Vascular Myogenic or Stretch-Dependent Tone

Ja, Bevan

doi:10.1097/00005344-198500073-00015

Cited by 23 publications

(15 citation statements)

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“…Resistance artery tone is mainly regulated by mechanical (pressure and shear stress) and humoral factors such as Ang-II and bradykinin (4,17,19,20). The two mechanical factors antagonize each other.…”

Section: Discussionmentioning

confidence: 99%

Role of ACE/AT2R complex in the control of mesenteric resistance artery contraction induced by ACE/AT1R complex activation in response to Ang I

Palen

Boulares

et al. 2007

Mol Cell Biochem

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Objectives-In this study we will determine the function of the interaction between AT 2 R and ACE, and AT 1 R and ACE in the control of mesenteric resistance artery (MRA) tone from normotensive and Angiotensin II (AII)-dependent hypertensive mice.Methods-results-Hypertension (HT) was induced by infusion of Ang-II (200ng/kg/day) for 3 weeks. Freshly MRA (100-120μm) were isolated from HT and normotensive (NT) mice and mounted in an arteriograph. Dose-response of Ang-I induced a similar contraction of MRA from NT and HT mice, which was increased after endothelium removal. AT 2 R antagonist (PD123319, 1μM) significantly increased Ang-I-induced contraction of MRA from NT but not from HT mice. In addition, PD123319 significantly increased in vivo blood pressure in response to Ang-I. Luminal incubation with ACE-antibody (50ng/mL) to block only endothelial ACE function significantly enhanced Ang-I-induced contraction of MRA from NT mice. ACE inhibitor (captopril, 10μM) completely blocked Ang-I-induced contraction of MRA from both animals and prevented the increased blood pressure. Freshly isolated MRA subjected to immunoprecipitation, western blot analysis and RT-PCR revealed AT 1 R/ACE and AT 2 R/ACE complexes formation, and similar AT 1 R, AT 2 R, and ACE expression level in both groups.Conclusion-The present findings show the existence of ACE/AT 2 R and ACE/AT 1 R complexes on endothelial cells and VSMC respectively. ACE/AT 2 R complex plays a modulator effect on ACE/ AT 1 R-SMC-induced contraction of MRA, which is altered in hypertension.

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Section: Discussionmentioning

confidence: 99%

Role of ACE/AT2R complex in the control of mesenteric resistance artery contraction induced by ACE/AT1R complex activation in response to Ang I

Palen

Boulares

et al. 2007

Mol Cell Biochem

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“…As remodeling in response to hypertension has been shown to be inhomogeneous across the wall cross thickness (23,34), one would thus expect that the VSM tone and changes in local stress and strain acting on the VSM cells would be inhomogeneous during the remodeling process. Furthermore, we have observed (49) changes of VSM tone in response to axial elongation of the porcine carotid artery in addition to the widely appreciated sensitivity to circumferential deformation or myogenic response (3,6,7,33,40,41). We thus identified the need for a more detailed description of the arterial wall mechanics through a SEF that describes the orthotropic and dynamic VSM embedded in the passive arterial matrix.…”

mentioning

confidence: 86%

A constitutive formulation of arterial mechanics including vascular smooth muscle tone

Zulliger

Rachev²,

Stergiopulos

2004

American Journal of Physiology-Heart and Circulatory Physiology

170

136

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A pseudo-strain energy function (pseudo-SEF) describing the biomechanical properties of large conduit arteries under the influence of vascular smooth muscle (VSM) tone is proposed. In contrast to previous models that include the effects of smooth muscle contraction through generation of an active stress, in this study we consider the vascular muscle as a structural element whose contribution to load bearing is modulated by the contraction. This novel pseudo-SEF models not only arterial mechanics at maximal VSM contraction but also the myogenic contraction of the VSM in response to local increases in stretch. The proposed pseudo-SEF was verified with experimentally obtained pressure-radius curves and zero-stress state configurations from rat carotid arteries displaying distinct differences in VSM tone: arteries from normotensive rats displaying minimal VSM tone and arteries from hypertensive rats exhibiting significant VSM tone. The pressure-radius curves were measured in three different VSM states: fully relaxed, maximally contracted, and normal VSM tone. The model fitted the experimental data very well (r2 > 0.99) in both the normo- and hypertensive groups for all three states of VSM activation. The pseudo-SEF was used to illustrate the localized reduction of circumferential stress in the arterial wall due to normal VSM tone, suggesting that the proposed pseudo-SEF can be of general utility for describing stress distribution not only under passive VSM conditions, as most SEFs proposed so far, but also under physiological and pathological conditions with varying levels of VSM tone.

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“…Furthermore, endothelium dependent flow mediated dilatation52 would be lost, thereby enabling the myogenic response to operate unopposed. 8 We could not assess endothelium dependent responses to substance P after PTCA to test this hypothesis because progressive vasoconstriction occurs after PTCA.2122 As substance P was infused over a two minute period in our protocol, the end result would represent the sum of two opposing actionsthat is, dilatation with substance P and progressive vasoconstriction as a result of PTCA. Thus, it would not be possible to dissect out the contributions from these two opposing mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Endothelium dependent and independent responses in coronary artery disease measured at angioplasty.

Holdright

Clarke²,

Poole-Wilson³

et al. 1993

Heart

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Objective-To investigate the effects of substance P and papaverine, two drugs that increase coronary blood flow by different mechanisms, on vasomotion in stenotic coronary arteries at percutaneous transluminal coronary angioplasty (PTCA).Design-Coronary blood flow responses to substance P and papaverine were measured in stenotic coronary arteries at the time of PTCA with quantitative angiography and a Doppler flow probe. Setting-A cardiothoracic referral centre.Patients-15 patients undergoing elective PTCA of a discrete epicardial coronary artery stenosis. Interventions-Pharmacological coronary flow reserve was determined with papaverine 5-10 minutes before and after successful PTCA. Endothelium dependent responses to 2 minute infusions of substance P (10-15 pmol.min-1) were assessed immediately before PTCA. Main outcome measures-Coronary blood flow responses and changes in epicardial coronary artery area at stenotic, proximal, and distal sites with papaverine and substance P. Results-Stenotic sites dilated with papaverine before PTCA (17.7%(6.9%) (mean (SEM)) area increase, p < 0 05 v baseline). Substance P dilated stenotic sites (16-8%(5-7%) area increase, p < 0.05) and proximal (14-3%(5-4%), p < 0.05) and distal sites (41.7%(9.3%), p < 0.005). Coronary flow reserve increased but did not reach normal values after PTCA (2-3(0.4) before PTCA v 3-0(0.4) after PTCA, p < 0.05) and was associated with an increase in peak flow with papaverine. Angioplasty did not alter baseline flow. After PTCA papaverine caused significant vasoconstriction at the stenotic site (-13.6%(4-3%) area decrease, p < 0.05). There was a negative correlation (r = -068, p < 0.05) between the dilator response with papaverine before PTCA and the constrictor response after PTCA. Conclusions-Substance P causes endothelium dependent dilatation in atheromatous coronary arteries, even at sites of overt atheroma. The cause of the paradoxical constrictor response to papaverine after PTCA is uncertain, but unopposed flow mediated vasoconstriction (the myogenic response) after balloon induced endothelial denudation may be one of several contributory factors. (Br Heartj_ 1993;70:35-42)

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Vascular Myogenic or Stretch-Dependent Tone

Cited by 23 publications

References 0 publications

Role of ACE/AT2R complex in the control of mesenteric resistance artery contraction induced by ACE/AT1R complex activation in response to Ang I

Role of ACE/AT2R complex in the control of mesenteric resistance artery contraction induced by ACE/AT1R complex activation in response to Ang I

A constitutive formulation of arterial mechanics including vascular smooth muscle tone

Endothelium dependent and independent responses in coronary artery disease measured at angioplasty.

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