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Spinal Arginine Vasopressin Elevates Renal Nerve Activity in the Rat
Author(s) -
Riphagen Colleen L.,
Pittman Quentin J.
Publication year - 1989
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.1989.tb00126.x
Subject(s) - vasopressin , endocrinology , medicine , arginine , arginine vasopressin receptor 1b , chemistry , arginine vasopressin receptor 2 , amino acid , antagonist , receptor , biochemistry
Intrathecal injections of arginine vasopressin increased activity recorded from multifiber renal nerve bundles of anesthetized rats by 47 + 14%. This response was significantly attenuated following perfusion of the intrathecal space with a vasopressin antagonist, d(CH 2 ) 5 Tyr(Me)AVP. It is unlikely that vasopressin leaked to the periphery as iv administration of 10 pmol vasopressin decreased renal nerve activity by 9 + 1%. Electrical stimulation of the paraventricular nucleus (three stimuli at 20 to 100 μA, 100 or 200 Hz) caused a biphasic excitatory response with the peaks of increased renal nerve activity occurring between 50 to 100 and 100 to 200 ms after stimulation. Intrathecal application of the vasopressin antagonist prior to repeating the stimulation of the paraventricular nucleus attenuated the second excitatory response without affecting the first excitatory episode. In animals in which the stimulating electrode was located adjacent to, but not within, the paraventricular nucleus, a monophasic excitatory response (at between 100 to 150 ms after the stimulation) was observed. This response was not attenuated by the intrathecal antagonist. These results are consistent with earlier studies which suggested that arginine vasopressin may function as a mediator of synaptic transmission at spinal levels in pathways influencing kidney function.