Sl. Hochstenbach et J. Ciriello, CARDIOVASCULAR EFFECTS OF NACL MICROINJECTIONS INTO THE NUCLEUS OF THE SOLITARY TRACT, Brain research, 644(2), 1994, pp. 233-242
The nucleus of the solitary tract (NTS) was systematically explored in
the alpha-chloralose-anesthetized rat for sites that elicited changes
in mean arterial pressure (MAP) and heart rate (HR) during microinjec
tions (20 nl) of phosphate-buffered saline (PBS; pH 7.2-7.4) or NaCl s
olutions containing various concentrations of NaCl (104-326 mM). Decre
ases in MAP (range 7-83 mmHg) and HR (range 10-70 bpm) were consistent
ly elicited from sites in the caudal medial and commissural subnuclei
of NTS. Microinjection of PBS or NaCl into other NTS subnuclei or area
postrema did not elicit cardiovascular responses. Microinjection of L
iCl in PBS elicited cardiovascular responses that were significantly s
maller than those elicited by microinjection of NaCl in PBS at the sam
e NTS site. Injections of either a hyperosmotic (400 mOsm/kg) or a hyp
osmotic (204 mOsm/kg) solution of mannitol into NaCl-sensitive sites d
id not elicit cardiovascular responses. Finally, most of the sites in
NTS that elicited cardiovascular responses during microinjection of gl
utamate (1 M) did not respond to microinjections of PBS. Administratio
n of atropine methyl bromide had no effect on the magnitude of the dep
ressor response to injections of PBS into NTS, but significantly atten
uated (32%) the HR response. Subsequent administration of the ganglion
ic blockers hexamethonium bromide or arfonad abolished both the depres
sor and bradycardic responses. These data suggest that within a restri
cted region of the caudal NTS there exists a pool of neurons sensitive
to changes in extracellular Na+ concentrations that, when activated b
y the sodium, elicit vasodepressor responses as a result of sympathoin
hibition and bradycardia as a result of vagal excitation and sympathoi
nhibition.