Evidence for a role of PTH in the reduced pressor response to norepinephrine in chronic renal failure.
Reduced pressor response to norepinephrine (NE) is present in patients with chronic renal failure (CRF) and is responsible partly for some of the manifestations of autonomic nervous system dysfunction in these patients. PTH blunts the pressor response to NE in normal rats, suggesting that excess PTH in CRF may be responsible for this abnormality. However, the relative roles of uremia and of excess PTH in the uremic state in the genesis of this abnormality are not defined. The present study examines this question. Rats with chronic renal failure display reduced pressor response to NE administration, but this derangement can be prevented by prior parathyroidectomy and abolished by administration of indomethacin. The role of PTH in the genesis of this abnormality can also be demonstrated in the hind limb preparation obtained from rats with CRF. Our data show that excess PTH and not other consequences of CRF plays a paramount pathogenetic role in the reduced pressor response to NE and that this effect of PTH is due to a direct action on the blood vessels. Further, this hormone action is most likely mediated through increased production of vasodilating prostaglandins. These observations are constant with the idea that PTH would contribute to the pathogenesis of some of the manifestations of autonomic nervous system dysfunction in CRF.[1]References
- Evidence for a role of PTH in the reduced pressor response to norepinephrine in chronic renal failure. Iseki, K., Massry, S.G., Campese, V.M. Kidney Int. (1985) [Pubmed]
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