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.

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.

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.

scholarly journals Stability of Carotid Artery Under Steady-State and Pulsatile Blood Flow: A Fluid–Structure Interaction Study

2015 ◽  
Vol 137 (6) ◽  
Author(s):  
Seyed Saeid Khalafvand ◽  
Hai-Chao Han
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Carotid Artery ◽  
Flow Rate ◽  
Pulsatile Flow ◽  
Fluid Structure Interaction ◽  
Steady State Flow ◽  
Structure Interaction ◽  
State Flow ◽  
Critical Buckling Pressure

It has been shown that arteries may buckle into tortuous shapes under lumen pressure, which in turn could alter blood flow. However, the mechanisms of artery instability under pulsatile flow have not been fully understood. The objective of this study was to simulate the buckling and post-buckling behaviors of the carotid artery under pulsatile flow using a fully coupled fluid–structure interaction (FSI) method. The artery wall was modeled as a nonlinear material with a two-fiber strain-energy function. FSI simulations were performed under steady-state flow and pulsatile flow conditions with a prescribed flow velocity profile at the inlet and different pressures at the outlet to determine the critical buckling pressure. Simulations were performed for normal (160 ml/min) and high (350 ml/min) flow rates and normal (1.5) and reduced (1.3) axial stretch ratios to determine the effects of flow rate and axial tension on stability. The results showed that an artery buckled when the lumen pressure exceeded a critical value. The critical mean buckling pressure at pulsatile flow was 17–23% smaller than at steady-state flow. For both steady-state and pulsatile flow, the high flow rate had very little effect (<5%) on the critical buckling pressure. The fluid and wall stresses were drastically altered at the location with maximum deflection. The maximum lumen shear stress occurred at the inner side of the bend and maximum tensile wall stresses occurred at the outer side. These findings improve our understanding of artery instability in vivo.

Oxygen transport during steady-state submaximal exercise in chronic hypoxia

1991 ◽  
Vol 70 (3) ◽  
pp. 1129-1136 ◽  
Author(s):  
E. E. Wolfel ◽  
B. M. Groves ◽  
G. A. Brooks ◽  
G. E. Butterfield ◽  
R. S. Mazzeo ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Steady State ◽  
Sea Level ◽  
Vascular Resistance ◽  
Barometric Pressure ◽  
Submaximal Exercise ◽  
Leg Blood Flow ◽  
Total Body ◽  
O2 Delivery

Arterial O2 delivery during short-term submaximal exercise falls on arrival at high altitude but thereafter remains constant. As arterial O2 content increases with acclimatization, blood flow falls. We evaluated several factors that could influence O2 delivery during more prolonged submaximal exercise after acclimatization at 4,300 m. Seven men (23 +/- 2 yr) performed 45 min of steady-state submaximal exercise at sea level (barometric pressure 751 Torr), on acute ascent to 4,300 m (barometric pressure 463 Torr), and after 21 days of residence at altitude. The O2 uptake (VO2) was constant during exercise, 51 +/- 1% of maximal VO2 at sea level, and 65 +/- 2% VO2 at 4,300 m. After acclimatization, exercise cardiac output decreased 25 +/- 3% compared with arrival and leg blood flow decreased 18 +/- 3% (P less than 0.05), with no change in the percentage of cardiac output to the leg. Hemoglobin concentration and arterial O2 saturation increased, but total body and leg O2 delivery remained unchanged. After acclimatization, a reduction in plasma volume was offset by an increase in erythrocyte volume, and total blood volume did not change. Mean systemic arterial pressure, systemic vascular resistance, and leg vascular resistance were all greater after acclimatization (P less than 0.05). Mean plasma norepinephrine levels also increased during exercise in a parallel fashion with increased vascular resistance. Thus we conclude that both total body and leg O2 delivery decrease after arrival at 4,300 m and remain unchanged with acclimatization as a result of a parallel fall in both cardiac output and leg blood flow and an increase in arterial O2 content.(ABSTRACT TRUNCATED AT 250 WORDS)

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

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