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Endothelial cell calcium and vascular control
1Texas A&M University Health Science Center, Department of Medical Physiology, College Station 77845-1114, USA.
Insights
Endothelial cells regulate vascular smooth muscle tone by increasing intracellular calcium in response to acetylcholine and high flow. This study reveals the critical role of the endothelium in mediating arteriolar dilation.
Area of Science:
- Vascular Biology
- Cell Physiology
- Microcirculation Research
Background:
- The endothelium plays a crucial role in regulating vascular smooth muscle tone.
- Endothelial cell calcium signaling is a key mechanism in vascular function.
Purpose of the Study:
- To investigate the role of endothelial cell calcium in skeletal muscle arteriole tone modulation.
- To determine the relationship between endothelial calcium and arteriolar responses to various stimuli.
Main Methods:
- Isolated rat cremaster muscle first-order arterioles were cannulated and pressurized.
- Digital imaging microscopy with Fura-2-AM was used to measure endothelial cell calcium.
- Vessels were stimulated with acetylcholine, adenosine, intraluminal pressure, and flow.
Main Results:
- Acetylcholine (endothelium-dependent) increased endothelial calcium and caused dilation.
- Adenosine (endothelium-independent) caused dilation without affecting endothelial calcium.
- High flow (40 cm H2O) increased endothelial calcium preceding arteriolar dilation.
- Endothelium removal abolished responses to acetylcholine and high flow but not adenosine.
Conclusions:
- Endothelial cell calcium signaling is essential for acetylcholine- and flow-induced arteriolar dilation.
- The endothelium is a critical mediator of vascular smooth muscle tone regulation in skeletal muscle arterioles.
Abstract:
The endothelium has been shown to contribute to the modulation of vascular smooth muscle tone. Using digital imaging microscopy, we measured calcium in endothelial cells of isolated skeletal muscle arterioles. First-order arterioles (N = 6) were isolated from rat cremaster muscle and cannulated. All vessels developed spontaneous tone (99.4 microns; 60%-80% of passive diameter). Endothelial cells were loaded with Fura-2-AM (5 microM), a ratiometric calcium-sensitive fluorescent dye. The Fura-2-AM was placed in the lumen of the vessel for approximately 10 min and removed. Fluorescent images of endothelial cells were acquired following excitation at 340- and 380-nm wavelengths and the data expressed as the 340/380 ratio which is directly proportional to intracellular calcium. Acetylcholine (Ach; 10(-6) M), an endothelium-dependent dilator, caused significant dilation (132% of control) and increased calcium to 186% of control. Adenosine (Adn; 10(-4) M), an endothelium-independent agent, produced similar dilation (127% of control) but did not alter endothelial cell calcium. Increasing intraluminal pressure produced a myogenic constriction with no change in endothelial calcium. Flow, induced by a 20 cm H2O pressure gradient, failed to dilate the arterioles and produced no increase in endothelial cell calcium. However, flow induced by a 40 cm H2O pressure difference did increase endothelial cell calcium prior to a significant arteriolar dilation. Removal of the endothelium by physically rubbing the intimal surface eliminated both the dilation and increase in calcium to Ach or flow (40 cm H2O) while the response to Adn remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)