Renal Response to Electrical Stimulation in the Septum and Diencephalon of Rabbits
The septum and diencephalon were electrically stimulated with stereotaxically placed bipolar, concentric electrodes in pentobarbital anesthetized rabbits with one kidney acutely denervated. Transient changes (30-60 seconds) in renal blood flow and urine flow were estimated with electromagnetic flowmeters and drop recorders and persistent changes (20-30 minutes) by clearance techniques. Hypothalamic stimulation, particularly in the perifornical region, caused increased blood pressure, reflex bradycardia (blocked by atropine), and intense renal vasoconstriction in the innervated kidney with a latency of about 2 seconds. In the denervated kidney renal blood flow increased with the rise in blood pressure but after 10-15 seconds decreased, possibly in response to catecholamines released from the adrenal glands. Clearance studies during hypothalamic stimulation showed persistent decreases in renal blood flow, glomerular filtration, maximal tubular transport of glucose and paraaminohippurate, and water and electrolyte excretion in the innervated kidney. The parallel decreases in the maximum tubular transport of glucose and glomerular filtration rate suggest nephron closure rather than flow redistribution as the major component of the response. Ventral thalamic and septal stimulation decreased blood pressure and renal blood flow in the denervated kidney to about the same extent. Ventral thalamic stimulation also decreased renal blood flow in the innervated kidney whereas septal stimulation transiently increased renal blood flow, suggesting inhibition of existing sympathetic vasoconstriction (not blocked by atropine). In clearance studies, effects of septal stimulation on the intact kidney (relative to the denervated kidney) were similar to the effects of acute denervation and consistent with redistribution of intrarenal blood flow.
- neural control of the kidney
- renal nerves
- pressor responses
- Received July 26, 1971.
- Accepted December 16, 1971.
- © 1972 American Heart Association, Inc.