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Influence of experimental reduction of arterial media : lumen ratio on agonist-stimulated contractions in hypertension

Hughes, Jennifer M; Bund, Stuart J

Original papers: Blood vessels

Objective This study investigated the relationship between the arterial media thickness : lumen diameter (M : L) ratio and arterial contractile responses in the spontaneously hypertensive rat (SHR) and its Wistar–Kyoto control (WKY) under isobaric conditions.

Methods Femoral arteries with an experimentally reduced M : L ratio were produced in one hindlimb of both rat strains, by partial ligation of the ipsilateral iliac artery. Arterial structure and contractile responses were assessed in an arteriograph. Contractile responses of these vessels to the vasoconstrictor agonists noradrenaline and phenylephrine were determined after generation of spontaneous myogenic tone and compared with those from contralateral hindlimbs determined at both estimated in-vivo pressures and at 80 mmHg. Control SHR and WKY arterial responses were also compared.

Results Under both pressure conditions, relaxed M : L ratios were significantly greater in SHR than in WKY arteries and were also significantly reduced in arteries distal to the ligature in both strains. In no comparison was a greater M : L associated with a greater agonist-stimulated contractile response. However, increased M : L were associated with narrower lumens across the concentration response relationships under some, but not all, conditions.

Conclusion An increased arterial M : L ratio does not effect an exaggerated contractile function in myogenically active resistance arteries in vitro. However, narrower lumen diameters associated with the increased M : L would provide a means for increased vascular resistance. These observations support the hypothesis that an increased M : L does not provide a means for a contractile response amplifier but may provide a means for a vascular resistance amplifier under some circumstances.

Department of Human Anatomy and Physiology, Conway Institute of Biomolecular and Biomedical Research, University College Dublin, Dublin 2, Ireland.

Sponsorship: The work was funded by a grant from the Health Research Board of Ireland.

Reprints will not be available.

Correspondence to Dr Stuart J. Bund, Department of Human Anatomy and Physiology, University College Dublin, Earlsfort Terrace, Dublin 2, Ireland. Tel: +353 1 716 7424; fax: +353 1 716 7417; e-mail:

Received 2 July 2003 Revised 3 October 2003 Accepted 6 November 2003

© 2004 Lippincott Williams & Wilkins, Inc.