Victor Forge
Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state. It is influenced by the contractile activity of vascular smooth muscle cells in the walls of small arteries and arterioles, which is the major determinant of resistance to blood flow through the circulation. The contractile activity of vascular smooth muscle cells is influenced by a complex interplay of vasodilator and vasoconstrictor stimuli from circulating hormones, neurotransmitters, endothelium-derived factors, and blood pressure. Ion channels in the plasma membrane of vascular muscle cells, particularly voltage-gated Ca2+ channels, play a central role in the regulation of vascular tone. The autonomic nervous system (ANS) also plays an important role in maintaining vascular tone and blood pressure through its parasympathetic and sympathetic branches.
| Characteristics | Values |
|---|---|
| Definition | Degree of constriction experienced by a blood vessel relative to its maximally dilated state |
| Types of Smooth Muscle | Multi-unit smooth muscle, Single-unit smooth muscle |
| Factors Influencing Vascular Tone | Basal vascular tone, Contractile activity of VSM, Central (remote) control mechanisms, Local influences, Myogenic tone, Sympathetic nerve activity, Parasympathetic nerve activity, Ion channels, Calcium channels, Voltage-gated sodium channels, Neurotransmitters, Endothelium-derived factors, Blood pressure, Rho-kinase, Smooth muscle tension, Actin polymerization, Autoregulation, MLC phosphorylation |
| Functions | Regulation of blood pressure, Distribution of blood flow, Maintenance of blood vessel tone |
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What You'll Learn
The role of ion channels
Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state. It is the major determinant of the resistance to blood flow through the circulation. Thus, vascular tone plays a crucial role in regulating blood pressure and the distribution of blood flow between and within the tissues and organs of the body.
Ion channels play a central role in the regulation of vascular tone. Calcium (Ca2+) influx through channels in the plasma membrane and Ca2+ release from intracellular stores are the major sources of activator Ca2+. The movement of ions through ion channels determines, to a large extent, membrane potential. Membrane potential, along with cytosolic Ca2+ concentration, regulates and modulates the influx and release of Ca2+ through ion channels and the sensitivity of the contractile machinery to Ca2+.
Vascular smooth muscle cells express at least four different types of K+ channels, one to two types of voltage-gated Ca2+ channels, two types of Cl- channels, store-operated Ca+ (SOC) channels, and stretch-activated cation (SAC) channels in their plasma membranes. All of these channels may be involved in the regulation of vascular tone.
Potassium channels are the dominant ion conductive pathways in vascular muscle cells. Their activity is crucial for determining and regulating membrane potential and vascular tone. The opening of K+ channels results in the diffusion of this cation out of the cells and membrane hyperpolarization. Conversely, the closure of K+ channels leads to membrane depolarization. Voltage-gated Ca2+ channels also play a central role in the regulation of vascular tone by membrane potential. Hyperpolarization closes these channels and leads to vasodilation, whereas depolarization opens them, resulting in vasoconstriction.
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The influence of sympathetic nerves
Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state. It is the major determinant of resistance to blood flow through the circulation. The vascular smooth muscle is constantly under the influence of competing drives, and the degree of contraction is the result of the balance of these forces.
The skeletal muscle vasculature is richly innervated by the sympathetic nervous system and exhibits high sympathetic tone at rest. This high level of basal sympathetic activity, coupled with myogenic tone, maintains the arteries and arterioles supplying skeletal muscle in a partially constricted state. The tonic basal activity in the sympathetic vasoconstrictor nerves helps maintain vascular tone.
Additionally, the sympathetic nervous system's activation is associated with pro-hypertensive stimuli, promoting vasoconstriction, vascular hypertrophy, fibrosis, inflammation, and calcification. This activation influences vascular reactivity and tone, which are crucial factors in determining vascular resistance and blood pressure.
Furthermore, the relatively high activity of sympathetic nerves supplying the vasculature of skeletal muscle helps maintain a high level of vascular resistance during inactivity. This ensures that oxygen delivery by blood flow matches the low metabolic requirements of the resting state.
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Calcium as a trigger for contraction
Calcium is a key component in the contraction of vascular smooth muscle. Calcium ions (Ca2+) are required for the activation of contractile proteins actin and myosin, which are responsible for muscle contraction. The entry of calcium ions into the cytosol of vascular smooth muscle cells is facilitated by various calcium entry channels, including voltage-operated channels (VOCs), receptor-operated channels (ROCs), and store-operated calcium entry (SOCE) mechanisms.
The concentration of cytosolic calcium is regulated by signalling pathways, which can induce an increase in calcium levels through the promotion of calcium influx from extracellular sources or the release of calcium from intracellular stores. This increase in cytosolic calcium stimulates calcium-dependent signalling pathways that lead to muscle contraction. In vascular smooth muscle, calcium entry is particularly important for the regulation of vascular tone, which refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state.
Vascular tone is influenced by competing vasoconstrictor and vasodilator factors. Calcium entry channels, such as VOCs, play a crucial role in agonist-induced vasoconstriction. Activation of VOCs through membrane depolarization promotes calcium entry and subsequent vasoconstriction. Additionally, the interaction of STIM1 and Orai1 proteins is critical for calcium-induced vascular contraction in various vascular beds and vessel types, including the aorta, coronary, and cerebral arteries.
Furthermore, calcium entry through voltage-gated calcium channels can trigger calcium-induced calcium release (CICR), leading to further calcium-induced contraction. This process involves the activation of ryanodine-sensitive Ca2+ release (RyR) channels in the sarcoplasmic reticulum, which increases the frequency of "Ca2+ sparks" and enhances contraction. The activation of receptor-operated channels (ROCs) also contributes to calcium-induced contraction by enabling calcium influx and stimulating additional calcium release from intracellular stores.
While calcium is a critical trigger for contraction in vascular smooth muscle, it is important to note that calcium-insensitive pathways of excitation-contraction coupling also exist in these muscle cells. The balance between calcium-dependent and calcium-insensitive pathways contributes to the overall regulation of vascular tone and blood flow.
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The impact of membrane potential
Vascular tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state. It is determined by competing vasoconstrictor and vasodilator influences acting on the blood vessel. These influences can be separated into extrinsic factors that originate from outside the organ or tissue in which the blood vessel is located, and intrinsic factors that originate from the vessel itself or the surrounding tissue.
Vascular smooth muscle cells express at least 4 different types of K+ channels, 1 to 2 types of voltage-gated Ca2+ channels, ≥2 types of Cl− channels, store-operated Ca+ (SOC) channels, and stretch-activated cation (SAC) channels in their plasma membranes, all of which may be involved in the regulation of vascular tone. Calcium influx through voltage-gated Ca2+, SOC, and SAC channels provides a major source of activator Ca2+ used by resistance arteries and arterioles. In addition, K+ and Cl− channels and the Ca2+ channels mentioned previously are all involved in the determination of the membrane potential of these cells.
The opening of K+ channels results in the diffusion of this cation out of the cells and membrane hyperpolarization. Hyperpolarization closes the voltage-gated Ca2+ channels and leads to vasodilation, whereas depolarization opens them, resulting in vasoconstriction. The L-type Ca2+ channel, the ryanodine receptor (RyR) channel, and the KCa channel appear to function as a coupled unit with a negative feedback relationship regulating membrane potential and arterial tone. An increase in sarcoplasmic reticulum [Ca2+] and/or in [Ca2+]i through L-type Ca2+ channels activates RyR channels and KCa channels, increasing “Ca2+ sparks” and “STOCs” frequency.
In summary, membrane potential is a key variable that regulates Ca2+ influx through voltage-gated Ca2+ channels and influences the release of Ca2+ from intracellular stores. The movement of ions through ion channels, particularly K+ and Ca2+ channels, plays a central role in determining membrane potential and, consequently, vascular tone.
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The function of vascular smooth muscle
Vascular smooth muscle (VSM) is a type of smooth muscle that contracts and regulates blood vessel tone, blood pressure, and blood flow. It is responsible for the control of total peripheral resistance, arterial and venous tone, and the distribution of blood flow throughout the body. VSM is found in the walls of small arteries and arterioles, and it is constantly under the influence of competing drives, with the degree of contraction resulting from a balance of these forces.
VSM can be divided into two types: multi-unit smooth muscle and single-unit smooth muscle. Multi-unit smooth muscle fibres are independently innervated and do not exhibit spontaneous contraction or basal tone, and they respond to phasic stimulation. Single-unit smooth muscle acts like a syncytium, with impulse propagation facilitated by gap junctions. A stimulus spreads beyond the initial effector smooth muscle cell, and the smooth muscle behaves functionally as one. VSM falls into the latter category.
The contractile activity of VSM is influenced by a complex interplay of vasodilator and vasoconstrictor stimuli from circulating hormones, neurotransmitters, endothelium-derived factors, and blood pressure. Ion channels play a central role in this process, with calcium influx through voltage-gated Ca2+, store-operated Ca+ (SOC), and stretch-activated cation (SAC) channels providing a major source of activator Ca2+ used by resistance arteries and arterioles. The movement of ions through ion channels also determines, to a large extent, membrane potential, which regulates Ca2+ influx through voltage-gated channels and influences the release of Ca2+ from intracellular stores.
VSM in resistance arteries and arterioles develop and maintain an intrinsic, steady-state degree of contraction or myogenic tone at their normal intravascular pressure. Myogenic tone helps to maintain resistance artery and arteriolar diameter at some intermediate level of constriction, allowing changes in vessel calibre to occur in response to vasodilator or vasoconstrictor stimuli.
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Frequently asked questions
Vascular muscle tone refers to the degree of constriction experienced by a blood vessel relative to its maximally dilated state.
There are several factors that influence vascular muscle tone, including:
- Ion channels in the plasma membrane of vascular muscle cells
- Calcium influx and release from intracellular stores
- Endothelial cells and neurons releasing endothelial nitric oxide synthase (eNOS) and neuronal nitric oxide synthase (nNOS) vasodilators
- Sympathetic nervous system activity
- Circulating hormones, neurotransmitters, and endothelium-derived factors
Vascular muscle tone plays a crucial role in regulating blood pressure and controlling blood flow distribution within the body's tissues and organs. It helps match oxygen delivery by blood flow to the metabolic requirements of the tissues.
