Response to Letter Regarding Article, “Advanced Glycation End Products Accumulate in Vascular Smooth Muscle and Modify Vascular but Not Ventricular Properties in Elderly Hypertensive Canines”
We thank Dr Hartog and colleagues for their interest in our study1 and agree with their conclusion that other advanced glycation end product (AGE) structures could be present in vascular (or ventricular) tissue. As acknowledged in the limitations section of the discussion, “We did not assess the presence of other AGE structures …” (p 1008). We would have liked to have measured other AGE structures but were unable to find reliable methodologies to do so, and we emphasized that, “although CML [Nε-(carboxymethyl)lysine] is commonly used as a marker of AGE accumulation, the relationship of CML content to that of other AGEs and differences in tissue deposition of CML and other AGEs throughout the body are poorly defined” (p 1008) and cited a review of the technical difficulties in assessing different AGE structures in vivo.2
We further agree that despite our findings, this area is deserving of further study, as outlined in the final sentence of the article: “Furthermore, the potential for AGE-modifying therapies to improve vascular or ventricular properties deserves further study but should include careful attention to potential changes in vascular size.”
Drug and partial financial support for the study was provided by Alteon, Inc. Drs Redfield (HL 63281 and HL 76611), Mohammad (HL 76611), and Owan (HL07111) were funded in part by the National Institute of Health.