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ENDOTHELIUM‐SMOOTH MUSCLE INTERACTIONS IN BLOOD VESSELS
Author(s) -
Breemen Cornells,
Skarsgard Peter,
Laher Issy,
McManus Bruce,
Wang Xiaodong
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb02737.x
Subject(s) - endoplasmic reticulum , serca , plasma membrane ca2+ atpase , extracellular , chemistry , vascular smooth muscle , intracellular , endothelium , myocyte , biophysics , cytoplasm , medicine , endocrinology , atpase , biochemistry , biology , smooth muscle , enzyme
SUMMARY 1. Blood vessel tone is determined both by smooth muscle and endothelial functions. In coronary arteries taken from rat (Fisher‐Lewis) cardiac transplanted hearts, the inducible form of NOS (iNOS) in smooth muscle is more active, while acetylcholine‐induced nitric oxide production in the endothelium is greatly diminished. This causes a greatly reduced myogenic constriction, in pressurized septal arteries taken from immunologically challenged transplanted hearts. 2. The sarcoplasmic reticulum (SR) of smooth muscle and the endoplasmic reticulum (ER) of endothelial cells sequeste. Ca 2+ from the cytoplasm. This reduces the intracellular concentration of free Ca 2+ , which is necessary for the activation of cellular processes. The release of Ca 2+ from internal stores occurs through ryanodine and IP3 recoptors located on the SR membrane. 3. The superficial SR/ER also interacts with ion exchangers and pumps in the plasma membrane. This allows for the superficial SR/ER to function in Ca 2+ extrusion; for example, inhibition of the SR/ER Ca 2+ ‐ATPase (SERCA) partially inhibits the rate of loss Ca 2+ from the cell. Recent data suggest that the SR Ca 2+ ‐ATPase and the Na + ‐Ca 2+ exchanger of smooth muscle cells function in series; that is, Ca 2+ uptake by the SR followed by release towards the exchanger to mediate extrusion. This interaction between the SERCA of the superficial SR and ion exchangers and pumps creates intracellular Ca 2+ gradients. 4. The SERCA of the superficial, peripherally distributed SR/ER also serves to regulat. Ca 2+ entry from the extracellular space. This occurs in part by inhibition of the superficial buffer barrier function of the SR as well as by depletion of stimulated Ca 2+ entry. 5. Ca 2+ entry is also regulated in endothelial and smooth muscle cells by the membrane potential. Membrane hyperpolar‐ization increases the driving force for Ca 2+ entry into endothelial cells, which lack voltage‐gated Ca 2+ channels, and reduces open ate probability of voltage‐gated Ca 2+ channels in vascular smooth muscle cells. The two cell types have electrical contact and interact in a dynamic manner to regulate blood vessel diameter