title: Intracoronary angiotensin II potentiates coronary sympathetic vasoconstriction in humans.
abstract: BACKGROUND
  In humans with coronary artery disease, ACE inhibition attenuates coronary sympathetic vasoconstriction. Whether this is due to removal of angiotensin (Ang) II production or to a reduced bradykinin breakdown, however, is unknown.
  
  
  RESULTS
  In eight normotensive patients with angiographic evidence of mild left coronary artery lesions (< or = 50%), mean arterial pressure (MAP, intra-arterial catheter), heart rate (HR, ECG lead), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between MAP and CBF) were measured before and during a 15-minute left intracoronary infusion of Ang II at a dose that had no direct coronary or systemic vasomotor effects. The same measurements were made before and during a 15-minute infusion of saline. A 2-minute cold pressor test (CPT) and a 45-second diving were performed at the end of either infusion period. These maneuvers were used because their coronary vasomotor effects are abolished by phentolamine and thus depend on sympathetic activation. During saline infusion, both CPT and diving caused a marked increase in MAP. HR increased with CPT and fell with diving. CBF increased in parallel to the MAP increase, with little change in CVR. The MAP and HR responses were similar during Ang II infusion, which, however, caused either no change or a reduction in CBF with a consequent marked increase in CVR with both CPT and diving. In four additional patients, the diameter of the stenotic vessels remained unchanged during the CPT performed under saline and Ang II infusion.
  
  
  CONCLUSIONS
  Ang II markedly enhances sympathetic influences on coronary circulation in humans, presumably by acting at the arteriolar level. This may explain the blunting effect of ACE inhibition on sympathetic coronary vasoconstriction in patients with coronary artery disease.
authors.affiliation: Centro di Fisiologia Clinica e Ipertensione, Università di Milano, Ospedale Maggiote, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Saino
authors.forename: G
authors.initials: G
authors.lastname: Pomidossi
authors.forename: R
authors.initials: R
authors.lastname: Perondi
authors.forename: R
authors.initials: R
authors.lastname: Valentini
authors.forename: A
authors.initials: A
authors.lastname: Rimini
authors.forename: L
authors.initials: L
authors.lastname: Di Francesco
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000368:Aged; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D014662:Vasoconstrictor Agents; D000804:Angiotensin II; D002216:Captopril