vasoconstrictor Agents
Sympathetic Ganglia
Ganglionic Blockers
Vasopressin Receptors
Hexamethonium
Chloralose
Vascular Smooth Muscle
Synaptic Transmission
Electric Stimulation
Extremities
Perfusion
Pressure

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Cite this

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title = "Vasopressin inhibits sympathetic ganglionic transmission but potentiates sympathetic neuroeffector responses in hindlimb vasculature of rabbits",
abstract = "To determine whether vasopressin (AVP) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or i.a. norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1-8 Hz), or administration of NE (50-200 ng), in the isolated constant-flow perfused hind limb of chloralose-anesthetized rabbits (n = 7), before and after i.a. infusion of AVP (0.65 mU/kg/min). AVP significantly potentiated responses to LSNS (relative potency (RP) = 1.59) and to NE (RP = 5.17). The potentiation of LSNS and NE by AVP infusion was abolished by the AVP V1 antagonist, d(CH2)5[Tyr(Me)2]AVP, 400 ng, total dose (n = 6). Because there was a significant difference between the RP of LSNS (stimulation of both preganglionic and postganglionic nerves) and NE (direct effect on the vascular smooth muscle), we verified whether this difference might represent disparate actions of AVP on the ganglia and/or sympathetic neuroeffector sites. To evaluate responses to stimulating only the postganglionic sympathetic nerves, we repeated the above study in animals pretreated with a supramaximal dose of the ganglionic blocking agent hexamethonium (25 mg/kg i.v.). After ganglionic blockade the responses to LSNS were reduced to 22{\%} of control. In the presence of ganglionic blockade, AVP potentiated responses to LSNS (RP = 4.09) (n = 6). Potentiation was now no different between postganglionic LSNS and NE. We draw the following conclusions from these data: 1) AVP potentiates vasoconstrictor responses to both LSNS and NE; 2) AVP-mediated potentiation of vasoconstrictor responses to these stimuli is mediated via V1 receptors; and 3) AVP seems to have disparate actions, i.e., inhibition of neurotransmission at the sympathetic ganglia and potentiation at the neuroeffector site.",
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T1 - Vasopressin inhibits sympathetic ganglionic transmission but potentiates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

AU - Patel, K. P.

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N2 - To determine whether vasopressin (AVP) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or i.a. norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1-8 Hz), or administration of NE (50-200 ng), in the isolated constant-flow perfused hind limb of chloralose-anesthetized rabbits (n = 7), before and after i.a. infusion of AVP (0.65 mU/kg/min). AVP significantly potentiated responses to LSNS (relative potency (RP) = 1.59) and to NE (RP = 5.17). The potentiation of LSNS and NE by AVP infusion was abolished by the AVP V1 antagonist, d(CH2)5[Tyr(Me)2]AVP, 400 ng, total dose (n = 6). Because there was a significant difference between the RP of LSNS (stimulation of both preganglionic and postganglionic nerves) and NE (direct effect on the vascular smooth muscle), we verified whether this difference might represent disparate actions of AVP on the ganglia and/or sympathetic neuroeffector sites. To evaluate responses to stimulating only the postganglionic sympathetic nerves, we repeated the above study in animals pretreated with a supramaximal dose of the ganglionic blocking agent hexamethonium (25 mg/kg i.v.). After ganglionic blockade the responses to LSNS were reduced to 22% of control. In the presence of ganglionic blockade, AVP potentiated responses to LSNS (RP = 4.09) (n = 6). Potentiation was now no different between postganglionic LSNS and NE. We draw the following conclusions from these data: 1) AVP potentiates vasoconstrictor responses to both LSNS and NE; 2) AVP-mediated potentiation of vasoconstrictor responses to these stimuli is mediated via V1 receptors; and 3) AVP seems to have disparate actions, i.e., inhibition of neurotransmission at the sympathetic ganglia and potentiation at the neuroeffector site.

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