CARDIOVASCULAR EFFECTS OF NACL MICROINJECTIONS INTO THE NUCLEUS OF THE SOLITARY TRACT

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.