AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 1 193-R200, Copyright © 1989 by American Physiological Society
Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats
A. Martinez-Arizala, J. W. Holaday and J. B. Long
Department of Medical Neurosciences, Walter Reed Army Institute of Research, Washington, DC 20307.
Increases in mean arterial pressure and heart rate have been documented
after the intrathecal administration of [Arg8]vasopressin (AVP) in rats.
Prior studies in our laboratories with conscious rats indicated that these
cardiovascular changes were associated with a marked hindlimb sensorimotor
dysfunction. In this study, which represents the first systematic
comparison of the effects of intrathecal AVP in conscious and anesthesized
rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the
motor dysfunction induced by intrathecal AVP is accompanied by a rise in
mean arterial pressure that is significantly greater than that produced by
an equal intravenous dose of AVP, and 2) both paralytic and pressor effects
of intrathecal but not intravenous AVP are blocked by the intrathecal
administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT)
but are not blocked by intravenous phenoxybenzamine, hexamethonium, or
[Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in
anesthesized rats the arterial pressor response to intrathecal AVP was
blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous
phenoxybenzamine. Furthermore, conscious but not anesthesized rats
exhibited a tachyphylaxis to intrathecal AVP. These results indicate that
intrathecal AVP produces both the cardiovascular changes and the
sensorimotor deficits through interactions with centrally located
V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate
the rise in mean arterial pressure produced by intrathecal AVP in
anesthesized rats, but they do not in conscious rats.
