Differential sympathetic responses initiated by angiotensin and sodium chloride

Angiotensin II (ANG II) and NaCl act on central receptors to cause pressor responses that may be mediated in part by the sympathetic nervous system. The inhibitory or excitatory nature of effects on central sympathetic outflow are not well defined. This study was undertaken to evaluate further the potential contribution of the sympathetic nervous system to central actions of angiotensin or hypertonic NaCl. Experiments were performed using anesthetized, sinoaortic denervated, vagotomized cats. Intracarotid injection of NaCl produced increased splenic sympathetic nerve activity and decreased renal sympathetic nerve activity. Intracerebroventricular (icv) administration of NaCl caused slight excitatory responses in splenic nerves and no change in renal nerve activity. Intracarotid injection of ANG II caused significantly greater splenic than renal excitation. Administration of ANG II icv caused excitation of splenic nerve activity and no change in renal nerve activity. These findings illustrate that stimulation of sodium-sensitive and angiotensin-sensitive CNS receptors produces differential responses in sympathetic outflow. These differential sympathetic responses may contribute to the complex cardiovascular responses to increased plasma or brain concentrations of angiotensin or sodium.