Excision of the thoracic portion of the splanchnic nerves and the lower four dorsal sympathetic ganglia on both sides failed to prevent the development of persistent hypertension which, in dogs, follows the production of renal ischemia by partial clamping of the renal arteries (1). In dogs with this type of experimental renal hypertension existent for varying lengths of time (up to about 4 years), excision of the splanchnic nerves and the lower four dorsal sympathetic ganglia failed to effect any degree of permanent lowering of the blood pressure.
For the dog, at least, these results tend to minimize the importance of the splanchnic vasomotor mechanism in the pathogenesis of renal hypertension. This is in agreement with the conclusions of Prinzmetal and Wilson (6) and of Pickering (7) about the part played by the vasomotor system in human hypertension. It is also in agreement with the work of Page (8), and of Collins (9), who showed that in dogs excision of the extrinsic renal nerves alone does not prevent experimental hypertension due to renal ischemia. Although the results of this investigation fail to give experimental support for the operation that is being practised on human beings with hypertension, yet they do not necessarily controvert the reports of beneficial effects in some cases of human hypertension. Further study of the effects on man is necessary before the results of this operation can be adequately evaluated.