A functional morphometric study of the cremaster muscle microcirculation in young spontaneously hypertensive rats

Jl, le Noble; Gj, Tangelder; Dw, Slaaf; H, van Essen; Rs, Reneman; Ha, Struyker-Boudier

doi:10.1097/00004872-199008000-00008

Cited by 50 publications

(22 citation statements)

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“…7,8 Vice versa, we may detect functional, but not structural capillary rarefaction in patients with mild blood pressure elevation. 9 Microvascular rarefaction can be a primary event 10 because remodelling of resistance arteries and microvessels can be totally [11][12][13] or partially 14 independent of blood pressure. Patients with borderline essential hypertension have skin capillary densities that are as low or even lower than those in patients with established hypertension.…”

Section: The Microvasculature Is Rarefied In Hypertensionmentioning

confidence: 99%

Angiogenesis and hypertension: an update

2009

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The purpose of this review is to provide a basic understanding of the important relationship between microvascular remodelling, angiogenesis and hypertension, that is, provide an overview of recent experimental and clinical evidence from anti-hypertensive and pro-and anti-angiogenic therapy with respect to hypertension and microvascular structure. Microvascular rarefaction, that is, a loss of terminal arterioles and capillaries, is found in most forms of human and experimental arterial hypertension. This further increases peripheral resistance, and aggravates hypertension and hypertension-induced target organ damage. In some cases with a genetic predisposition, hypertension is preceded by a loss of microvessels. Therefore, new therapies aimed at reversing microvascular rarefaction potentially represent candidate treatments of hypertension. The microvasculature is formed by the continuous balance between de novo angiogenesis and microvascular regression. Imbalanced angiogenesis, in addition to functional shut-off of blood flow, contributes to microvascular rarefaction. Numerous clinical trials assessing anti-angiogenic agents in cancer patients show that this therapy leads to microvascular rarefaction and causes or aggravates hypertension. The development of specific pro-angiogenic treatment to correct hypertension or ischaemic disorders, however, it is still in its infancy. On the other hand, long-term treatment by classic anti-hypertensive therapies that present vasodilator activity can correct for hypertension-associated rarefaction in man.

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Section: The Microvasculature Is Rarefied In Hypertensionmentioning

confidence: 99%

Angiogenesis and hypertension: an update

2009

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“…Circumstantial evidence along this line comes from measurements of tissue partial pressure of oxygen in rat models of hypertension, where relative hypoxia occurred in the cremaster, 76,77 a muscle in which rarefaction was consistently demonstrated, 30,31 but not the spinotrapezius, 78 a muscle in which no rarefaction was found. 79 The theoretical impact of rarefaction on tissue oxygenation was investigated by modeling the spatial distribution of partial pressure of oxygen with a finite element method; in that simulation, suppression of 25% of microvessels generated extended areas of profound hypoxia, especially in the presence of high cellular demand for oxygen.…”

Section: Consequences Of Microvascular Rarefactionmentioning

confidence: 99%

Hypertension

et al. 2006

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“…2 Thus far, evidence is largely based on animal models. 2,5 Spontaneously hypertensive rats had decreased arteriolar diameters compared with control rats before the onset of hypertension. 6,7 Studies in humans suggested that persons with familial predisposition had arteriolar narrowing in the prehypertensive stage.…”

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confidence: 95%

Retinal Vessel Diameters and Risk of Hypertension

Ikram

Witteman²,

Vingerling³

et al. 2006

Hypertension

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Abstract-Generalized retinal arteriolar narrowing is an important sign of systemic hypertension, and a lower arteriolar:venular diameter ratio predicts the risk of hypertension. We investigated whether this association was based on arteriolar or venular diameters or both. This study was based on the prospective population-based Rotterdam Study (1990 -1993) and included 1900 participants (Ն55 years of age) of whom 739 persons had normal blood pressure (systolic Ͻ120 mm Hg and diastolic Ͻ80 mm Hg) and 1161 prehypertension (systolic 120 to 139 mm Hg or diastolic 80 to 89 mm Hg). For each participant, retinal arteriolar and venular diameters were measured on digitized images of 1 eye. After a mean follow-up of 6.6 years, 808 persons developed hypertension, defined as either systolic blood pressure Ն140 mm Hg or diastolic blood pressure Ն90 mm Hg or use of antihypertensive medication. Adjusted for age, gender, follow-up time, body mass index, smoking, diabetes mellitus, total and high-density lipoprotein cholesterol, C-reactive protein, and intima-media thickness, arteriolar narrowing was associated with an increased risk of hypertension (odds ratio per SD: 1.38; 95% CI, 1.23 to 1.55); for venular narrowing this was less striking (OR: 1.17; 95% CI, 1.04 to 1.32). Each SD decrease in the arteriolar:venular diameter ratio significantly increased the risk of hypertension by 24%. To examine the effect of baseline blood pressure, we stratified persons into those with "normal blood pressure" or "prehypertension." Within these strata, arteriolar narrowing was still related to incident hypertension. These data show that both retinal arteriolar and venular narrowing may precede the development of systemic hypertension. Key Words: population Ⅲ risk factors Ⅲ arterioles Ⅲ vasoconstriction Ⅲ hypertension I ncreased peripheral vascular resistance, a hallmark of hypertension, is mainly determined by arteriolar narrowing. 1-3 It remains uncertain whether generalized arteriolar narrowing antedates high blood pressure or occurs as a secondary adaptation. 2 A primary role has been attributed to impaired renal sodium homeostasis, leading to fluid expansion and, subsequently, to increased cardiac output and blood pressure. 3,4 According to this hypothesis, physiological and morphological alterations in the peripheral circulation arise as a secondary reaction.In recent years, other hypotheses, postulating alterations in arterioles as the initiating event in the development of hypertension, have gained support. 2 Thus far, evidence is largely based on animal models. 2,5 Spontaneously hypertensive rats had decreased arteriolar diameters compared with control rats before the onset of hypertension. 6,7 Studies in humans suggested that persons with familial predisposition had arteriolar narrowing in the prehypertensive stage. 8 Recently, a semiautomated system was developed to noninvasively measure retinal vessel diameters in vivo. 9 To avoid a potential problem of magnification differences because of refractive errors of an eye, an arteriol...

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A functional morphometric study of the cremaster muscle microcirculation in young spontaneously hypertensive rats

Cited by 50 publications

References 0 publications

Angiogenesis and hypertension: an update

Angiogenesis and hypertension: an update

Hypertension

Retinal Vessel Diameters and Risk of Hypertension

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