Hemodynamic and renal functional changes after acute unilateral nephrectomy in the dog: role of carotid sinus baroreceptors.

Abstract

We examined the role of the carotid sinus baroreceptors in the hemodynamic and renal functional changes initiated by acute unilateral nephrectomy (AUN). In 15 anesthetized dogs, AUN caused increases in sodium (UNaV) and potassium excretion (UKV) without significant changes in GFR, renal blood flow, or mean arterial pressure. Cardiac output (CO) was measured in five of these animals and decreased from 2.5 +/- 0.2 to 1.9 +/- 0.3 liter/min as total peripheral resistance (TPR) increased. In 11 dogs with bilateral acute surgical carotid sinus denervation, AUN failed to cause any change in renal hemodynamics, UNaV, or UKV that could be distinguished from sham-operated time controls. CO was measured in seven of these dogs and also did not change. AUN caused an immediate, transient elevation in blood pressure that returned to control levels 15 min after nephrectomy. When bilateral carotid occlusion (BCO) was carried out prior to AUN in animals with intact carotid sinus baroreceptors, AUN again caused an immediate increase in blood pressure but no changes in CO or electrolyte excretion. In separate studies, AUN increased UNaV and UKV significantly; when BCO was then carried out after AUN, cation excretion remained elevated. In seven dogs undergoing continuous perfusion of the carotid circulation bilaterally at constant pressure, AUN again failed to increase cation excretion despite a 30 mmHg rise in arterial blood pressure. These studies demonstrate that AUN fails to initiate hemodynamic or compensatory renal functional changes in dogs with bilateral carotid sinus denervation or in animals in which intact baroreceptors are shielded from the systemic circulation by BCO or perfusion at constant pressure, indicating the importance of these baroreceptors in the early changes after AUN.