The major objective is to determine if endogenous vasopressin (reflexly stimulated secretion) contributes to the neural regulation of the circulation. The underlying hypothesis is that vasopressin at low concentrations may increase the gain of the arterial baroreflex to inhibit sympathetic nerve activity while at higher concentrations vasopressin may decrease the gain of the arterial baroreflex. At these higher concentrations of vasopressin, the reflex increase in sympathetic nerve activity to decreases in arterial pressure will be reduced. A second hypothesis is that the area postrema is necessary for the interaction of vasopressin with the arterial and cardiopulmonary baroreflexes. The third hypothesis is that circulating vasopressin may increase the arterial and cardiopulmonary inhibitions of vasopressin release thereby providing a mechanism whereby vasopressin might feedback to regulate its own release. Studies will be performed in conscious rabbits instrumented with arterial and venous catheters and electrodes on the renal, splanchnic and lumbar sympathetic nerves. By altering plasma vasopressin concentrations (osmotically or reflexly) we will be about to determine if endogenous vasopressin alters the arterial and cardiopulmonary baroreflex control of sympathetic nerve activity. The studies will be repeated in rabbits with lesion of the area postrema. We expect that in the lesioned rabbit the interactions of vasopressin with the arterial and cardiopulmonary baroreflex will be abolished. Additional studies are proposed to determine the arterial pressure, heart rate and sympathetic nerve responses to chemical and electrical stimulation of the area postrema.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Method to Extend Research in Time (MERIT) Award (R37)
Project #
5R37HL012415-18
Application #
3485315
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1975-02-01
Project End
1992-03-31
Budget Start
1988-04-01
Budget End
1989-03-31
Support Year
18
Fiscal Year
1988
Total Cost
Indirect Cost
Name
University of Texas Health Science Center San Antonio
Department
Type
School of Medicine & Dentistry
DUNS #
800772162
City
San Antonio
State
TX
Country
United States
Zip Code
78229
Sanderford, Max G; Bishop, Vernon S (2002) Central mechanisms of acute ANG II modulation of arterial baroreflex control of renal sympathetic nerve activity. Am J Physiol Heart Circ Physiol 282:H1592-602
Sanderford, M G; Bishop, V S (2000) Angiotensin II acutely attenuates range of arterial baroreflex control of renal sympathetic nerve activity. Am J Physiol Heart Circ Physiol 279:H1804-12
Nishida, Y; Sugimoto, I; Morita, H et al. (1998) Suppression of renal sympathetic nerve activity during portal vein infusion of hypertonic saline. Am J Physiol 274:R97-103
Farrell, D M; Bishop, V S (1997) The roles of cGMP and cAMP in active thermoregulatory vasodilation. Am J Physiol 272:R975-81
Nishida, Y; Hosomi, H; Bishop, V S (1997) Long-term effects of AVP-induced neurohumoral interaction via area postrema on body fluid and blood pressure. Am J Physiol 273:R1696-703
Qu, L; Hay, M; Bishop, V S (1997) Administration of AVP to the area postrema alters response of NTS neurons to afferent inputs. Am J Physiol 272:R519-25
Ryuzaki, M; Stahl, L K; Lyson, T et al. (1997) Sympathoexcitatory response to cyclosporin A and baroreflex resetting. Hypertension 29:576-82
DiCarlo, S E; Stahl, L K; Bishop, V S (1997) Daily exercise attenuates the sympathetic nerve response to exercise by enhancing cardiac afferents. Am J Physiol 273:H1606-10
Ryan, K L; Taylor, W F; Bishop, V S (1997) Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear. J Appl Physiol 83:2091-7
Cai, Y; Hay, M; Bishop, V S (1996) Synaptic connections and interactions between area postrema and nucleus tractus solitarius. Brain Res 724:121-4

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