Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin.

Greene, Andrew S.; Lombard, Julian H.; Cowley, Allen W.; Hansen-Smith, Fay M.

doi:10.1161/01.hyp.15.6.779

Cited by 75 publications

(64 citation statements)

References 14 publications

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“…In comparison to tissues harvested from WKY rats, SHR mesenteric tissues contain smaller microvascular networks, consistent with previously documented microvascular rarefaction in other organs of the SHR (Chen et al, 1981;Greene et al, 1990;Hutchins and Darnell, 1974;Kobayashi et al, 2005;Prewitt et al, 1982). 15/15 SHR isolated networks from 6 tissues were classified as small defined by being contained to a 10× field of view.…”

Section: Resultssupporting

confidence: 84%

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Murfee

Schmid‐Schönbein

2008

Methods in Enzymology

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Microvascular rarefaction, defined by a loss of terminal arterioles, small venules and/or capillaries, is a common characteristic of the hypertension syndrome. While rarefaction has been associated with vessel specific free radical production, deficient leukocyte adhesion, and cellular apoptosis, the relationships of rarefaction with structural alterations at the network and cellular level remain largely unexplored. The objective of this study was to examine the architecture and perivascular cell phenotypes along microvascular networks in hypertensive versus normotensive controls in the context of imbalanced angiogenesis. Mesenteric tissues from age-matched adult male spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were harvested and immnolabeled for PECAM and neuron-glia antigen 2 (NG2). Evaluation of intact rat mesenteric microvascular networks rats suggests that network alterations associated with hypertension are more complex than just a loss of vessels. Typical SHR versus WKY networks demonstrate a reduced branching architecture marked by more proximal arteriole/venous anastomoses and an absence of NG2 labeling along arterioles. Although less frequent, larger SHR microvascular networks display regions of dramatically increased vascular density. SHR and WKY lymphatic networks demonstrate increased vessel diameters and vascular density compared to networks in normotensive Wistar rats (the strain from which both the SHR and WKY originated). These observations provide a rationale for investigating the presence of local angiogenic factors and response of microvascular networks to therapies aimed at reversing rarefaction in genetic hypertension.

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Section: Resultssupporting

confidence: 84%

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Murfee

Schmid‐Schönbein

2008

Methods in Enzymology

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“…10 Other studies with a longer duration have shown similar findings. 9,19,27 It is possible that salt, rather than working through BP, may have a direct effect on microvascular network and could be one of the underlying causes for the microvascular rarefaction that occurs in hypertension.…”

Section: Discussionmentioning

confidence: 99%

Effect of Modest Salt Reduction on Skin Capillary Rarefaction in White, Black, and Asian Individuals With Mild Hypertension

Marciniak

Markandu

et al. 2010

Hypertension

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Abstract-Microvascular rarefaction occurs in hypertension. We carried out a 12-week randomized double-blind crossover trial to determine the effect of a modest reduction in salt intake on capillary rarefaction in 71 whites, 69 blacks, and 29 Asians with untreated mildly raised blood pressure. Both basal and maximal (during venous congestion) skin capillary density were measured by capillaroscopy at the dorsum and the side of the fingers. In addition, we used orthogonal polarization spectral imaging to measure skin capillary density at the dorsum of the fingers and the hand web. With a reduction in salt intake from 9.7 to 6.5 g/day, there was an increase in capillary density (capillaries per millimeter squared) from 101Ϯ21 to 106Ϯ23 (basal) and 108Ϯ22 to 115Ϯ22 (maximal) at the dorsum, and 101Ϯ25 to 107Ϯ26 (basal) and 110Ϯ26 to 116Ϯ26 (maximal) at the side of the fingers (PϽ0.001 for all). Orthogonal polarization spectral imaging also showed a significant increase in capillary density both at the dorsum of the fingers and the web. Subgroup analysis showed that most of the changes were significant in all of the ethnic groups. Furthermore, there was a significant relationship between the change in 24-hour urinary sodium and the change in capillary density at the side of the fingers. These results demonstrate that a modest reduction in salt intake, as currently recommended, improves both functional and structural capillary rarefactions that occur in hypertension, and a larger reduction in salt intake would have a greater effect. The increase in capillary density may possibly carry additional beneficial effects on target organs. (Hypertension. 2010;56:253-259.)Key Words: sodium Ⅲ dietary Ⅲ microcirculation Ⅲ capillary rarefaction Ⅲ hypertension Ⅲ randomized trial M icrovascular rarefaction, that is, a reduction in the number of arterioles and capillaries, is found in many animal models of hypertension and in human hypertension. 1,2 We have shown previously that much of the reduction in capillary density in essential hypertension was because of the structural (anatomic) absence of capillaries, 2 although functional capillary rarefaction (because of nonperfusion) also existed. 1 Our previous studies also suggested that capillary rarefaction was likely to be a primary vascular abnormality. 3,4 Microvascular rarefaction increases peripheral vascular resistance, thereby increasing blood pressure (BP) and aggravating BP-related target organ damage. 1 At the same time, a reduction in the microvascular network may decrease tissue perfusion 5 and cause gradual impairments of tissues and organs. Two studies have implied that long-term effective antihypertensive treatments may reverse microvascular rarefaction in nondiabetic individuals with raised BP. 6 -8 Studies in rats demonstrated that a high-salt intake caused a significant loss of microvessels, 9,10 which occurred within a few days. 10 However, no controlled trial in humans has studied whether a modest reduction in salt intake has an effect on microcirculation.Direct in...

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“…The remaining TA was lightly fixed overnight in 0.25% formalin solution and sectioned longitudinally. TA sections were stained with lectin, and vessel density was determined as previously described (21,38).…”

Section: Experimental Protocol the Medical College Of Wisconsin (Mcw)mentioning

confidence: 99%

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

Resende

Amaral

Munzenmaier

et al. 2006

Physiological Genomics

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. Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Physiol Genomics 25: 325-335, 2006. First published February 7, 2006 doi:10.1152/physiolgenomics.00253.2005.-Angiogenesis, under normal conditions, is a tightly regulated balance between pro-and antiangiogenic factors. The goal of this study was to investigate the mechanisms involved in the control of the skeletal muscle angiogenic response induced by electrical stimulation during the suppression of plasma renin activity (PRA) with a high-salt diet. Rats fed 0.4% or 4% salt diets were exposed to electrical stimulation for 7 days. The tibialis anterior (TA) muscles from stimulated and unstimulated hindlimbs were removed and prepared for gene expression analysis, CD31-terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) double-staining assay, and Bcl-2 and Bax protein expression by Western blot. Rats fed a low-salt diet showed a dramatic angiogenesis response in the stimulated limb compared with the unstimulated limb. This angiogenesis response was significantly attenuated when rats were placed on a high-salt diet. Microarray analysis showed that in the stimulated limb of rats fed a low-salt diet many genes related to angiogenesis were upregulated. In contrast, in rats fed a high-salt diet most of the genes upregulated in the stimulated limb function in apoptosis and cell cycle arrest. Endothelial cell apoptosis, as analyzed by CD31-TUNEL staining, increased by fourfold in the stimulated limb compared with the unstimulated limb. There was also a 48% decrease in the Bcl-2-to-Bax ratio in stimulated compared with unstimulated limbs of rats fed a high-salt diet, confirming severe apoptosis. This study suggests that the increase in endothelial cell apoptosis in TA muscle might contribute to the attenuation of angiogenesis response observed in rats fed a high-salt diet.Bax; Bcl-2; gene expression THE GROWTH OF NEW BLOOD VESSELS plays a critical role in normal physiological processes but is also central to the progression of many diseases. Angiogenesis is involved in several disorders such as cancer, diabetic retinopathy, macular degeneration, and endometriosis (15). In an attempt to control pathological angiogenesis, a growing interest in better understanding prosurvival and prodeath signals has emerged (7,8,26,34). Each endothelial cell within a vessel wall is exposed to a combination of prosurvival and prodeath signals. The sum of these signals determines whether the cell remains viable or undergoes apoptosis (10).Our laboratory has demonstrated that physiological, pharmacological, or genetic manipulation of the renin-angiotensin system (RAS) has an important impact on both the basal number of microcirculatory blood vessels and the ability of tissues to undergo angiogenesis induced by exercise (3) or electrical stimulation (2). In previous studies (4), we demonstrated that transfer of a region of chromosome 13 containing the renin gene from Dahl R into Dahl S rats restores both p...

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Microvessel changes in hypertension measured by Griffonia simplicifolia I lectin.

Cited by 75 publications

References 14 publications

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Chapter 12 Structure of Microvascular Networks in Genetic Hypertension

Effect of Modest Salt Reduction on Skin Capillary Rarefaction in White, Black, and Asian Individuals With Mild Hypertension

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

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