title: Endothelin-A receptor antagonism promotes decreased vasodilation but has no differential effect on coronary artery compliance in hypertensive patients.
abstract: The importance of endothelin-1 in the pathophysiology of essential hypertension is unclear. We therefore examined whether there is a differential effect of endothelin-A antagonism on vasodilation and coronary artery compliance in hypertensive compared to normotensive patients. We examined atherosclerotic non-stenotic arteries from 18 non-diabetic, 10 normotensive patients and eight hypertensive patients, before and after intracoronary infusion of BQ-123 (6 mumol), an endothelin-A receptor antagonist. The systolic and diastolic artery lumen area in the proximal segment was measured using an intravascular ultrasound catheter. Systolic blood pressure decreased only in hypertensive patients (F = 5.44, P = 0.03), after BQ-123 administration. The diastolic artery lumen increased from 8.9 +/- 2.9 mm at baseline to 10.8 +/- 3.0 mm after BQ-123 administration (P < 0.05) in normotensive patients and from 10.6 +/- 4.6 mm to 10.8 +/- 4.0 mm (P = NS) in the hypertensive patients (F = 3.98, P = 0.01). The respective values for the systolic artery lumen, in the two groups, before and after BQ-123 were: 10.2 +/- 3.4 mm and 12.7 +/- 3.2 mm (P < 0.01) in the normotensive group and 12.0 +/- 5.5 mm and 12.8 +/- 5.0 mm (P = NS) in the hypertensive group (F = 3.37, P = 0.08). Artery compliance did not have a differential response to BQ-123. In conclusion, endothelin-A antagonism causes decreased vasodilation but does not have a differential effect on coronary artery compliance in hypertensive patients.
authors.affiliation: B Cardiology Department, Hellenic Red Cross Hospital, Athens, Greece.Erythrou Stavrou str., Athens 115 26, Greece. zskyr@otenet.gr
authors.forename: Zenon
authors.initials: Z
authors.lastname: Kyriakides
authors.forename: Stamatis
authors.initials: S
authors.lastname: Kyrzopoulos
authors.forename: Ioannis
authors.initials: I
authors.lastname: Paraskevaidis
authors.forename: Fotis
authors.initials: F
authors.lastname: Kolokathis
authors.forename: Ioannis
authors.initials: I
authors.lastname: Tsopotos
authors.forename: Theodore
authors.initials: T
authors.lastname: Lyras
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Kremastinos
mesh_terms: D000328:Adult; D000368:Aged; D000959:Antihypertensive Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D003187:Compliance; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1 / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D007263:Infusions, Parenteral; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000008:administration & dosage / Q000627:therapeutic use*; D011446:Prospective Studies; D044022:Receptor, Endothelin A / Q000378:metabolism; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D000959:Antihypertensive Agents; D065130:Endothelin A Receptor Antagonists; D019332:Endothelin-1; D010456:Peptides, Cyclic; D044022:Receptor, Endothelin A; C072247:cyclo(Trp-Asp-Pro-Val-Leu)