Efferent Renal Nerve Activity Research Articles

Reflex effects of hepatic baroreceptors on renal and cardiac sympathetic nerve activity.

The reflex effects of hepatic low-pressure baroreceptors on renal and cardiopulmonary sympathetic efferent nerve activity were studied in mongrel dogs anesthetized with pentobarbital sodium. Systemic blood pressure, central venous pressure, hepatic, renal, and portal venous pressures were all measured during occlusion of the thoracic vena cava above the diaphragm, below the liver, and during occlusion of the portal vein. Renal and cardiopulmonary sympathetic efferent nerve activity was continuously recorded along with the hepatic efferent nerve activity during the caval occlusions. Hepatic baroreceptor excitation resulted in marked increases in hepatic afferent nerve activity and reflex increases in renal and cardiopulmonary sympathetic efferent nerve activity without a change in heart rate. Section of the anterior hepatic nerves eliminated the reflex increase in renal efferent nerve activity, but did not eliminate the increase in cardiopulmonary sympathetic efferent nerve activity. Carotid sinus denervation, bilateral cervical vagotomy, and phrenectomy did not alter the reflex responses to hepatic baroreceptor excitation. These hepatorenal and hepatocardiopulmonary reflexes may be important reflex mechanisms that are activated during congestive heart failure and cirrhosis of the liver.

Denervated and intact kidney responses to saline load in awake and anesthetized dogs.

The function of the innervated and denervated kidney was examined in clearance studies with unilaterally renal-denervated conscious and anesthetized dogs before and after saline loading. Barbiturate anesthesia distinctly depressed hemodynamics and excretory function of both kidneys and increased the difference between the denervated and innervated organ. In conscious moderately hydrated dogs the denervated kidney excreted slightly more sodium and water, while after saline loading higher excretion was observed on the innervated side. The denervated-to-innervated kidney ratios for UNaV, UNaV/100 ml GFR, and urine flow fell significantly from mean control values of 1.27, 1.27, and 1.20, respectively, to 0.80, 0.87, and 0.77 after extracellular volume expansion. Similar alterations of the ratios were observed in anesthetized dogs, but higher excretion of the denervated kidney persisted after saline loading. It is concluded that the greater natriuretic response of the intact kidney to saline infusion was due to inhibition of sodium-retaining action of renal efferent nerve activity by acute extracellular volume expansion.

Reflex effects of thoracic sympathetic afferent nerve stimulation on the kidney.

Thoracic sympathetic afferents may play a role in the reflex control of renal vascular resistance during hypotension. Mongrel dogs were anesthetized with ketamine hydrochloride and maintained on a 50-50, O2-N2O mixture supplemented with 0.5%-1.0% halothane. Systemic arterial blood pressure was lowered to 50 mmHg with use of a constant pressure hemorrhage technique. The renal circulation was perfused with a constant-flow perfusion system. Low-frequency (3 Hz) stimulation of thoracic sympathetic afferents produced renal vasodilation. A reduction of renal vascular resistance was measured as a decrease in constant-flow perfusion pressure. Vagotomy accentuated the dilator response to stimulation. High-frequency (30 Hz) afferent stimulation produced renal vasoconstriction. Renal efferent nerve activity and renal blood flow responded to afferent stimulation (3 Hz) by transient inhibition of efferent activity and increases in renal blood flow. Afferent stimulation (30 Hz) caused increases in renal efferent nerve activity and decreases in renal blood flow. The thoracic sympathetic afferents carry information from cardiopulmonary structures that alter renal efferent nerve activity and renal hemodynamics during hypotension.

Effects of a beta-adrenergic blocking drug, atenolol, on efferent renal nerve activity in rabbits (author's transl)

Postganglionic sympathetic nerve activity (renal nerve) decreased significantly during i.v. infusion of a beta-adrenergic blocking drug, atenolol, in anesthetized rabbits. This phenomenon, at least in part reflex in nature, may contribute to the hypotensive effect of atenolol.