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Angiotensin II contractions in coronary artery. Nature of receptors and calcium pools

Grover, A K ; Fomin, V P ; Samson, S E

Molecular and cellular biochemistry, 1994-06, Vol.135 (1), p.11-19 [Revista revisada por pares]

Netherlands

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  • Título:
    Angiotensin II contractions in coronary artery. Nature of receptors and calcium pools
  • Autor: Grover, A K ; Fomin, V P ; Samson, S E
  • Materias: Angiotensin II - metabolism ; Angiotensin II - pharmacology ; Animals ; Cell Membrane - drug effects ; Cells, Cultured ; Coronary Vessels - drug effects ; Egtazic Acid - pharmacology ; In Vitro Techniques ; Models, Biological ; Muscle Contraction - drug effects ; Muscle, Smooth, Vascular - cytology ; Muscle, Smooth, Vascular - drug effects ; Nitrendipine - pharmacology ; Receptors, Angiotensin - metabolism ; Swine
  • Es parte de: Molecular and cellular biochemistry, 1994-06, Vol.135 (1), p.11-19
  • Notas: ObjectType-Article-1
    SourceType-Scholarly Journals-1
    ObjectType-Feature-2
    content type line 23
  • Descripción: Pig coronary artery rings denuded of endothelium contract to the vasoactive hormone angiotensin II (Ang II). The nature of Ang II receptors and their Ca(2+)-pool utilization were examined for contraction of the artery rings and for increase in ultracellular [Ca2+] ([Ca2+]i) in smooth muscle cells cultured from them. Ang II contracted the arteries (EC50 = 7 +/- 4 nM) but with a lower maximal force (1.4 +/- 0.25 N/g tissue) than the contraction with 60 mM K+ (6.11 +/- 0.63 N/g tissue). In the cultured cells it caused a transient increase in [Ca2+]i with an EC50 value of 11 +/- 4 nM. The cells bound Ang II with a dissociation constant (Kd) of 7 +/- 2 nM. Based on the effects of the Ang II antagonists saralasin, DuPont 753, dithiothreitol and PD123319, the Ang II receptors responsible for contraction, increase in [Ca2+]i and Ang II binding to coronary artery smooth muscle were of type AT1. The contraction to Ang II was abolished by EGTA but not by nitrendipine. The sarcoplasmic Ca2+ pump inhibitors cyclopiazonic acid (10 microM CPA) and thapsigargin (1 microM) produced contractions of 4.35 +/- 0.73 and 2.07 +/- 0.54 N/g, respectively. Ang II contractions in the control arteries were nearly abolished upon pretreatment with CPA and thapsigargin. CPA and thapsigargin induced contractions were abolished by exposure to EGTA for 1 h but short exposure of the cells to EGTA only modulated the CPA or thapsigargin induced increase in [Ca2+]i; Ang II induced increase in [Ca2+]i was not inhibited by 1 microM nitrendipine but was reduced significantly by a 30-60 sec exposure to EGTA.
  • Editor: Netherlands
  • Idioma: Inglés
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