Nitric oxide influences ventrolateral medullary mechanisms of vasomotor control in the cat.

In acute experiments on cats changes in the background sympathetic activity in the renal nerve, chosen as a model of vaso-constrictor nerve, together with arterial pressure shifts have been found following injections of nitric oxide (NO) containing drugs into the ventrolateral medulla. This is the first report of evidence that both sodium nitroprusside, which produces NO spontaneously and thus mimics endothelium-derived relaxing factor (EDRF), and L-arginine, being a precursor for NO, as well as L-NG-monomethyl-L-arginine (L-NMMA) which inhibits synthesis of NO, induce remarkable changes in the background activity of the renal nerve and systemic arterial pressure (SAP) level shifts, following unilateral injections of drugs examined into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla. These sites are essential for the maintenance of arterial pressure level and vascular tone control. Injections of NO-containing drugs in the RVLM induce attenuation of the renal nerve sympathetic activity and lower the SAP level, while injections in the CVLM reverse these effects. After previous application of Methylene blue on the ventral medullary surface we failed to induce any of the effects following NO injections in the sites examined. Our results raise the possibility that NO influences mechanisms of the neurogenic vasomotor control, realized by neurons within the RVLM and the CVLM via activation of the guanylate cyclase.