Blood-borne angiotensin II and plasma hypernatremia can alter the discharge rate of subfornical organ neurons, potentially influencing arterial pressure and vasopressin release.
Experiments were done in urethan-anesthetized rats to investigate the effect of plasma angiotensin II (ANG II) and hypernatremia on the excitability of subfornical organ (SFO) neurons projecting directly to paraventricular nucleus of the hypothalamus (PVH), supraoptic nucleus (SON), and nucleus medianus (NM). Extracellular recordings were made from 106 antidromically identified neurons in the SFO. The firing frequency of 53 (50%) was increased by the intracarotid infusion of ANG II and/or 0.5 M hypertonic NaCl. The intracarotid infusion of isotonic saline or the intravenous infusion of phenylephrine did not alter the discharge rate of these SFO neurons. Of 38 PVH projecting neurons, 21 (55%) responded to ANG II and/or hypertonic NaCl: 9 to ANG II only, 8 to hypertonic NaCl only, and 4 to both. Similarly, of 42 SON projecting neurons, 30 (71%) responded to ANG II and/or hypertonic NaCl: 10 to ANG II only, 15 to hypertonic NaCl only, and 5 to both. Finally, of 26 NM projecting neurons, one increased its firing frequency to ANG II and one other to 0.5 M NaCl. An additional eight SFO neurons were found to send collateral axons to both the PVH and SON (n = 6) and PVH and NM (n = 2): four responded in various combinations to intracarotid infusion of ANG II and 0.5 M NaCl. These data suggest that blood-borne ANG II and plasma hypernatremia can influence arterial pressure and the release of vasopressin from the neurohypophysis by altering the discharge rate of SFO neurons projecting to forebrain structures that contain magnocellular neurosecretory vasopressin neurons and neurons that are components of sympathoexcitatory pathways.
Gutman et al. (1988) studied this question.