This research is designed to describe how information from the kidney is organized within the spinoreticular and spinothalamic pathways. Renal mechanoreceptors and chemoreceptors initiate cardiovascular reflexes and cause renal pain. The neural mechanisms that underlie these functions are unknown. The following hypotheses will be tested: 1) activation of renal receptors by noxious stimuli leads to increased activity of the spinoreticular and spinothalamic pathways; 2) the spinoreticular pathway participates in cardiovascular reflex changes associated with noxious renal events; whereas 3) the spinothalamic pathway mediates the perception of renal pain including its referral to somatic structures. The hypotheses will be tested in experiments on alpha-chloralose anesthetized cats and monkeys. Extracellular potentials will be recorded from spinoreticular cells in cats and spinothalamic cells in monkeys. Cells that are responsive to electrical stimulation of renal nerves will be tested for responses to other more natural renal stimuli as well as somatic stimuli. Primate spinothalamic tract cells will be examined for responses to increased renal vein and ureteral pressure and to intrarenal injection of algesic chemicals. Both spinothalamic and spinoreticular cells will be tested for responses to renal chemoreceptor stimuli, renal ischemia, and backflow of nondiuretic urine into the renal pelvis. The axon terminals of spinoreticular cells will be located and glutamate injected in order to activate cell bodies in the region of the axon terminal. The resulting changes in cardiovascular parameters and in the activity of the spinoreticular cell will be recorded. Information from these experiments will increase our understanding of mechanisms of renal pain and its referral to somatic structures. In addition, these experiments will provide information about the role of the spinoreticular tract in cardiovascular reflexes during painful or pathophysiological renal states.
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