Increased expression of endothelin ET(B) and angiotensin AT(1) receptors in peripheral resistance arteries of patients with suspected acute coronary syndrome.
Patients who experience chest pain, in which ischemic heart disease has been ruled out, still have an increased risk of future ischemic cardiac events and premature death, possibly due to subclinical endothelial dysfunction. A feature of endothelial dysfunction is an increased expression of arterial vasoconstrictor endothelin (ET) and angiotensin (AT) receptors. Our aim was to investigate if the arterial expressions of these receptors are changed in patients with suspected but ruled out acute coronary syndrome (ACS). Small subcutaneous arteries (diameter of 100 microm) were surgically removed in an abdominal biopsy from 12 patients suspicious of ACS (susp ACS), admitted to the medical telemetry unit for chest pain. The vessels were analyzed for their receptor protein expression by quantitative immunohistochemistry using specific antibodies directed against ET(A), ET(B), AT(1), and AT(2) receptors. The control group (controls) consisted of eight healthy volunteers matched for age and sex with no previous cardiac illness or medication. The susp ACS group had an increased expression of ET(B) (by 94%) and AT(1) (by 34%) receptors in the smooth muscle cells of resistance arteries as compared to the control group. There were no significant differences in AT(2) and ET(A) receptor expression between the groups. The results indicate that the expression of arterial smooth muscle ET(B) and AT(1) receptors are increased in patients with suspected but ruled out ACS. These receptor changes could be important in the regulation of coronary tone and in the development of atherosclerosis, and may be related to increased cardiovascular risk.
Dimitrijevic
Ivan
I
Divisions of Emergency Medicine and Experimental Vascular Research, Department of Clinical Sciences, Lund University Hospital, BMC A13, SE-221 84 Lund, Sweden. ivan.dimitrijevic@med.lu.se
Ekelund
Ulf
U
Edvinsson
Marie-Louise
ML
Edvinsson
Lars
L
D054058:Acute Coronary Syndrome / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001158:Arteries / Q000737:chemistry / Q000503:physiopathology; D001706:Biopsy; D016022:Case-Control Studies; D002637:Chest Pain / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000737:chemistry* / Q000503:physiopathology; D044140:Receptor, Angiotensin, Type 1 / Q000032:analysis*; D044023:Receptor, Endothelin B / Q000032:analysis*; D040521:Subcutaneous Tissue / Q000098:blood supply*; D015854:Up-Regulation; D014655:Vascular Resistance
C544065:AGTR1 protein, human; D044140:Receptor, Angiotensin, Type 1; D044023:Receptor, Endothelin B