Mesenteric Small Artery Changes After Vasoconstrictor Infusion in Young Rats

Boonen, Harrie C. M.; Daemen, M. J. A. P.; Eerdmans, Pedro; Fazzi, Gregorio E.; Kleef, E. M. Van; Schiffers, P. M. H.; Mey, Jo G. R. De

doi:10.1097/00005344-199309000-00007

Cited by 30 publications

(14 citation statements)

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“…We confirmed that in mesenteric small arteries hyper trophy develops during chronic low dose administration of All [ 13,22,29] and that this is associated with quanti tative rather than qualitative changes in mesenteric small artery reactivity [13,22]. The nonselective hyperreactivi ty to various vasoconstrictor stimuli could fully be ac counted for by the hypertrophy and no modification in sensitivity to vasoconstrictor stimuli, including nerve stimulation, could be detected.…”

Section: Other Types O F Arteriessupporting

confidence: 76%

“…Arteries were mounted on two stainless steel wires ( 0 = 40 pm) as ring segments in an isometric myograph between a force transducer (Kistle Morse DSC6, Seattle, Wash., USA) and a displacement device [22] for recording of isometric force development. Subse quently, arteries were stretched to their individual optimal lumen diameter, i.e.…”

Section: React I Vity Measurementsmentioning

confidence: 99%

“…In general, experiments involving local surgical and systemic chemical or immunosympathectomy have indicated that sympathetic nerves exert a trophic influence in the young and stabilize arterial smooth mus cle cell contractile phenotype in the adult [39]. Because ai-adrenoceptor antagonists inhibit the mitogenic but not the hypertrophic action of All in large arteries [18] and because phenylephrine fails to induce MrA hypertrophy in vivo [22], it is unlikely that the nervous contribution to the hypertrophic action of All is brought about by increased stimulation of arterial ai-adrenoceptors. Other adrenergic receptors and other sympathetic neurotrans mitters may be worth considering.…”

Section: Other Types O F Arteriesmentioning

confidence: 99%

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Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

et al. 1997

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We examined effects of a 2-week infusion of angiotensin II (All, 250 ng· kg^-1•min^-1) on properties of mesenteric resistance arteries (MrA) and superior epigastric arteries (SEA) of male Wistar rats. Histochemistry and pharmacological tools showed that MrA are densely innervated, whereas SEA are only sparsely innervated. All infusion resulted in a significant elevation in mean arterial pressure and in plasma All and noradrenaline levels. Organ chamber studies and morphometry were used to determine arterial contractile reactivity and structure. After All infusion, in MrA (i) maximal contractile responses to 125 mM K⁺, noradrenaline, serotonin and adrenergic nerve stimulation were significantly increased, without modification of the sensitivity to these stimuli and (ii) a significant increase in media cross-sectional area and media thickness was observed without alterations in lumen diameter. The observed increase in vascular reactivity could fully be attributed to the observed increase in wall mass since no alterations in maximal active wall stress were noted. In SEA, no significant changes in responsiveness to vasoconstrictor stimuli or in wall structure were observed. These findings suggest that perivascular nerves are involved in the hypertrophy and subsequent hyperreactivity of small arteries in rats exposed for 2 weeks to a low dose of AII

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Section: Other Types O F Arteriessupporting

confidence: 76%

Section: React I Vity Measurementsmentioning

confidence: 99%

Section: Other Types O F Arteriesmentioning

confidence: 99%

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Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

et al. 1997

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“…Cross sections (4 m) were stained with Lawson's solution (Boom BV), which highlights the elastic laminae. Medial cross-sectional area (CSAm), lumen diameter, and medial thickness were determined as previously described 29 with the use of video images generated by a Zeiss Axioscope, a standard CCD camera (Sony), and commercial software (JAVA 1.21, Jandell Scientific).…”

Section: Morphometrymentioning

confidence: 99%

Altered Flow–Induced Arterial Remodeling in Vimentin-Deficient Mice

Schiffers

Henrion

Boulanger

et al. 2000

ATVB

110

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Abstract-The endothelial cytoskeleton plays a key role in arterial responses to acute changes in shear stress. We evaluated whether the intermediate filament protein vimentin is involved in the structural responses of arteries to chronic changes in blood flow (BF). In wild-type mice (Vϩ/ϩ) and in vimentin-deficient mice (VϪ/Ϫ), the left common carotid artery (LCA) was ligated near its bifurcation, and 4 weeks later, the structures of the occluded and of the contralateral arteries were evaluated and compared with the structures of arteries from sham-operated mice. 3 m 2 for LCA and RCA, respectively). In Vϩ/ϩ, LCA ligation eliminated BF in the occluded vessel (before ligation, 0.35Ϯ0.02 mL/min) and increased BF from 0.34Ϯ0.02 to 0.68Ϯ0.04 mL/min in the RCA. In VϪ/Ϫ, the BF change in the occluded LCA was comparable (from 0.38Ϯ0.05 mL/min to zero-flow rates), but the BF increase in the RCA was less pronounced (from 0.33Ϯ0.02 to 0.50Ϯ0.05 mL/min). In the occluded LCA of Vϩ/ϩ, arterial diameter was markedly reduced (Ϫ162 m), and CSAm was significantly increased (5ϫ10 3 m 2 ), whereas in the high-flow RCA of Vϩ/ϩ, carotid artery diameter and CSAm were not significantly modified. In the occluded LCA of VϪ/Ϫ, arterial diameter was reduced to a lesser extent (Ϫ77 m) and CSAm was increased to a larger extent (10ϫ10 3 m 2 ) than in Vϩ/ϩ. In contrast to Vϩ/ϩ, the high-flow RCA of VϪ/Ϫ displayed a significant increase in diameter (52 m) and a significant increase in CSAm (5ϫ10 3 m 2 ). These observations provide the first direct evidence for a role of the cytoskeleton in flow-induced arterial remodeling.

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“…Historically, many studies examining pathways activated by contractile agonists have been limited to relatively acute exposures to these agents, whereas studies aimed at delineating events related to compensatory growth responses, such as remodeling in hypertension, have often considered long-term responses to trophic stimuli including catecholamines and angiotensin II (4,5). Furthermore, growth-related studies have often been performed on cultured cells, which typically exhibit phenotypic changes compared with cells in the in vivo state.…”

mentioning

confidence: 99%

Delayed arteriolar relaxation after prolonged agonist exposure: functional remodeling involving tyrosine phosphorylation

Hill

Potocnik²,

Martinez‐Lemus³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

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. Delayed arteriolar relaxation after prolonged agonist exposure: functional remodeling involving tyrosine phosphorylation. Am J Physiol Heart Circ Physiol 285: H849-H856, 2003. First published April 24, 2003 10.1152/ajpheart.00986.2002-Although arteriolar contraction is dependent on Ca 2ϩ -induced myosin phosphorylation, other mechanisms including Ca 2ϩ sensitization and time-dependent phenomena such as cytoskeletal and cellular reorganization may contribute to contractile events. We hypothesized that if arteriolar smooth muscle exhibits time-dependent behavior this may be manifested in differences in relaxation after short-and long-term exposure to contractile agonists. Studies were conducted in isolated arterioles pressurized to 70 mmHg. In initial experiments (n ϭ 10), rate of relaxation was measured after acute (5 min) or prolonged (4 h) exposure to 5 M norepinephrine (NE). Prolonged exposure to NE resulted in significantly (P Ͻ 0.05) increased time for relaxation in physiological salt solution. Rapid relaxation of vessels exposed to NE for 4 h was observed after superfusion with 0 mM Ca 2ϩ buffer, indicating that the alteration in relaxation was reversible and Ca 2ϩ dependent. A similarly impaired dilation was not observed with 4-h exposure to KCl (75 mM). To determine mechanisms contributing to the effects of prolonged NE exposure, studies were performed in the presence of the microtubule depolymerizing agent demecolcine (10 M) or a series of tyrosine phosphorylation inhibitors. Although demecolcine caused significant vasoconstriction (P Ͻ 0.05) and potentiated NE vasoconstriction, it did not prevent the effect of long-term NE exposure on relaxation. Genistein, although having no effect on acute NE-induced contraction, concentration-dependently inhibited prolonged NE constriction. Similarly, Src (PP1) and p42/44 MAP kinase (PD-98059) inhibitors prevented maintenance of long-term NE contraction. The data indicate that prolonged exposure to NE induces biochemical alterations that impair relaxation after removal of the agonist. The contractile effects are Ca 2ϩ dependent and involve tyrosine phosphorylation but do not appear to involve the polymerization state of the microtubule network.

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Mesenteric Small Artery Changes After Vasoconstrictor Infusion in Young Rats

Cited by 30 publications

References 0 publications

Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

Angiotensin II Induces Media Hypertrophy and Hyperreactivity in Mesenteric but Not Epigastric Small Arteries of the Rat

Altered Flow–Induced Arterial Remodeling in Vimentin-Deficient Mice

Delayed arteriolar relaxation after prolonged agonist exposure: functional remodeling involving tyrosine phosphorylation

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