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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Hypertens
2017 ; 30
(4
): 435-443
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Increased Expression of Macrophage Migration Inhibitory Factor in the Nucleus of
the Solitary Tract Attenuates Renovascular Hypertension in Rats
#MMPMID28158469
Barbosa RM
; Speretta GF
; Dias DPM
; Ruchaya PJ
; Li H
; Menani JV
; Sumners C
; Colombari E
; Colombari DSA
Am J Hypertens
2017[Apr]; 30
(4
): 435-443
PMID28158469
show ga
BACKGROUND: Macrophage migration inhibitory factor (MIF) is an intracellular
inhibitory regulator of the actions of angiotensin II in the central nervous
system. Renovascular hypertensive 2-kidney, 1-clip (2K1C) rats have an increased
activity of the renin-angiotensin system and a decrease in baroreflex function
compared to normotensive (NT) rats. In the present study, we tested the effects
of MIF overexpression within the nucleus of the solitary tract (NTS), a key
brainstem region for cardiovascular regulation, on the development of
hypertension, on baroreflex function, and on water and food intake in 2K1C rats.
METHODS: Holtzman NT rats received a silver clip around the left renal artery to
induce 2K1C hypertension. Three weeks later, rats were microinjected in the NTS
with AAV2-CBA-MIF, to increase the expression of MIF, or with the control vector
AAV2-CBA-enhanced green fluorescent protein. Mean arterial pressure (MAP) and
heart rate were recorded by telemetry. Baroreflex function was tested, and water
and food intake were also measured. RESULTS: Increasing MIF expression in the NTS
of 2K1C rats attenuated the development of hypertension, reversed the impairment
of baroreflex function, and reduced the increase in water intake. In contrast to
2K1C rats, similar increases in MIF expression in the NTS of NT rats produced no
changes in baseline MAP, baroreflex function, or water intake. CONCLUSIONS: These
results indicate that an increased expression of MIF within the NTS attenuates
the development of hypertension and restores the baroreflex function in 2K1C
rats.