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Acta Physiologica 2010; Volume 199, Supplement 680
Abstracts for the 12th Symposium on Vascular Neuroeffector Mechanisms
7/24/2010-7/26/2010
Odense, Denmark
PROTECTIVE POTENTIAL ROLE OF CGRP IN THE ONSET OF MURINE HYPERTENSION.
Abstract number: 14
SMILLIE1 S-J, FERNANDES1 E, LIANG1 L, MARSHALL1 NJ, BRAIN1 SD
1Cardiovascular Division, King's College London, UK
We have evidence that sensory nerves play an essential role in homeostasis. These comprise C- and Ad- fibres which contain and release the potent vasodilator calcitonin gene-related peptide, CGRP. This peptide is considered to play a positive role in wound healing and protects in neuro-vascular conditions and vascular related stress (Brain and Grant 2004). However, these protective mechanisms are less well understood. The purpose of this study was to determine the role of CGRP in Angiotensin II (Ang II) induced hypertension. We hypothesise that CGRP becomes important in resisting the hypertension. Sex and age matched (>2 months) CGRP wildtype (WT) and knockout (KO) C57BL/6 mice were administered either saline (control) or Ang II (1.1mg/kg/day) via implantation of osmotic mini pumps for 14 days. Blood pressure was recorded routinely via tail cuff plethysmography and tissues were collected at termination of the study for post analysis. At baseline there is no significant difference in systolic pressure in WT's (119.3±0.53, n=8) and CGRP KO's (120.2±0.53, n=8). Following 14 days of Ang II infusion, systolic pressure is significantly increased (p<0.001). At day 7, hypertension is significantly increased in the CGRP KO mice in comparison to their WT counterparts, with a significantly higher maximum response in CGRP KO's at day 14, (p<0.001). This interesting data gives light to a potentially protective role of CGRP in Ang II induced hypertension, however the mechanisms behind this still need to be elucidated. This project is funded by the BBSRC Brain, S.D. and Grant, A.D. 2004 Physiol Rev 84,903934.
To cite this abstract, please use the following information:
Acta Physiologica 2010; Volume 199, Supplement 680 :14