Renal afferent fibers relay information from renal mechanoreceptors and chemoreceptors to the central nervous system. This information is responsible for activating renorenal reflexes, initiating renal pain, and contributing to regulation of blood pressure. The mechanisms by which renal afferent information alters activity in the central nervous systems are unknown. This research will test the following hypotheses: 1) electrical stimulation of renal afferent fibers alters activity of spinoreticular and spinothalamic neurons in the lower thoracic and upper lumbar spinal cord; 2) spinoreticular neurons are responsive to renal stimuli which elicit cardiovascular and renorenal reflexes; 3) noxious renal stimuli activate spinothalamic neurons. These hypotheses will be tested in experiments on alphachloralose anesthetized cats. Extracellular potentials will be recorded from cells in the spinal cord which project either to the medial reticular formation or the contralaternal thalamus. After locating a cell, its responsiveness to electrical stimulation of the renal nerves will be examined and the type of fiber input responsible for the responses determined. Each cell will also be tested for responsiveness to somatic stimuli. More natural stimuli will be used to excite renal receptors, including increases in renal venous pressure, renal arterial pressure, and ureteral pressure to activate renal mechanoreceptors. Renal chemoreceptors will be activated by prolonged renal artery occlusion and by back perfusion of various solutions into the renal pelvis. Noxious stimuli will include injections of algesic chemicals into the renal circulation and severe distention of the renal pelvis. The responses of spinoreticular and spinothalamic neurons to these maneuvers will be determined as well as the stimulus intensity - cell response relationship. The information gained from these experiments will provide a basis for understanding renal pain, renorenal reflexes, and the possible participation of renal receptors in hypertension.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
7R01HL036378-01
Application #
3351354
Study Section
Experimental Cardiovascular Sciences Study Section (ECS)
Project Start
1985-09-30
Project End
1987-03-31
Budget Start
1985-09-30
Budget End
1986-03-31
Support Year
1
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Thomas Jefferson University
Department
Type
Schools of Medicine
DUNS #
061197161
City
Philadelphia
State
PA
Country
United States
Zip Code
19107
Standish, A; Vizzard, M A; Ammons, W S (1993) Tonic descending modulation of spinal neuronal responses to activation of renal receptors. Am J Physiol 265:R1291-303
Ammons, W S (1992) Bowditch Lecture. Renal afferent inputs to ascending spinal pathways. Am J Physiol 262:R165-76
Standish, A; Vizzard, M A; Ammons, W S (1992) Tonic descending modulation of spinal neurons with renal input. Brain Res 576:12-24
Ammons, W S (1991) Responses of spinoreticular cells to graded increases in renal venous pressure. Am J Physiol 260:R27-31
Ammons, W S (1989) Primate spinothalamic cell responses to ureteral occlusion. Brain Res 496:124-30
Ammons, W S (1989) Responses of primate spinothalamic tract neurons to renal pelvic distension. J Neurophysiol 62:778-88
Ammons, W S (1989) Electrophysiological characteristics of primate spinothalamic neurons with renal and somatic inputs. J Neurophysiol 61:1121-30
Ammons, W S; Sinha, R (1989) Responses of thoracolumbar spinal neurons to renal artery occlusion. Am J Physiol 256:H1515-23
Ammons, W S (1988) Spinoreticular cell responses to intrarenal injections of bradykinin. Am J Physiol 255:R994-1001
Ammons, W S (1988) Renal and somatic input to spinal neurons antidromically activated from the ventrolateral medulla. J Neurophysiol 60:1967-81

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