Ultraviolet Light May Contribute to Geographic and Racial Blood Pressure Differences

10. Teerlink JR, Breu V, Sprecher U, Clozel M, Clozel JP. Potent vasoconstriction mediated by endothelin ETB receptors in canine coronary arteries. Circ Res. 1994;74:105–114. Response: Dr Rossi and colleagues suggest an alternative explanation of the antinatriuretic effects of ET-1 infusion through its secretory effects on plasma aldosterone levels. Their hypothesis is certainly of interest. However, we feel that from our data this interpretation cannot be supported. First, the difference in plasma aldosterone, which was measured immediately before and at the end of the ET-1 infusion, was not significant. If we use a logarithmic transformation, the increments become even smaller (270 to 288 pmol/L for control; 256 to 267 pmol/L for enalapril; and 270 to 284 pmol/L for nifedipine). The within-assay variance coefficient of our assay was 9%, and the between-assay variance coefficient was 14%. The absence of an effect of pathophysiological increments in plasma ET-1 on aldosterone is in agreement with observations from other groups using similar infusion protocols. Moreover, to really identify the magnitude of a change in plasma aldosterone from our study, one would need a time-control study because there are important diurnal changes in the secretion of the hormone. Second, there was an immediate decrease in sodium excretion after ET-1 infusion, whereas one would expect a delay in the onset of the antinatriuretic effect if it were secondary to aldosterone stimulation. Finally, from our data there are no indications that effects of ET-1 on aldosterone can be modulated by calcium channel blockade. Rossi et al also offer an alternative explanation for some of our hemodynamic findings, ie, the absence of initial vasodilation in response to ET-1 infusion. Although we cannot exclude that impaired endothelium-dependent relaxation could contribute to this phenomenon in these hypertensive subjects, we also did not see this initial vasodilation in previous studies in healthy volunteers, who are assumed to have normal endothelial function. Moreover, we recently performed a study in healthy subjects in whom we infused ET-3, a relatively selective ETB agonist. In this study we did not see any vasodilation or vasoconstriction in the kidney despite a threefold increase in plasma ET-3 levels, suggesting that the renal effects of exogenously administered ET-1 in the human kidney are predominantly mediated through ETA receptors. Karin A.H. Kaasjager Hein A. Koomans Ton J. Rabelink Department of Nephrology and Hypertension University Hospital Utrecht Utrecht, The Netherlands