Dilator response of rat mesenteric arcading arterioles to increased blood flow velocity

Smiesko, V; Lang, Douglas J.; Johnson, Paul C.

doi:10.1152/ajpheart.1989.257.6.h1958

Cited by 80 publications

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“…The parameter governing shear-dependent sensitivity was assumed to be equal in both arteriolar segments. It has been observed that the shear-dependent response is greater in small arteries and large arterioles than in small arterioles (18,32), and thus this model may overestimate the shear-dependent response in small arterioles. NO scavenging by RBCs is not considered in the model, causing a possibly greater overestimation of the shear stress contribution to autoregulation.…”

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

146

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

146

160

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“…flow rate; furthermore, this effect was blocked by LNMMA, but not by indomethacin. Although most reports of flowinduced dilation suggest mediation by NO (3,12,13), some have reported a role for endothe lium-der ived eicosanoids (4). Cyclooxygenase products did not appear to mediate this phenomenon in newborn intestine.…”

Section: Discussionmentioning

confidence: 99%

Flow-Induced Dilation in Newborn Intestine

Nowicki¹,

Miller²

1995

Pediatr Res

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The goal of these experiments was to determine the presence and mechanistic basis of flow-induced dilation in mesenteric artery from 3-d-old swine. In the first experiment, in vitro gut loops were perfused from a blood-filled reservoir under controlled-flow conditions, and flow was progressively increased from~40 % to~170% in six increments by manipulation of pump speed. Under control conditions, vascular resistance significantly decreased after each step increase in flow rate. WMonomethyl-t-arginine (LNMMA; 10-4 M), an arginine analog that blocks nitric oxide production, eliminated this flow-induced dilation, but only for the step increases in flow at rates above the baseline flow rate. For step increases below the baseline rate, LNMMA caused a simple parallel shift of the resistance-flow rate curve upward. Phenylephrine (10-6 M), an (X l-agonist which has no effect on nitric oxide production or half-life, did not eliminate flow-induced dilation, but instead caused a simple parallel shift of the resistance-flow rate curve upward across the entire range of flows studied. In the second experiment, a 3-cm segment of mesenteric artery was perfused with Krebs buffer at two flow rates: 10 and 25 mU min. The effluent from the rnesFlow-induced dil ation is a vascular phenomenon wh erein aug me ntation of flow rate throu gh an art ery res ults in vasodilation of that ves sel (1). Th e proc ess was init iall y described in large conduit arteries and was presumed to be part of series of va scular adjustments which facilitate oxygen delivery during exercise (1, 2). In this sce nario, resistance vessels within the microcir cul ation of co ntrac ting muscle dil ate in response to a metaboli c feedb ack signal, an action which decre ases downstrea m vascular resista nce. This hemodynamic ch ange increases flow rate throu gh the co nduit ves se ls leading to the mu scl e. Th e stimulus of inc reas ed flow rate induces dil ation of the conduit vessels, an action which maximizes vascular conduct ance . Subsequent studies hav e identified flow-induced dilation within arterioles (3) and have establ ish ed that flowinduced dil ation is an endo thelium-dependent process, that is, enteric artery segment was suffused onto a deendothelialized, phenylephrine-precontracted ring of swine carotid artery; relaxation of this bioassay vessel served as an index of release of relaxing factors from the mesenteric artery segment. Under control conditions, increase in the mesenteric artery flow rate caused a 60% relaxation of the bioassay vessel. This effect was eliminated by the addition of LNMMA to the buffer (10-4 M), but not by the addition of indomethacin (10-5 M). Flow-induced dilation occurs in the mesenteric artery of 3-d-old swine. This vascular phenomenon appears to be mediated by nitric oxide, but only at flows above the baseline flow rate. The mechanism(s) responsible for this phenomenon at lower flow rates is not clear. (Pediatr Res 38: 783-791, 1995) Abbreviations NO, nitric oxide LNMMA, W-monomethyl-i. -arginine (a-v)02' arteriov...

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“…If so, one role of these nitrergic neurons could be to detect distortion from moving internal fluids by way of stretch receptors and to transmit output signals to other neurons or musculo-epithelial cells thereby directly adjusting muscle tension levels and peristalsis. This postulated mechanism has some analogy with the shearing forces acting on the luminal surface of mammalian vascular endothelium to regulate the release of NO (Buga et al, 1991;Smiesko et al, 1989). The location of these neurons in the tentacles and oral disc also suggest a role in feeding, but preliminary experiments with NO donors and NOS inhibitors failed to affect the posture of tentacles or mouth opening.…”

Section: Histochemistry Of Putative Nos-containing Cellsmentioning

confidence: 93%

Nitric oxide modulates peristaltic muscle activity associated with fluid circulation in the sea pansyRenilla koellikeri

Anctil

Poulain

Pelletier

2005

Journal of Experimental Biology

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SUMMARY Nitric oxide (NO) is a well-known regulator of vascular activities in vertebrates and it has also been implicated as a vasodilatatory agent in a cephalopod. In the sea pansy Renilla koellikeri, an octocorallian representative of the most basal animals with a nervous system, we investigated the role of NO in peristalsis, an activity that moves body fluids through the coelenteron (gastrovascular cavity) of the polyps across the colony. NO donors increased the amplitude of peristaltic contractions and increased tonic contractions in relaxed preparations, but caused a relaxation of basal tension in contracted preparations. The NO synthase (NOS) inhibitors L-NAME (N(ω)-nitro-L-arginine methyl ester) and 7-nitroindazole reduced the amplitude of peristaltic contractions and lowered basal tension. In contrast, aminoguanidine, a specific inhibitor of inducible NOS, increased the amplitude but reduced the rate of peristalsis. Zaprinast, a cGMP-specific phosphodiesterase inhibitor, decreased the amplitude of peristaltic contractions, a decrease that was amplified by dibutyryl cGMP. In contrast,the inhibitor of soluble guanylyl cyclase ODQ(1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one) enhanced peristalsis. Putative NOS-containing neurons, revealed by NADPH-diaphorase activity and citrulline immunohistochemistry, were observed in the basiectoderm at the base of the autozooid polyp tentacles and in a nerve-net around the oral disc. Their neurites ran up the tentacles and down to the polyp body wall, crossing from the ectoderm through the mesoglea and into the endoderm musculature where musculo-epithelial cells were also reactive. These data suggest that two distinct nitrergic pathways, one of which is mediated by cGMP, regulate peristalsis and muscle tone in the sea pansy and that these pathways may involve NOS-containing ectodermal neurons and musculo-epithelial cells.

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Dilator response of rat mesenteric arcading arterioles to increased blood flow velocity

Cited by 80 publications

References 0 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

Flow-Induced Dilation in Newborn Intestine

Nitric oxide modulates peristaltic muscle activity associated with fluid circulation in the sea pansyRenilla koellikeri

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