• Br J Anaesth · Apr 2009

    Urotensin II receptor expression in human right atrium and aorta: effects of ischaemic heart disease.

    • A D Leonard, J P Thompson, E L Hutchinson, S P Young, J McDonald, J Swanevelder, and D G Lambert.
    • Department of Cardiovascular Sciences (Pharmacology and Therapeutics Group), Division of Anaesthesia, Critical Care and Pain Management, University of Leicester, Leicester Royal Infirmary, Leicester LE1 5WW, UK.
    • Br J Anaesth. 2009 Apr 1; 102 (4): 477-84.

    BackgroundUrotensin II (UII) and its receptor UT are involved in control of the cardiovascular system and are implicated in heart failure. We measured UT expression by quantitative PCR (Q-PCR) in atrial and aortic tissue, and plasma UII while simultaneously assessing cardiac function in 40 patients undergoing coronary artery bypass surgery.MethodsRNA extracted from atrial and aortic samples was probed with specific Q-PCR UT and housekeeper (glyceraldehyde-3-phosphate dehydrogenase, GAPDH) TaqMan primers. Plasma UII was measured using radioimmunoassay. Left ventricular ejection fraction (LVEF) was measured using preoperative trans-thoracic echocardiography and ventriculography, and intraoperatively using transoesophageal echocardiography. Q-PCR data are expressed as difference in cycle threshold (DeltaC(t)=C(tUT)-C(tGAPDH): high number indicates low expression).ResultsThere was no difference in DeltaC(t) in either atrium or aorta between patients with normal (LVEF >50%) or those with impaired (LVEF <50%) preoperative systolic function. There was a weak negative correlation (r(2)=0.245, P=0.031) between intraoperative LVEF and DeltaC(t) in 19 patients possibly indicating down-regulation of UT with worsening LVEF. Atria expressed significantly more UT than aorta (P=0.011). In the absence of non-diseased controls, plasma UII was higher than a historical control group.ConclusionsThis is the first study to simultaneously measure UT (mRNA), UII, and cardiovascular function. Collectively, these pilot data may suggest a down-regulation of UT within the right atrium of patients with heart failure.

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