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We read with interest the paper by M. Wolzt et al. (1) related to the hemodynamic effects of parathyroid hormone-related peptide (PTHrP) in man. These authors observed a dose-dependent increase in pulse rate, renal plasma flow, and hand vein diameter without any change in blood pressure in response to the infusion of the PTHrP analog PTHrP (1–34). Although this interesting study is the first to evaluate the effect of PTHrP in man, some conclusions are overdrawn beyond the information provided, mainly because of the lack of hemodynamic and hormonal assessment. As heart rate increased but blood pressure remained unchanged, determination of cardiac output and systemic vascular resistances would have allowed to attribute a peripheral vasodilating effect definitely to PTHrP. Measurement of catecholamines would have helped to differentiate tachycardia due to reflex baroreceptor responses from a direct chronotropic effect of PTHrP, as suggested in experiments using isolated rat hearts (2). The authors also claim that no effect was noted on parameters of cardiac inotropic performance, which were not evaluated as such by the present study even by noninvasive methods (echocardiography). On the contrary, based on a presumable baroreflex-induced tachycardia, there might be an indirect positive inotropic effect. In addition, others have shown that PTHrP might exert inotropic effects mediated via coronary vasodilation (3). Finally, the most important concern is the lack of PTHrP concentration monitoring during the infusion, which would have demonstrated whether the responses were of pharmacological or of pathophysiological relevance. Indeed, in humoral hypercalcemia of malignancy, associated with increased PTHrP concentrations, no cardiovascular changes are systematically present.

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Letters to the Editor
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