Anne-Maj Samuelsson's picture

Anne-Maj Samuelsson

Postdoctoral Fellow
  • E-mailAnne-Maj.Samuelsson@uib.no
  • Phone+47 404 83 979
  • Visitor Address
    University of Bergen
    Jonas Lies vei 91
    5011 Bergen
    Biomedicine (7th floor)
  • Postal Address
    Postboks 7804
    5020 Bergen

I am a research scientist who, after spending a decade at King’s College London (KCL), recently joined Prof. Wiig’s lab here at the Department of Biomedicine in Bergen. Along the way I have gathered extensive experience in lecturing, tutoring, research, development and technology.

My research interests lie in the field of primary hypertension, to identify novel pathways and intervention during early life that may reverse/ameliorate heightened blood pressure. 

Salty brain, salty heart ? Heightened response to salt may intimately leads to development of hypertension and chronic heart failure. Brain (meningeal) lymphatic system (mL) could potentially be used to manipulate and treat salt-induced hypertension.

My research enables me to explore novel methods for interrogating blood pressure (telemetry), cardiac function (echo), and lymphatic function (optical imaging, PET) in experimental models of salt sensitivity.  

Future prospects include the relevance to man by studying the relationship between high salt diet and childhood autonomic dysfunction in existing human cohorts (apply Na-MRI).



I am a medical scientist who, after spending a decade at King’s College London (KCL), recently joined Prof. Wiig’s lab here at the Department of Biomedicine in Bergen. Along the way I have gathered extensive experience in lecturing, tutoring, research, development and technology.

2017-present 2ndsupervisor for Jianhua Han, Department of Biomedicine, UiB, NO.

2016-present 2ndsupervisor for Julie Sigurd, Imaging and Biomedical Engineering Clinical Academic Group, KCL, UK

2011-2016 2ndsupervisor for Emmanuel Domfeh, Department of Women and Children's Health, KCL, UK.


  1. Pataia V, Papacleovoulou,G, Nikolova V, Samuelsson AMet al. Int J Obesity. Feb 2018. Paternal cholestasis exacerbates obesity-associated hypertension in male offspring but is prevented by paternal ursodeoxycholic acid treatment. In press.
  2. Oosterhuis NR, Fernandes R, Maicas N, Bae SE, Pombo J, Gremmels H, Poston L, Joles JA, Samuelsson AM. Extravascular renal denervation ameliorates juvenile hypertension and renal damage resulting from experimental hyperleptinemia in rats. J. Hypertension. 2017 Dec 35; 12:2537-2547.
  3. Cordero P, Li J, Nguyen V, Pombo J, Maicas N, Novelli M, Taylor PD, Samuelsson AM, et al. Developmental Programming of obesity and liver metabolism by maternal perinatal nutrition involves the melanocortin system. Nutrient.2017 Sep 20;9 (9).
  4. Samuelsson AM, et al. A central role for melanocortin-4 receptors in offspring arising from maternal obesity.PNAS. 2016 Oct 25; 113(43): 12298–12303.
  5. Samuelsson AM.Essential Hypertension in Children: New Mechanistic Insights. Book Chapter 2 in Update on Essential Hypertension, ISBN 978-953-51-2615-7.
  6. Samuelsson AM. New perspectives on the origin of hypertension; the role of the hypothalamic melanocortin system. Exp. Physiol. 2014 Sep;99. 1110-1115.
  7. Lager S, Samulesson AM, et al. Diet-induced obesity in mice reduces placental efficiency and inhibits placental mtor signaling. Physiol reports. 2014;2:e00242
  8. Taylor PD, Samuelsson AM, Poston L. Maternal obesity and the developmental programming of hypertension: A role for leptin. Acta physiologica. 2014;210:508-523(Times  Cited 25).
  9. Samuelsson AM, et al. Response to role of hyperleptinemia in the regulation of blood pressure and cardiac function. Hypertension. 2014;63:e2Editorial.
  10. Samuelsson AM, et al. Experimental hyperleptinemia in neonatal rats leads to selective leptin responsiveness, hypertension, and altered myocardial function. Hypertension. 2013;62:627-633(Times Cited 19).
  11. Samuelsson AM, et al. Sucrose feeding in mouse pregnancy leads to hypertension, and sex-linked obesity and insulin resistance in female offspring. Frontiers in physiology. 2013;4:14(Times Cited 23)
  12. Mouralidarane A, Soeda J, Visconti-Pugmire C, Samuelsson AM, et al. Maternal obesity programs offspring nonalcoholic fatty liver disease by innate immune dysfunction in mice. Hepatology. 2013;58:128-138(Times Cited 28).
  13. Fernandes C, Grayton H, Poston L, Samuelsson AM, et al. Prenatal exposure to maternal obesity leads to hyperactivity in offspring. Mol psychiat. 2012;17:1159-1160(Times Cited 11).
  14. Matthews PA, Samuelsson AM, et al. Fostering in mice induces cardiovascular and metabolic dysfunction in adulthood. J physiol. 2011;589:3969-3981(Times Cited 22).
  15. Samuelsson AM, et al. Evidence for sympathetic origins of hypertension in juvenile offspring of obese rats. Hypertension. 2010;55:76-82(Times Cited 71).
  16. Oben JA, Patel T, Mouralidarane A, Samuelsson AM, et al. Maternal obesity programmes offspring development of non-alcoholic fatty pancreas disease. Biochem biophysical res comm.2010;394:24-28.
  17. Oben JA, Mouralidarane A, Samuelsson AM, et al. Maternal obesity during pregnancy and lactation programs the development of offspring non-alcoholic fatty liver disease in mice. J hepatol. 2010;52:913-920(Times Cited 95*).
  18. Kirk SL, Samuelsson AM, et al. Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring. PloS one. 2009;4:e5870 (Times Cited 165).
  19. Samuelsson AM,et al. Diet-induced obesity in female mice leads to offspring hyperphagia, adiposity, hypertension, and insulin resistance: A novel murine model of developmental programming. Hypertension. 2008;51:383-392(Times Cited 402*)
  20. Armitage JA, Gupta S, Wood C, Jensen RI, Samuelsson, AM, et al. Maternal dietary supplementation with saturated, but not monounsaturated or polyunsaturated fatty acids, leads to tissue-specific inhibition of offspring na+,k+-atpase.  J Physiology. 2008;586:5013-5022.
  21. Dahlgren J, Samuelsson AM, Jansson T, Holmang A. Interleukin-6 in the maternal circulation reaches the rat fetus in mid-gestation. Pediatric Research. 2006;60:147-151(Times Cited 67).
  22. Samuelsson AM, Alexanderson C, Molne J, Haraldsson B, Hansell P, Holmang A. Prenatal exposure to interleukin-6 results in hypertension and alterations in the renin-angiotensin system of the rat.  J Physiology. 2006;575:855-867(Times Cited 21).
  23. Samuelsson AM, et al. Prenatal exposure to interleukin-6 results in inflammatory neurodegeneration in hippocampus with nmda/gaba(a) dysregulation and impaired spatial learning. Am J Physiol. Regul, integr and comp physiol. 2006;290:R1345-1356(Times Cited 124*).
  1. Samuelsson AM, et al. Prenatal exposure to interleukin-6 results in hypertension and increased hypothalamic-pituitary-adrenal axis activity in adult rats. Endocrinology. 2004;145:4897-4911 (Times Cited 39).
  2. Samuelsson AM, et al. Hyperinsulinemia: effect on cardiac mass/function, angiotensin II receptor expression, and insulin signaling pathways. Am J Physiol Heart Circ Physiol.2006;291 (2): H787-H796 (Times Cited 31).
  3. Johansson, A-K, Sjostrand, M, Tomaki, M, Samuelsson, AM, Lotvall, J. Allergen stimulates bone marrow CD34(+) cells to release IL-5 in vitro; a mechanism involved in eosinophilic inflammation? Allergy. 2004; 59:1080-6.



Salty brain, salty heart ? 

Today, children and adults alike consume twice as much salt as recommended. Processed foods and ready-made meals are well-known culprits and are commonplace in the diets of today’s Norwegian children. WHO has urged nations to take population wide action to reduce salt intake in order to decrease the number of deaths from CVD in adults. Thus far, the impact of high salt (HS) intake in children CVD has not been addressed. 

Current project investigate whether lymphatics in brain and heart are key components in the protection against salt-induced hypertension and CVD, thus providing a target for future prevention. To investigate if early HSD exposure contributes to salt-sensitivity, priming the neuro/immune responsiveness to salt will be conducted in experimental models of salt-sensitive (VEGF-ctransgenic mice, DOCA-SD rats) from weaning until adulthood. 

During the tenure of the project additional EU- funding will be sought to address the relevance to humans by studying the relationship between high salt intake in Norwegian children and development of CVD. Salt intake is high among the Norwegian population and salt reduction may be an important step towards improving public health. Only when the underlying mechanisms have been mapped can effective countermeasures be developed and implemented. 

Research groups