Micropressure-flow relationships in a skeletal muscle of spontaneously hypertensive rats.

Zweifach, Benjamin W.; Kovalcheck, Steven; Lano, F De; Chen, P

doi:10.1161/01.hyp.3.5.601

Cited by 113 publications

(89 citation statements)

References 37 publications

(15 reference statements)

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“…This discrepancy may reflect an interspecies difference in the relative importance of structural versus functional adjustments at the microvascular level during maturational changes in tissue metabolism. With the assumption that changes in arcade bridge volume flow accurately reflect changes in total network blood flow, the 25% volume flow increase from weanling to juvenile rats (Table 2) is consistent with previous reports of growth-related increases in total blood flow to rat spinotrapezius muscle (36) and rat cremaster muscle (33). However, from our recent finding that spinotrapezius muscle mass increases by almost 2.5-fold over this same period (19), blood flow per gram of tissue must actually decrease with growth.…”

Section: Discussionsupporting

confidence: 88%

“…During juvenile growth, rapid increases in tissue mass are accompanied by extensive growth of the arteriolar, venular, and capillary networks (11,19,31,33) and by increases in microvascular pressure (36) and tissue blood flow (33,36). In light of these structural and hemodynamic changes, it is reasonable to expect an accompanying change in the functional relationship between endothelium and vascular smooth muscle.…”

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confidence: 99%

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Growth-related changes in the influence of nitric oxide on arteriolar tone

Linderman

Boegehold

1999

American Journal of Physiology-Heart and Circulatory Physiology

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Linderman, J. R., and M. A. Boegehold. Growth-related changes in the influence of nitric oxide on arteriolar tone. Am. J. Physiol. 277 (Heart Circ. Physiol. 46): H1570-H1578, 1999.-This study was designed to determine whether juvenile growth is accompanied by changes in the local influence of nitric oxide (NO) or prostaglandins on arteriolar tone. In vivo microscopy was used to study proximal arterioles in the spinotrapezius muscle of rats 4-5 wk (weanling), 7-8 wk (juvenile), and 11-12 wk (mature) of age. From 4 to 12 wk of age, arterioles underwent an increase in resting diameter (from 31 Ϯ 2 to 49 Ϯ 2 µm) and volume flow (from 7 Ϯ 1 to 10 Ϯ 1 nl/s) but a decrease in resting wall shear rate (from 1,901 Ϯ 150 to 748 Ϯ 50 s Ϫ1 ). NO synthase inhibition with N G -monomethyl-L-arginine (L-NMMA) had no effect on arteriolar diameters in weanling rats but reduced diameters by 14 Ϯ 4% in juvenile rats and by 13 Ϯ 4% in mature rats. Cyclooxygenase inhibition with meclofenamate reduced arteriolar diameters by a similar amount (13 Ϯ 4 to 18 Ϯ 3%) in all age groups. There were no age-related differences in arteriolar responsiveness to locally applied sodium nitroprusside or prostaglandin E 2 . Arteriolar responsiveness to ACh was also similar in all groups, but the L-NMMA-sensitive portion of this response was smaller in mature rats than in weanling rats. Elevation of flow-related shear stress caused arteriolar dilation in juvenile rats but not in weanling rats. These findings suggest that arteriolar smooth muscle responsiveness to NO or prostaglandins does not change during juvenile growth and that basally released vasodilator prostaglandins exert a constant influence on arteriolar tone throughout this period. Basal NO activity also modulates arteriolar tone in juvenile and mature rats but not in weanling rats. In contrast, agonist-stimulated NO release is prominent in weanling and juvenile rats but somewhat decreased in mature rats, where cyclooxygenase products also contribute to ACh induced dilation.

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Section: Discussionsupporting

confidence: 88%

mentioning

confidence: 99%

Growth-related changes in the influence of nitric oxide on arteriolar tone

Linderman

Boegehold

1999

American Journal of Physiology-Heart and Circulatory Physiology

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“…These results indicate that the smaller diameters of the renal preglomerular vasculature of young SHR vs normotensive rats are due to differences in active vascular tone rather than a structural narrowing of the vessels. Previous studies have demonstrated an increased cerebral vascular tone in young SHR, 19 and studies of the skeletal muscle microcirculation have shown an increased vascular resistance 20 -22 that was due, in part, to vascular rarefaction. 22 The present study is the first to observe directly an increase in active renal vascular tone as early as 4 weeks in the SHR.…”

Section: Discussionmentioning

confidence: 98%

Elevated renovascular tone in young spontaneously hypertensive rats. Role of cytochrome P-450.

et al. 1993

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The present study examined the role of cytochrome P-450 metabolites of arachidonic acid in elevating renal vascular resistance in young spontaneously hypertensive rats (SHR). Differences in vascular tone were assessed in the preglomerular vasculature of 3-to 4-week-old prehypertensive SHR ( n = l l ) and normotensive Wistar-Kyoto (WKY, n=10) and Wistar-Lewis (n=10) rats. Pressure-diameter relations to changes in renal perfusion pressure were compared using the juxtamedullary nephron microvascular preparation perfused in vitro with a physiological salt solution. At a pressure of 60 mm Hg, the basal diameters of the interlobular arteries and proximal and distal afferent arterioles of the SHR averaged 43±2, 17±0.3, and 11 ±0.4 /u,m, respectively. The diameters of the interlobular arteries and afferent arterioles were 9% to 14% smaller than those of corresponding vessels in WKY and Wistar-Lewis rats. Addition of P-450 inhibitors, ketoconazole (100 /imol/L) or 7-ethoxyresorufin (1 /imol/L), to the perfusate dilated the afferent arteriole of SHR by 7% to 12%, whereas it increased the diameter by only 0% to 6% in control rats and significantly reduced the differences in the pressure-diameter relation in the preglomerular vasculature of SHR and control rats. Inhibitors of P-450 eliminated the contractile response of afferent arterioles to increases in renal perfusion pressure in all three groups. Removal of calcium from the perfusate eliminated differences in the diameters of the preglomerular vasculature in SHR and normotensive rats. Renal P-450 activities in SHR and normotensive rats were compared by incubating cortical microsomes with [ In the SHR, the blunted pressure-natriuretic response is associated with a reduction in papillary blood flow 3 and renal interstitial hydrostatic pressure. 4 Recent studies by Gebremedhin et al 5 suggest that the decline in papillary blood flow in adult SHR is due to an enhanced vascular tone rather than structural changes in the preglomerular vasculature of the deep nephrons. However, little is known about the renal vasculature of very young SHR, and it remains to be determined if changes in renal vascular reactivity occur very early in the development of hypertension.

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“…This is particularly important in the large arterioles, which contribute the major portion of the overall resistance of the vascular bed. Zweifach et al (51) showed that, in the rat spinotrapezius, ϳ60% of the pressure drop occurs before the transverse arterioles (diameter 8-30 m). Similar results have been observed in other tissues (7,35,48), although the distribution of resistances in larger, conscious animals has not been determined.…”

Section: Anatomical Evidence For Venular-arteriolar Communicationmentioning

confidence: 99%

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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Micropressure-flow relationships in a skeletal muscle of spontaneously hypertensive rats.

Cited by 113 publications

References 37 publications

Growth-related changes in the influence of nitric oxide on arteriolar tone

Growth-related changes in the influence of nitric oxide on arteriolar tone

Elevated renovascular tone in young spontaneously hypertensive rats. Role of cytochrome P-450.

Venular-arteriolar communication in the regulation of blood flow

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