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  • Title: A study of the role of renal nerves in the renal responses to 60 degree head-up tilt in the anaesthetized dog.
    Author: DiBona GF, Johns EJ.
    Journal: J Physiol; 1980 Feb; 299():117-26. PubMed ID: 7381761.
    Abstract:
    1. Renal responses to 10 min of 60 degrees head-up tilt were measured in anaesthetized dogs in which renal perfusion pressure was maintained at a relatively constant value.2. Tilting was associated with a fall in systemic blood pressure and an increase in heart rate. Renal blood flow and glomerular filtration rate remained constant while there was a significant decrease in both absolute and fractional excretion of sodium.3. Animals which had undergone acute renal denervation were tilted. The cardiovascular responses were similar to intact animals. A fall in renal blood flow was observed but the glomerular filtration rate was maintained at a steady value during tilting. The decreased renal tubular excretion of sodium measured in intact animals was abolished.4. Alpha-adrenergic blockade of the kidney was achieved by infusion of phentolamine into the renal artery. Tilting of these animals caused cardiovascular changes similar to those observed in control animals but renal blood flow, glomerular filtration rate and sodium handling remained unchanged.5. Animals in which both carotid sinuses had been acutely denervated were tilted. Systemic blood pressure fell as in intact animals, but the rise in heart rate was significantly less. Renal blood flow, glomerular filtration rate and the rate of sodium excretion were unchanged.6. A 10 min period of 60 degrees head-up tilt in anaesthetized dogs resulted in an unchanged renal blood flow and glomerular filtration rate which was associated with a decrease in both fractional excretion of sodium and sodium excretion. The renal sympathetic nerves were shown to be responsible for these changes in tubular sodium handling which appeared to exert their action via renal tubular alpha-adrenergic receptors. This activation of the renal nerves appeared to be mediated by the carotid sinus baroreceptor reflex.
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