The Arterial Lumen Is Controlled by Flow-Related Shear Stress

Smiesko, V; Pc, Johnson

doi:10.1152/physiologyonline.1993.8.1.34

Cited by 55 publications

(67 citation statements)

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“…Shear stress is determined by blood flow and blood viscosity. Smiesko et al (32) show an increase in arterial lumen by increasing flow. Melkumyants et al (26) report that increased shear stress, induced by elevated blood viscosity, causes vasodilation in the femoral artery of the cat, which returns shear stress to baseline values.…”

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Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

106

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-Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 7-13% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function (R 2 ϭ 0.57 and P Ͻ 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by Ͻ19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and L-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring A1 arteriolar diameters (55.0 Ϯ 21.5 m) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 Ϯ 0.1 relative to baseline) and microcirculatory blood flow (1.39 Ϯ 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (Ͼ19% of baseline) led blood viscosity to increase Ͼ50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values. nitric oxide; shear stress; vascular resistance; hypertension IT IS A GENERAL MEDICAL and clinical perception that an increase in blood viscosity may lead to short-and long-term negative physiological conditions, and there appears to be universal agreement that increased blood viscosity is a factor in hypertension. Lowering blood viscosity, however, is not advocated as a means for controlling hypertension with the exception of erythrocytosis, substantial Hct increases consequent to adaptation to high altitudes, and cardiovascular impairment in premature infants. These conditions represent extremes of an increase in blood viscosity and clearly must be corrected by lowering Hct, because the extreme excess of red blood cells (RBCs) is superfluous in providing adequate oxygen-carrying capacity and is in fact a hindrance to blood flow and therefore oxygen delivery.Clinical studies (14, 37) report a significant relationship between hypertension and high Hct levels. Hypertensive patients have higher Hct values than normotensive control individuals (23). Patients suffering from polycythemia vera or other erythrocytoses present with pathologically high Hcts leading to hypertension, thromboembolism, and other severe clinical complications (2, 15). There is evidence, however, that individuals, such as Peruvian miners, survive with Hct levels of 75-91% (18), suggesting the existence of an adaptive mechanism.Endothelial cells play a key role in the regulation of blood pressure and blood flow beca...

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confidence: 96%

Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

106

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“…Key Words: blood vessels Ⅲ myogenic Ⅲ arteries Ⅲ stress, mechanical Ⅲ angiotensin II Ⅲ bradykinin F low (shear stress)-induced vasodilation and pressure (tensile stress)-induced tone (myogenic tone) play a key role in the control of vascular tone. [1][2][3][4][5][6] In resistance arteries, pressure or stretch induces myogenic tone, 6 -8 which is opposed by flow-induced dilation, in vitro as well as in vivo. 3,5,6,8,9 Whereas myogenic tone is mainly independent of endothelial factors, 6,8 shear stress has been widely shown to induce the release of endothelium-derived vasoactive agents.…”

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confidence: 99%

“…3,5,6,8,9 Whereas myogenic tone is mainly independent of endothelial factors, 6,8 shear stress has been widely shown to induce the release of endothelium-derived vasoactive agents. 1,4,5,10,11 The local tissue renin-angiotensin system [12][13][14] is another potent regulator of vascular tone. At physiological concentrations, angiotensin II amplifies agonist-induced contractions.…”

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Activation of AT ₂ Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries

et al. 1999

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Abstract-Pressure-induced tone (myogenic, MT) and flow (shear stress)-induced dilation (FD) are potent modulators of resistance artery tone. We tested the hypothesis that locally produced angiotensin II interacts with MT and FD. Rat mesenteric resistance arteries were perfused in situ. Arterial diameter was measured by intravital microscopy after a bifurcation on 2 distal arterial branches equivalent in size (150 m, nϭ7 per group). One was ligated distally and thus submitted to pressure only (MT, no FD). The second branch was submitted to flow and pressure (MT and FD). The difference in diameter between the 2 vessels was considered to be FD. Flow-diameter-pressure relationship was established in the absence and then in the presence of 1 of the following agents. In the nonligated segment (MTϩFD), angiotensin II type 1 (AT 1 ) receptor blockade (losartan) had no significant effect, whereas angiotensin II type 2 (AT 2 ) receptor blockade (PD123319) or saralasin (AT 1 ϩAT 2 blocker) decreased the diameter significantly, by 9Ϯ1 and 10Ϯ0.8 m, respectively. Angiotensin II in the presence of losartan increased the diameter by 18Ϯ0.6 m (inhibited by PD123319). PD123319 or saralasin had no effect after NO synthesis blockade or after endothelial disruption. In the arterial segment ligated distally (MT only), AT 1 or AT 2 receptor blockade had no significant effect. AT 2 -dependent dilation represented 20% to 39% of FD (shear stress from 22 to 37 dyn/cm 2 ), and AT 2 -receptor mRNA was found in mesenteric resistance arteries. Thus, resistance arterial tone was modulated in situ by locally produced angiotensin II, which might participate in flow-induced dilation through endothelial AT 2 receptor activation of NO release. Key Words: blood vessels Ⅲ myogenic Ⅲ arteries Ⅲ stress, mechanical Ⅲ angiotensin II Ⅲ bradykinin F low (shear stress)-induced vasodilation and pressure (tensile stress)-induced tone (myogenic tone) play a key role in the control of vascular tone. [1][2][3][4][5][6] In resistance arteries, pressure or stretch induces myogenic tone, 6 -8 which is opposed by flow-induced dilation, in vitro as well as in vivo. 3,5,6,8,9 Whereas myogenic tone is mainly independent of endothelial factors, 6,8 shear stress has been widely shown to induce the release of endothelium-derived vasoactive agents. 1,4,5,10,11 The local tissue renin-angiotensin system 12-14 is another potent regulator of vascular tone. At physiological concentrations, angiotensin II amplifies agonist-induced contractions. [13][14][15] Angiotensin II also activates nitric oxide (NO) production by vascular endothelial cells through angiotensin II type 1 receptor (AT 1 ) activation 16 or through angiotensin II type 2 (AT 2 ) receptor activation. 17,18 Although no relation between flow-induced dilation and angiotensin II is known as yet, angiotensin II production may be activated by stretch in cardiac myocytes. 19.20 Moreover, in the aorta, stretch and angiotensin II synergistically activate DNA and protein synthesis. 21 Nevertheless, the role of angiotensin...

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“…1,2,6 -8 These 2 mechanical stimuli determine a basal vascular tone in resistance arteries and allow a rapid adaptation to changes in flow and pressure. 1,8 Whereas myogenic tone is mainly independent of endothelial factors, 1,5 flow produces shear stress and triggers an endothelium-dependent dilation. 1,7,8 Flow-induced dilation depends in part on the production of NO 8 -11 and cyclooxygenase (COX) products 10 -13 by endothelial cells.…”

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Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

Henrion¹,

Iglarz²,

Lévy³

1999

ATVB

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Abstract-Endothelin-1 (ET-1) is released on stimulation by shear stress of the vascular wall. In several pathological situations, an involvement of ET-1 is suspected. Nevertheless, the effect of a chronic increase in circulating ET-1 on vascular tone in resistance arteries is not yet fully understood. We investigated the response to tensile stress (pressure-induced myogenic tone) and shear stress (flow-induced dilation, FD) of rat mesenteric resistance arteries cannulated in an arteriograph. Intraluminal diameter was measured continuously. Rats (normotensive Wistar-Kyoto rats [WKYs] and spontaneously hypertensive rats [SHRs]) were treated for 2 weeks with ET-1 (5 pmol ⅐ kg Ϫ1 ⅐ min Ϫ1 SC; nϭ8 to 16 per group). Systolic arterial blood pressure increased significantly in ET-1-treated rats (171Ϯ7 versus 196Ϯ6 mm Hg in WKYs and 216Ϯ8 versus 245Ϯ6 mm Hg in SHRs, PϽ0.05). Passive arterial diameter in isolated resistance arteries ranged from 78Ϯ9 to 169Ϯ4 m in WKYs and from 62Ϯ6 to 149Ϯ7 m in SHRs (pressure from 10 to 150 mm Hg). Myogenic tone was not significantly affected by chronic ET-1. Flow (9 to 150 L/min) significantly increased the arterial diameter by 2Ϯ0.5 to 22Ϯ2 m in WKYs and by 1.3Ϯ0.7 to 8.3Ϯ0.8 m in SHRs (PϽ0.001 versus WKYs). The NO synthesis blocker N G -nitro-L-arginine methyl ester (L-NAME; 100 mol/L) attenuated FD in WKYs (eg, 22Ϯ2 versus 15Ϯ3 m after L-NAME, flowϭ150 L/min) and, to a lesser extent, in SHRs (PϽ0.001 versus WKYs). The cyclooxygenase inhibitor indomethacin (3 mol/L) attenuated the remaining FD in WKYs (eg, 15Ϯ3 versus 8Ϯ3 m, flowϭ150 L/min) and in SHRs (eg, 7.5Ϯ0.5 versus 5.0Ϯ0.6 m). Chronic ET-1 significantly increased FD in SHRs but not in WKYs. In both strains, NO-dependent FD was significantly increased by chronic ET-1. Furthermore, indomethacin-sensitive FD was increased by chronic ET-1 in SHRs only. Thus, chronic ET-1 increased NO-dependent FD in resistance mesenteric arteries from both WKYs and SHRs and increased indomethacin-sensitive Key Words: myogenic tone Ⅲ shear stress Ⅲ resistance arteries Ⅲ endothelin Ⅲ hypertension P ressure-induced tone (myogenic tone) is a characteristic of small resistance arteries and of some veins. [1][2][3][4][5] It is opposed by flow-induced dilation in vitro as well as in vivo. 1,2,6 -8 These 2 mechanical stimuli determine a basal vascular tone in resistance arteries and allow a rapid adaptation to changes in flow and pressure. 1,8 Whereas myogenic tone is mainly independent of endothelial factors, 1,5 flow produces shear stress and triggers an endothelium-dependent dilation. 1,7,8 Flow-induced dilation depends in part on the production of NO 8 -11 and cyclooxygenase (COX) products 10 -13 by endothelial cells.Endothelial cells stimulated by hormonal 14 or mechanical 15-17 factors can produce endothelin-1 (ET-1). Mechanical factors such as pressure or wall stretch increase ET-1 gene expression and ET-1 production. 16,17 Flow, or shear stress, exerts a flow rate-dependent effect on the production of ET-1. A low flow rate or a short-term increas...

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The Arterial Lumen Is Controlled by Flow-Related Shear Stress

Abstract: An increase in blood flow velocity through both arteries and arterioles induces a dilation that is mediated by the endothelium. This is a significant mechanism of flow regulation at normal flow rates and is critically important during high flow conditions.

Cited by 55 publications

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Paradoxical hypotension following increased hematocrit and blood viscosity

Paradoxical hypotension following increased hematocrit and blood viscosity

Activation of AT ₂ Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries

Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

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The Arterial Lumen Is Controlled by Flow-Related Shear Stress

Abstract: An increase in blood flow velocity through both arteries and arterioles induces a dilation that is mediated by the endothelium. This is a significant mechanism of flow regulation at normal flow rates and is critically important during high flow conditions.

Cited by 55 publications

References 0 publications

Paradoxical hypotension following increased hematocrit and blood viscosity

Paradoxical hypotension following increased hematocrit and blood viscosity

Activation of AT 2 Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries

Chronic Endothelin-1 Improves Nitric Oxide–Dependent Flow-Induced Dilation in Resistance Arteries From Normotensive and Hypertensive Rats

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Activation of AT ₂ Receptors by Endogenous Angiotensin II Is Involved in Flow-Induced Dilation in Rat Resistance Arteries