Acta Physiologica 2011; Volume 202, Supplement 685
Scandinavian Physiological Society's Annual Meeting
ACETYLCHOLINE SENSITIVITY IN ABDOMINAL SUBCUTANEOUS ARTERIES FROM OBESE PATIENTS
Abstract number: 6.1.5
BRONDUM1 ET, GRUNNET1 M, BORG1 M, RAMLOV1 P, FUNCH-JENSEN1 P, AALKJAER1 C
1Institute of Biophysics, Aarhus University, Ole Worms All build 1160, 8000 Aarhus C, Denmark; Email: firstname.lastname@example.org
Patients with obesity have an increased risk for cardiovascular disease, possibly related to endothelial-dysfunction. This study investigates the acetylcholine mediated relaxation in subcutaneous resistance arteries from obese patients (BMI>40) undergoing gastric-bypass operation or undergoing surgery for non-cardiovascular related reasons. (i.e. kidney transplant donors).
Arteries dissected from biopsies taken from 12 control and 12 obese matched for age and sex were mounted in an isometric myograph. Endothelium-dependent relaxation was investigated by increasing concentrations of acetylcholine on noradrenaline pre-contracted vessels. The EDHF-like response was investigated in the presence of eNOS and COX inhibitors and pharmacological modulators of the pathways involved in the EDHF response.
There was no difference between the groups in maximal relaxation under control conditions (86±6 and 89±3%, obese and control, respectively). However, the sensitivity to acetylcholine was significantly higher in obese (logEC50 was -7.4±0.1and -7.1±0.1, obese and control, respectively (p =0.02)). Also after blocking eNOS and COX the sensitivity to acetylcholine was higher in obese (logEC50 -6.6±0.1 and -6.2±0.1 (p =0.02)) while maximal relaxation was not different (61±9 and 70±4%(p> 0.5), obese and control, respectively). Treatment with the IK and SK channel opener NS309 (1mM) abolished the difference in sensitivity (logEC50 -7.3±0.1 and -7.2±0.2) while increasing maximal relaxation (77±4 and 79±14%, n= 11 and 3) obese and control, respectively.
Subcutaneous resistance arteries from obese patients seem to have increased sensitivity to the endothel.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 685 :6.1.5