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Cell‐To‐Cell Communication in the Resistance Vasculature

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The arterial vasculature can be divided into large conduit arteries, intermediate contractile arteries, resistance arteries, arterioles, and capillaries. Resistance arteries and arterioles primarily function to control systemic blood pressure. The resistance arteries are composed of a layer of endothelial cells oriented parallel to the direction of blood flow, which are separated by a matrix layer termed the internal elastic lamina from several layers of smooth muscle cells oriented perpendicular to the direction of blood flow. Cells within the vessel walls communicate in a homocellular and heterocellular fashion to govern luminal diameter, arterial resistance, and blood pressure. At rest, potassium currents govern the basal state of endothelial and smooth muscle cells. Multiple stimuli can elicit rises in intracellular calcium levels in either endothelial cells or smooth muscle cells, sourced from intracellular stores such as the endoplasmic reticulum or the extracellular space. In general, activation of endothelial cells results in the production of a vasodilatory signal, usually in the form of nitric oxide or endothelial‐derived hyperpolarization. Conversely, activation of smooth muscle cells results in a vasoconstriction response through smooth muscle cell contraction. © 2022 American Physiological Society. Compr Physiol 12: 3833–3867, 2022.

Figure 1. Figure 1. The contractile state of the resistance arteries is important in determining systemic blood pressure.
Figure 2. Figure 2. In the resistance vasculature, a number of signaling pathways become integrated to produce the final response.
Figure 3. Figure 3. Cells of the resistance vascular wall are directly coupled to one another through connexin comprised gap junctions.
Figure 4. Figure 4. Pannexin‐1 has been demonstrated to function as a purine release channel (ATP and UTP). Adapted, with permission, from Lohman AW, et al., 2015 338.
Figure 5. Figure 5. Nitric oxide (NO) is a primary regulator of vascular tone.
Figure 6. Figure 6. A key regulator of transmembrane Ca2+ flux is change in the transmembrane potential (Em). “?” indicates that while voltage‐gated potassium channels (Kv) are present it is unclear which specific isoforms are expressed in endothelial cells.
Figure 7. Figure 7. A key component in the regulation of vascular tone is an alteration in free cytosolic/intracellular Ca2+.

Figure 1. The contractile state of the resistance arteries is important in determining systemic blood pressure.

Figure 2. In the resistance vasculature, a number of signaling pathways become integrated to produce the final response.

Figure 3. Cells of the resistance vascular wall are directly coupled to one another through connexin comprised gap junctions.

Figure 4. Pannexin‐1 has been demonstrated to function as a purine release channel (ATP and UTP). Adapted, with permission, from Lohman AW, et al., 2015 338.

Figure 5. Nitric oxide (NO) is a primary regulator of vascular tone.

Figure 6. A key regulator of transmembrane Ca2+ flux is change in the transmembrane potential (Em). “?” indicates that while voltage‐gated potassium channels (Kv) are present it is unclear which specific isoforms are expressed in endothelial cells.

Figure 7. A key component in the regulation of vascular tone is an alteration in free cytosolic/intracellular Ca2+.
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D. Ryan King, Meghan W. Sedovy, Xinyan Eaton, Luke S. Dunaway, Miranda E. Good, Brant E. Isakson, Scott R. Johnstone. Cell‐To‐Cell Communication in the Resistance Vasculature. Compr Physiol 2022, 12: 3833-3867. doi: 10.1002/cphy.c210040