title: Vasodilator action of docosahexaenoic acid (DHA) in human coronary arteries in vitro.
abstract: Coronary arterial tissues obtained from mammalian hearts are known to develop spontaneous phasic contractions. The aim of the present study was to investigate the vasodilatory effects of docosahexaenoic acid (DHA) on the rhythmic contractions of isolated human coronary arterial (HCA) preparations obtained from the recipient hearts of patients undergoing cardiac transplantation. Results from 8 hearts show that: (i) most HCA tissues displayed spontaneous rhythmic phasic contractions with a cycle length around 10 min in the absence or presence of PGF2alpha or elevated [K+]0 (20 mM); (ii) the rhythmic activity could be suppressed by a free fatty acid DHA (30 microM); (iii) high [K+]0 (20 and 80 mM) could induce sustained tonic contraction in addition to phasic contractions in HCA tissues, the tonic contraction could be antagonized by L-type Ca(2+) channel blockers or by DHA (depending on [K+]0); (iv) a digitalis substance ouabain also could induce tonic contraction and suppress phasic contraction; (v) in isolated HCA vascular smooth muscle cells, DHA increased the magnitude of outward voltage-gated K+ (IKV) currents and the inwardly rectifying IK1 currents. Enhancement of K+ currents could be related to vasorelaxation induced by DHA in HCA preparations. Further studies on the effects of DHA on various ionic currents and intracellular Ca(2+) transient are needed to clarify the Ca(2+)-dependent and the Ca(2+)-independent actions of DHA in HCA.
authors.affiliation: Institutes of Physiology, National Defense Medical Center, Taipei, Taiwan, ROC.
authors.forename: Kuen-Tze
authors.initials: KT
authors.lastname: Wu
authors.forename: Ching-Ting
authors.initials: CT
authors.lastname: Huang
authors.forename: Jeng
authors.initials: J
authors.lastname: Wei
authors.forename: Lih-Min
authors.initials: LM
authors.lastname: Tsait
authors.forename: Chih-Hsueng
authors.initials: CH
authors.lastname: Hsu
authors.forename: Yao-Chang
authors.initials: YC
authors.lastname: Chen
authors.forename: Jung-Mou
authors.initials: JM
authors.lastname: Yangs
authors.forename: Cheng-I
authors.initials: CI
authors.lastname: Lin
mesh_terms: D000328:Adult; D000368:Aged; D003331:Coronary Vessels / Q000187:drug effects*; D015237:Dinoprost / Q000494:pharmacology; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008875:Middle Aged; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D004791:Enzyme Inhibitors; D014665:Vasodilator Agents; D004281:Docosahexaenoic Acids; D010042:Ouabain; D015237:Dinoprost; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium