Flow-induced responses in skeletal muscle venules:  modulation by nitric oxide and prostaglandins

Koller, Ákos; Dörnyei, Gabriella; Kaley, Gabor

doi:10.1152/ajpheart.1998.275.3.h831

Cited by 43 publications

(35 citation statements)

References 14 publications

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“…However, the relative contribution of venules to flow resistance increases when the arterioles are strongly dilated, such that changes in venular resistance might significantly affect flow. Shear-dependent vasodilation has been observed in venules, and this may contribute to the increase in blood flow in exercise (15). Such an effect could readily be incorporated in the model.…”

Section: Discussionmentioning

confidence: 99%

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

153

160

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Carlson BE, Arciero JC, Secomb TW. Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses. Am J Physiol Heart Circ Physiol 295: H1572-H1579, 2008. First published August 22, 2008; doi:10.1152/ajpheart.00262.2008The autoregulation of blood flow, the maintenance of almost constant blood flow in the face of variations in arterial pressure, is characteristic of many tissue types. Here, contributions to the autoregulation of pressure-dependent, shear stress-dependent, and metabolic vasoactive responses are analyzed using a theoretical model. Seven segments, connected in series, represent classes of vessels: arteries, large arterioles, small arterioles, capillaries, small venules, large venules, and veins. The large and small arterioles respond actively to local changes in pressure and wall shear stress and to the downstream metabolic state communicated via conducted responses. All other segments are considered fixed resistances. The myogenic, shear-dependent, and metabolic responses of the arteriolar segments are represented by a theoretical model based on experimental data from isolated vessels. To assess autoregulation, the predicted flow at an arterial pressure of 130 mmHg is compared with that at 80 mmHg. If the degree of vascular smooth muscle activation is held constant at 0.5, there is a fivefold increase in blood flow. When myogenic variation of tone is included, flow increases by a factor of 1.66 over the same pressure range, indicating weak autoregulation. The inclusion of both myogenic and shear-dependent responses results in an increase in flow by a factor of 2.43. A further addition of the metabolic response produces strong autoregulation with flow increasing by a factor of 1.18 and gives results consistent with experimental observation. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear response and lead to the autoregulation of blood flow. conducted response; microcirculation; blood flow regulation; vascular smooth muscle; vascular tone THE ABILITY OF VASCULAR BEDS to maintain a relatively constant blood flow over a large range of arterial pressures is known as vascular autoregulation. With increasing arterial pressure, the degree of vascular smooth muscle (VSM) activation, VSM tone, increases in arterioles, resulting in decreased vessel diameter and increased flow resistance. Several mechanisms contribute to changes in vascular tone, including responses to intraluminal pressure (myogenic response), shear stress on the endothelial lining of vessels (shear-dependent response), metabolite concentrations in vessels and/or tissue (metabolic response), and neural stimuli. The cerebral and renal vasculature show the most stable flow over a wide range of arterial pressures (2, 25), whereas in other beds, such as those in the mesentery, autoregulation is less effective.Several theoretical models for the autoregulation of blood flow have been developed using a multicompartmen...

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Section: Discussionmentioning

confidence: 99%

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Carlson¹,

Arciero²,

Secomb³

2008

American Journal of Physiology-Heart and Circulatory Physiology

153

160

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“…The cyclooxygenase and cytochrome P-450 systems in arteriolar endothelium are known to be activated by physiological stimuli such as hypoxia (8,33,37), hypercapnia (32), and increases in blood flow (28). Release of arachidonic acid metabolites from venous/ venular endothelial cells was also previously described (11,27).…”

Section: Physiological Role For Venular-arteriolar Communicationmentioning

confidence: 95%

Venular-arteriolar communication in the regulation of blood flow

Hester

Hammer

2002

American Journal of Physiology-Regulatory, Integrative and Comp

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Hester, Robert L., and Leah W. Hammer. Venular-arteriolar communication in the regulation of blood flow. Am J Physiol Regulatory Integrative Comp Physiol 282: R1280-R1285, 2002; 10.1152/ajpregu. 00744.2001.-Muscle blood flow is regulated to meet the metabolic needs of the tissue. With the vasculature arranged as a successive branching of arterioles and the larger, Ͼ50 m, arterioles providing the major site of resistance, an increasing metabolic demand requires the vasodilation of the small arterioles first then the vasodilation of the more proximal, larger arterioles. The mechanism(s) for the coordination of this ascending vasodilation are not clear and may involve a conducted vasodilation and/or a flow-dependent response. The close arteriolar-venular pairing provides an additional mechanism by which the arteriolar diameter can be increased due to the diffusion of vasoactive substances from the venous blood. Evidence is presented that the venular endothelium releases a relaxing factor, a metabolite of arachidonic acid, that will vasodilate the adjacent arteriole. The stimulus for this release is not known, but it is hypothesized that hypoxia-induced ATP release from red blood cells may be responsible for the stimulation of arachidonic release from the venular endothelial cells. Thus the venous circulation is in an optimal position to monitor the overall metabolic state of the tissue and thus provide a feedback regulation of arteriolar diameter. vasodilation; venular endothelium; relaxing factor TISSUE BLOOD FLOW is regulated to meet the metabolic needs of each tissue and can change quite dramatically. Increases in tissue metabolism cause increases in blood flow (functional hyperemia), whereas excess oxygen delivery causes a decrease in blood flow. Blood flow to skeletal or cardiac muscle increases proportionally with increases in metabolic rate to ensure adequate delivery of nutrients and removal of waste products. Although the precise mechanisms governing this close relationship between metabolic state of the tissue and blood flow remain to be elucidated, the anatomical arrangement of arteries and veins may provide a unique mechanism allowing the exchange of information or "cross-talk" between the pre-and postcapillary vessels.The vasculature is arranged as a series of blood vessels ranging in size from several millimeters to several micrometers, with the largest contribution of total resistance to blood flow coming from the large "feed" arterioles. Thus, to achieve optimal increases in blood flow during periods of increased muscle metabolism, large decreases in resistance of these arterioles must occur. As these upstream or feed vessels are not necessarily in contact with the metabolically active tissue, mechanisms other than or in addition to direct stimulation by tissue metabolites must be important in functional hyperemia. Mechanisms that have been proposed to regulate the diameter of upstream vessels include 1) conducted vasodilation (14), 2) flow-dependent vasodilation (29), and 3) myogenic vasodilation ...

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“…Különböző mechanikai stimulusok (például nyomás, nyírófeszültség) hatására is növekedhet az endothelialis anyagok szintézise és felszabadulása [40,41]. Az irodalomban ellentmondásos adatok találhatók azzal kapcsolatban, hogy az endothelialis faktorok befolyásolják-e, illetve szükségesek-e a nyomásindukált miogén tónus-hoz.…”

Section: Az Endothelialis Vazomotormechanizmusok Moduláló Szerepeunclassified

“…A venulák bazális átmérőjének szignifikáns csök-kenése L-NNA, illetve növekedése INDO és SQ 29,548 jelenlétében arra utal, hogy a NO és a PGH 2 nyugalmi körülmények között is termelődik a venulák endotheliumában és részt vesz a venulák átmérőjének a szabályozá-sában. Ugyanakkor az endothelium károsítása után a venulák bazális átmérője nem változott meg, feltehetően az endothelialis vazodilatátor és vazokonstriktor faktorok hatásának együttes kiesése miatt [33,41,42].…”

Section: Vazoaktív Anyagok Hatása a Vénás Mikroerekreunclassified

“…Az áramlás lépcsőzetes növelése dilatációt okozott a váz-izomvenulákban (maximum ~22%). Endothelium hiá-nyában az áramlás indukálta dilatáció megszűnt [41]. Vizsgálataink során azt találtuk, hogy tromboxán-A 2 , dilatátor prosztaglandinok és a nitrogén-monoxid együt-tesen felelősek az intraluminalis áramlás indukálta átmé-rőváltozások kialakulásáért.…”

Section: A Kisvénák áRamlás Indukálta Vazomotorválaszaunclassified

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Vázizomkisvénák vazomotortónusának intrinszik szabályozómechanizmusai

et al. 2016

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A legtöbb fejlett országban a vénás betegségek előfordulása és az abból adódó komplikációk meghaladják az artériás betegségekét, ezért nagyon fontos, hogy a vénák fiziológiás és patofiziológiás működését és az ezeket szabályozó mechanizmusokat minél pontosabban megismerjük. A kisvénák és venulák egyik fő feladata a vénás vér szívbe történő visszaáramlásának biztosítása és a kapillárisokban történő folyadékcsere és anyagcsere kontrollja a vazomotortónusuk szabályozása révén. Az ezeket a funkciókat szabályozó lokális mechanizmusokról azonban kevés az ismeretünk. Az elmúlt évtizedben a szerzők munkacsoportja izolált patkányvázizom-kisvénákon a vazomotortónust meghatározó "intrinszik" (érfalban található) mechanizmusokat kutatta. Eredményeik szerint a kisvénák tónusát az intraluminalis nyomás és nyíróerő változásai által aktivált mechanizmusok, továbbá számos, a simaizomból és az endotheliumból felszabaduló mediátorok integráltan szabályozzák. Ezek a mechanizmusok együttesen vesznek részt a posztkapilláris ellenállás és a szív telődésének szabályozásában, és ezáltal a megfelelő szöveti vérellátás és vénás visszaáramlás, illetve következményesen a perctérfogat biztosításában. Orv. Hetil., 2016, 157(21), 805-812.Kulcsszavak: patkány, vázizomvenula, vazomotortónus, endothelium, hidrogén-peroxid, prosztaglandinok, nitrogén-monoxid, arachidonsav, tromboxán-A 2 , nyomás, nyíróerő Regulation of vasomotor tone of small skeletal muscle veins by intrinsic mechanismsIn many developed countries the prevalence of venous disorders and its consequences are higher than that of arterial diseases. Thus it is very important to understand the exact physiological and pathophysiological function of small veins and their control mechanisms. Small veins and venules have an important role in the regulation of capillary fluid exchange, as well as return of the venous blood into the heart. However, there is only limited knowledge available regarding the role of local mechanisms controlling the vasomotor tone and diameter of small veins. In the last decade the authors focused on the elucidation of these mechanisms in isolated skeletal muscle venules of rats. Their results suggest that the tone of small veins is controlled by the integration of several mechanisms, activated by the intraluminal pressure and flow/wall shear stress, in addition to numerous local mediators synthesized and released from the smooth muscle and endothelium. These mechanisms are involved -in a complex manner -in the control of postcapillary resistance, thus regulation of tissue blood supply, venous return and consequently in the modulation of the cardiac output, as well.Keawords: rat, sceletal muscle venule, vasomotor tone, endothelium, hidrogen peroxide, prostaglandins, nitric oxide, arachidonic acid, tromboxane A 2 , pressure, flow/wall shear Szénási, A., Dörnyei, G., Rácz, A., Debreczeni, B., Koller, Á. [Regulation of vasomotor tone of small skeletal muscle veins by intrinsic mechanisms]. Orv. Hetil., 2016, 157(21), 805-812. (Beérkezett: 2016. március 5.; elfogadv...

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Flow-induced responses in skeletal muscle venules: modulation by nitric oxide and prostaglandins

Cited by 43 publications

References 14 publications

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Venular-arteriolar communication in the regulation of blood flow

Vázizomkisvénák vazomotortónusának intrinszik szabályozómechanizmusai

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