scholarly journals Myogenic Tone in Peripheral Resistance Arteries and Arterioles: The Pressure Is On!

2021 ◽  
Vol 12 ◽  
Author(s):  
William F. Jackson
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Signaling Pathways ◽  
Vascular Resistance ◽  
Myogenic Tone ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Fluid Exchange

Resistance arteries and downstream arterioles in the peripheral microcirculation contribute substantially to peripheral vascular resistance, control of blood pressure, the distribution of blood flow to and within tissues, capillary pressure, and microvascular fluid exchange. A hall-mark feature of these vessels is myogenic tone. This pressure-induced, steady-state level of vascular smooth muscle activity maintains arteriolar and resistance artery internal diameter at 50–80% of their maximum passive diameter providing these vessels with the ability to dilate, reducing vascular resistance, and increasing blood flow, or constrict to produce the opposite effect. Despite the central importance of resistance artery and arteriolar myogenic tone in cardiovascular physiology and pathophysiology, our understanding of signaling pathways underlying this key microvascular property remains incomplete. This brief review will present our current understanding of the multiple mechanisms that appear to underlie myogenic tone, including the roles played by G-protein-coupled receptors, a variety of ion channels, and several kinases that have been linked to pressure-induced, steady-state activity of vascular smooth muscle cells (VSMCs) in the wall of resistance arteries and arterioles. Emphasis will be placed on the portions of the signaling pathways underlying myogenic tone for which there is lack of consensus in the literature and areas where our understanding is clearly incomplete.

Intraluminal hyperglycaemia causes conduit and resistance artery dilatation and inhibits vascular autoregulation in the anaesthetised pig

2013 ◽  
Vol 91 (12) ◽  
pp. 1031-1036 ◽  
Author(s):  
Therese Ruane-O’Hora ◽  
Christine M. Shortt ◽  
Deirdre Edge ◽  
Farouk Markos ◽  
Mark I.M. Noble
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Steady State ◽  
Vascular Resistance ◽  
Iliac Artery ◽  
Resistance Artery ◽  
Steady State Flow ◽  
Resistance Vessel ◽  
Significant Impairment ◽  
Vascular Autoregulation

The effect of intraluminal hyperglycaemia was investigated in the iliac artery of 11 anaesthetised pigs. Following isolation of a test segment, hyperglycaemic blood (40 mmol·L–1) caused a significant dilatation of the artery of 167 ± 208 μm (mean ± SD; n = 6, P = 0.031). Dilatations were reduced by N(G)-nitro-l-arginine methyl esther (250 μg·mL–1) from 145 ± 199 to 38 ± 5 μm), but this was not statistically significant (n = 6, P = 0.18). Intra-arterial infusions of d-glucose (20–40 mmol·L–1·min–1), during graded constrictions, caused statistically significant increases in blood flow (n = 11, P = 0.0013). Vasodilatation was confirmed by measurements of the ratio of immediate pressure steps to flow steps (∂P/∂F) during the graded obstruction experiments, showing a decrease in instantaneous vascular resistance from a control of 0.62 ± 0.30 to 0.33 ± 0.34 mm Hg·mL–1·min–1 (n = 7, P = 0.016). Autoregulation was assessed from the slopes of the plots of steady-state flow versus pressure. There were significant increases in the slope from 2.32 ± 1.03 to 5.88 ± 5.60 mL·min–1·(mm Hg)–1 (n = 7, P = 0.0078), indicating significant impairment of autoregulation. In conclusion, luminal hyperglycaemia relaxes both arterial and resistance vessel smooth muscle.

Saline infusion into lumen of resistance artery and small vein causes contraction

1990 ◽  
Vol 259 (1) ◽  
pp. H23-H28 ◽  
Author(s):  
J. A. Bevan ◽  
E. H. Joyce
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Physiological Saline ◽  
Saline Infusion ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Surface Receptors ◽  
Calcium Dependent ◽  
Rate Dependent ◽  
Physiological Saline Solution

Infusion of saline into the lumen of a resistance artery from the rabbit ear at rates between 0.5 and 20 microliters/min causes a rate-dependent maintained contraction. This contraction is independent of the direction of saline flow and of the endothelium. The contraction is prevented by pretreatment with the vasodilator papaverine (0.1 mM), which also reversed the contraction during flow. Exclusion of calcium from the physiological saline solution plus ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (1 mM) prevents the contraction, as does pre-exposure to cobalt (1 mM) and manganese (1 mM). Both these ions depress saline flow contraction once it is established. Saline flow-dependent contraction changes in a complex manner with temperature. It is greatest in resistance arteries from the pial, ear (skin), and femoral (muscle) segments, moderate to poor in coronary, mesenteric, and renal segments, and absent in the pulmonary segments. A small ear vein adjacent to the ear resistance artery also contracts to saline infusion. Although an explanation based on the washout of a vasodilator metabolite cannot be excluded, we favor the hypothesis that saline flow-induced shear stress of the inner surface of the vessel wall mechanically activates the vascular smooth muscle cells causing an extracellular Ca2(+)-dependent contraction. This response takes place through indomethacin-insensitive calcium-dependent mechanisms in vascular smooth muscle that differ from those associated with commonly studied surface receptors and with stretch.

Steady-state autoregulation of renal blood flow: a myogenic model

1984 ◽  
Vol 247 (1) ◽  
pp. R89-R99 ◽  
Author(s):  
D. J. Lush ◽  
J. C. Fray
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Muscle Contraction ◽  
Intracellular Calcium ◽  
Renal Blood Flow ◽  
Smooth Muscle Contraction ◽  
Vascular Smooth Muscle Contraction ◽  
Calcium Permeability

This paper presents a model of myogenic control of renal blood flow based on the proposition that steady-state flow occurs when the distending and constricting forces acting on the afferent arteriole are equal. The distending force is represented by the Laplace relationship. The opposing force is governed by the properties of the arterioles and has two components--a purely passive component and an “active” component resulting from vascular smooth muscle contraction. Within the myogenic model, vascular smooth muscle contraction is initiated by “stretch”-induced changes in calcium permeability. Terms are developed describing the effect of stretch on calcium permeability, intracellular calcium, and contractile activity. The model is adapted to describe the myogenic control of blood flow in the dog kidney. Sigmoidal relationships between stretch and calcium permeability and between intracellular calcium and muscle tension seem to account for the shape of the autoregulatory curve. The model predicts a shifting of the autoregulatory pressure-flow curve upward and to the right in response to increased tissue hydrostatic pressure. The model is also exquisitely sensitive to changes in the parameters governing intracellular calcium. These predictions agree well with experimental observations.

1,25(OH)2D3 modulates intracellular Ca2+ and force generation in resistance arteries

1996 ◽  
Vol 270 (1) ◽  
pp. H230-H237 ◽  
Author(s):  
K. Bian ◽  
K. Ishibashi ◽  
R. D. Bukoski
Keyword(s):  
Smooth Muscle ◽  
Steady State ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Muscle Force ◽  
Force Generation ◽  
Myosin Light Chain Phosphorylation ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Active Stress

The mechanism by which 1 alpha,25-dihydroxycholecalciferol [1,25(OH)2D3] enhances smooth muscle force generation was examined. Rats were injected on three mornings with 1,25(OH)2D3 (35 ng/100 g) or vehicle, and on the fourth morning mesenteric resistance arteries were isolated and used for simultaneous measurement of intracellular Ca2+ and force or myosin light chain phosphorylation. 1,25(OH)2D3 did not affect media thickness or wall-to-lumen ratio, but it increased basal intracellular Ca2+ (vehicle = 49.2 +/- 2.2 nM vs. 1,25(OH)2D3 = 65.9 +/- 4.0 nM, P < 0.05, n = 24-26 rats). 1,25(OH)2D3 enhanced the active stress and intracellular Ca2+ responses to increasing doses of norepinephrine, and the increases were normalized by verapamil (10 microM). In a second group of animals, 1,25(OH)2D3 significantly increased both basal intracellular Ca2+ and light chain phosphorylation and the active stress and Ca2+ mobilization responses to norepinephrine (10 microM). The hormone did not affect peak or steady-state light chain phosphorylation. Myofilament Ca2+ sensitivity, determined during stimulation with 2 microM norepinephrine, was depressed in vessels isolated from rats treated with 1,25(OH)2D3 [vehicle Ca2+ 50% effective dose (ED50) = 82.7 +/- 3.8 nM vs. 1,25(OH)2D3 = 104.8 +/- 4.9 nM, P = 0.002]. We conclude that 1,25(OH)2D3 enhances resistance artery force generation by altering smooth muscle Ca2+ homeostasis, with effects on basal and verapamil-sensitive, agonist-induced Ca2+ mobilization.

Abstract P1120: Opioids Induce Proliferation in Vascular Smooth Muscle Cells Leading to an Increase in Myogenic Tone in Resistance Arteries

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Jeremy C Tomcho ◽  
Jonnelle Edwards ◽  
Nicole R Bearss ◽  
Cameron G McCarthy ◽  
Bina Joe ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Myogenic Tone ◽  
Resistance Arteries

scholarly journals Disruption of Pressure-Induced Ca 2+ Spark Vasoregulation of Resistance Arteries, Rather Than Endothelial Dysfunction, Underlies Obesity-Related Hypertension

Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 539-548 ◽  
Author(s):  
Adam S. Greenstein ◽  
Sharifah Zamiah Abdul Syed Kadir ◽  
Viktoria Csato ◽  
Sarah A. Sugden ◽  
Rachael A. Baylie ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Signaling Pathways ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Intraluminal Pressure ◽  
Pharmacological Intervention ◽  
Resistance Arteries ◽  
High Fat ◽  
Transient Receptor

Obesity-related hypertension is one of the world’s leading causes of death and yet little is understood as to how it develops. As a result, effective targeted therapies are lacking and pharmacological treatment is unfocused. To investigate underlying microvascular mechanisms, we studied small artery dysfunction in a high fat–fed mouse model of obesity. Pressure-induced constriction and responses to endothelial and vascular smooth muscle agonists were studied using myography; the corresponding intracellular Ca 2+ signaling pathways were examined using confocal microscopy. Principally, we observed that the enhanced basal tone of mesenteric resistance arteries was due to failure of intraluminal pressure-induced Ca 2+ spark activation of the large conductance Ca 2+ activated K + potassium channel (BK) within vascular smooth muscle cells. Specifically, the uncoupling site of this mechanotransduction pathway was at the sarcoplasmic reticulum, distal to intraluminal pressure-induced oxidation of Protein Kinase G. In contrast, the vasodilatory function of the endothelium and the underlying endothelial IP-3 and TRPV4 (vanilloid 4 transient receptor potential ion channel) Ca 2+ signaling pathways were not affected by the high-fat diet or the elevated blood pressure. There were no structural alterations of the arterial wall. Our work emphasizes the importance of the intricate cellular pathway by which intraluminal pressure maintains Ca 2+ spark vasoregulation in the origin of obesity-related hypertension and suggests previously unsuspected avenues for pharmacological intervention.

Vascular Actions of Insulin in Health and Disease

1995 ◽  
Vol 20 (2) ◽  
pp. 127-154 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Arend Bonen
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Resistance ◽  
Prolonged Exposure ◽  
Muscle Blood Flow ◽  
Metabolic Effects ◽  
Smooth Muscle Tissue

Insulin has well known metabolic effects. However, depending on the magnitude and duration of the insulin stimulus, this hormone can also produce vasodilation and vascular smooth muscle growth. The association of hyperinsulinemia with the metabolic disorders of obesity and non-insulin-dependent diabetes, as well as with the cardiovascular pathologies of hypertension and atherosclerosis, has led to suggestions that perhaps elevated insulin levels are causally related to these diseases. Alternatively, insulin resistance may develop following an increase in skeletal muscle vascular resistance, with or without hypertension, such that a reduction in skeletal muscle blood flow leads to an attenuated glucose delivery and uptake. These hypotheses are explored in this review by examining the effects of insulin on vascular smooth muscle tissue during both acute and prolonged exposure. An interaction among hyperinsulinemia, hyperglycemia, and hyperlipidemia associated with the insulin resistant state is described whereby insulin resistance can be both a cause and a result of elevated vascular resistance. The association between blood flow and insulin stimulated glucose uptake suggests that therapeutic intervention against the development of skeletal muscle vascular resistance should occur early in individuals genetically predisposed to cardiovascular pathology in order to attenuate, or avoid, insulin resistance and its sequelae. Key words: hyperinsulinemia, hyperglycemia, vascular smooth muscle, obesity, hypertension, atherosclerosis

Mechanisms of Direct Inhibitory Action of Isoflurane on Vascular Smooth Muscle of Mesenteric Resistance Arteries

2003 ◽  
Vol 99 (3) ◽  
pp. 666-677 ◽  
Author(s):  
Takashi Akata ◽  
Tomoo Kanna ◽  
Jun Yoshino ◽  
Shosuke Takahashi
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Reactivity ◽  
Channel Blocker ◽  
Isometric Force ◽  
Systemic Resistance ◽  
Resistance Arteries ◽  
Voltage Gated ◽  
Fura 2 ◽  
Force Relation

Background Isoflurane has been shown to directly inhibit vascular reactivity. However, less information is available regarding its underlying mechanisms in systemic resistance arteries. Methods Endothelium-denuded smooth muscle strips were prepared from rat mesenteric resistance arteries. Isometric force and intracellular Ca2+ concentration ([Ca2+]i) were measured simultaneously in the fura-2-loaded strips, whereas only the force was measured in the beta-escin membrane-permeabilized strips. Results Isoflurane (3-5%) inhibited the increases in both [Ca2+]i and force induced by either norepinephrine (0.5 microM) or KCl (40 mM). These inhibitions were similarly observed after depletion of intracellular Ca2+ stores by ryanodine. Regardless of the presence of ryanodine, after washout of isoflurane, its inhibition of the norepinephrine response (both [Ca2+]i and force) was significantly prolonged, whereas that of the KCl response was quickly restored. In the ryanodine-treated strips, the norepinephrine- and KCl-induced increases in [Ca2+]i were both eliminated by nifedipine, a voltage-gated Ca2+ channel blocker, whereas only the former was inhibited by niflumic acid, a Ca2+-activated Cl- channel blocker. Isoflurane caused a rightward shift of the Ca2+-force relation only in the fura-2-loaded strips but not in the beta-escin-permeabilized strips. Conclusions In mesenteric resistance arteries, isoflurane depresses vascular smooth muscle reactivity by directly inhibiting both Ca2+ mobilization and myofilament Ca2+ sensitivity. Isoflurane inhibits both norepinephrine- and KCl-induced voltage-gated Ca2+ influx. During stimulation with norepinephrine, isoflurane may prevent activation of Ca2+-activated Cl- channels and thereby inhibit voltage-gated Ca2+ influx in a prolonged manner. The presence of the plasma membrane appears essential for its inhibition of the myofilament Ca2+ sensitivity.

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