TY - JOUR
T1 - Vasopressin inhibits sympathetic ganglionic transmission but potentiates sympathetic neuroeffector responses in hindlimb vasculature of rabbits
AU - Patel, K. P.
AU - Schmid, P. G.
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1988
Y1 - 1988
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.
AB - 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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M3 - Article
C2 - 2898522
AN - SCOPUS:0023924407
VL - 245
SP - 779
EP - 785
JO - Journal of Pharmacology and Experimental Therapeutics
JF - Journal of Pharmacology and Experimental Therapeutics
SN - 0022-3565
IS - 3
ER -