The cardiocyte as a target for parathyroid hormone in end-stage renal disease.
Approximately 50% of the annual mortality in patients with end-stage renal disease (ESRD) is attributed to cardiovascular-related events. Multiple factors, including volume overload, hypertension, electrolyte abnormalities, and the presence of comorbid diseases, such as diabetes mellitus, may have an adverse effect on left ventricular function in ESRD. The purpose of this brief review is to advance the hypothesis that parathyroid hormone (PTH) is a cardiotoxin and a potential mediator of cardiac dysfunction in uremia. Recent studies have provided evidence that cardiocytes possess a distinct class of binding sites for PTH, and the PTH receptor has recently been cloned. Furthermore, the PTH receptor may be coupled to more than one effector pathway. Finally, the possibility that a PTH-related protein autocrine system may be present in cardiocytes and the implications of this signaling pathway on cardiocyte function are discussed.
Department of Medicine, New York Medical College, Valhalla, New York.
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D000818:Animals; D006333:Heart Failure / Q000503:physiopathology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology*; D010281:Parathyroid Hormone / Q000502:physiology*; D018016:Receptors, Parathyroid Hormone / Q000502:physiology*; D016277:Ventricular Function, Left / Q000502:physiology*
D010281:Parathyroid Hormone; D018016:Receptors, Parathyroid Hormone