Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Reichmuth, J.
Vasopressin and Aquaporin Changes in Young Healthy Volunteers Undergoing Orthostatic Challenge
Humanmedizin; [ Diplomarbeit ] Graz Medical University; 2016. pp.
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- Autor*innen der Med Uni Graz:
- Betreuer*innen:
- Goswami Nandu
- Rössler Andreas
- Altmetrics:
- Abstract:
- Introduction: Orthostatic syncope, caused by an inability of the cardiovascular system to compensate a reduction in venous return to the heart, is a major source of fall in the elderly often leading to injury and hospitalisation. Furthermore, women are known to be particularly prone to orthostatic syncope, for reasons which are still not clearly understood. In a recent review (see Appendix C), we have discussed the effect of aging on the vasoconstrictor hormone Arginine-Vasopressin (AVP). AVP regulates plasma osmolality and volume mainly by regulating the presence of a water channel called aquaporin 2 (AQP2) in the apical membrane of the principal cells of the renal collecting ducts, which is also excreted in the urine where its concentration correlates with plasma AVP. In recent years copeptin, a larger peptide released from the same precursor molecule as AVP has been established as a surrogate marker of plasma AVP. Its measurement is much cheaper and simpler and it is much more stable even at room temperature; thus, it offers considerable advantages over direct measurement of AVP. While it is known that AVP increases massively if syncope occurs, its role in conditions of orthostatic stress without syncope is still poorly understood. Aims & Goals: In the present study we assessed the effect of Lower Body Negative Pressure (LBNP) which simulates orthostatic challenge-induced central hypovolemia both on plasma copeptin and urinary AQP2 (uAQP2). We hypothesized that copeptin and uAQP2 increase upon graded LBNP and that there are gender differences in this response. Methodology: 38 (21 female and 17 male) healthy young volunteers were recruited for this study. Our experimental protocol consisted of a 30-minute supine baseline period followed by 20 min of LBNP, increasing every five min by -10 mmHg up to -40 mmHg followed by 10 min of supine rest. Blood was sampled at the end of baseline, at the end of the LBNP and at the end of the recovery period. 24-hours urine samples were collected as baseline before the experiment and another urine sample was collected immediately after the end of the experimental protocol. Results: Contrary to our expectations, copeptin and uAQP2 failed to increase upon 20 minutes of increasing LBNP; instead a significant drop in copeptin took place. Males had higher copeptin than females, a difference that became more pronounced after LBNP. There were no significant alterations of uAQP2 and no significant correlation between copeptin and uAQP2 could be found. Discussion: The observation that the difference between men and women in copeptin was more pronounced at the end of the experiments supports the notion of gender-specific kinetics and thus partly confirms our hypothesis. We consider the observed drop in copeptin to be most likely an effect of a slower elimination of copeptin compared to AVP in conjunction with the posture change into supine position at the beginning of the baseline period, 30 minutes before LBNP application.