Structural and reactivity alterations of the renal vasculature of spontaneously hypertensive rats prior to and during established hypertension.

Smeda, John S.; Lee, R. M. K. W.; Forrest, James B.

doi:10.1161/01.res.63.3.518

Cited by 92 publications

(64 citation statements)

References 23 publications

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“…In hypertension, the increased vascular resistance is most potently conferred by a structurally-based decrease in the radius of the lumen of arterioles and small arteries and also potentially by arteriolar rarefaction whereby even a small change in the average arteriolar radii throughout a vascular bed has a dramatic in¯uence on the resistance tō ow. Furthermore, Adams et al 6,7 and others 8,9 have demonstrated that structural changes can precede the onset of hypertension and therefore may be an initiating mechanism. The impact of such structural changes on erectile function however, has yet to be investigated.…”

Section: Introductionmentioning

confidence: 99%

The penis is not protected — in hypertension there are vascular changes in the penis which are similar to those in other vascular beds

et al. 1999

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In hypertension, small arteries in a variety of vascular beds undergo structural changes that increase resistance. To assess whether there are differential structural changes in the penis that accompany hypertension, we began with determining structurally-based vascular resistance properties in penile and hindlimb vascular beds of adult spontaneously hypertensive rats (SHR) and Sprague-Dawley (SD) rats.In anesthetized SHR, the penile and hindlimb vasculature were isolated and perfused, maximum dilation was induced, and a¯ow-pressure assessment and a 1 -adrenoceptor agonist concentration-response curves were generated.Both the baseline and maximum constrictor responses were similar in the two beds of each strain, and overall the maximum structurally-based vascular resistance in SHR was higher than in SD rats.Our data suggests that the penile vasculature is not protected from the structural changes that take place in the other vascular beds in hypertension. There does not appear to be an underlying functional control mechanism that protects the penile vasculature from structural changes that may have a negative impact on penile blood¯ow.

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Section: Introductionmentioning

confidence: 99%

The penis is not protected — in hypertension there are vascular changes in the penis which are similar to those in other vascular beds

et al. 1999

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“…7,9,18,19 Furthermore, given that the kidneys serve a critical role in the regulation of arterial pressure, 20,21 it is not surprising that …”

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confidence: 99%

Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

2012

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Abstract-Although it has been extensively scrutinized, the factor(s) involved in the initiation and development of hypertension in spontaneously hypertensive rats (SHRs) remains unresolved. The objective of the present study was to determine whether, early in development, the causal mechanism(s) for the development of hypertension in young SHRs involves an integration of 2 processes, specifically an upregulation of structurally based vascular resistance properties and a rightward shift in the hemodynamic component of pressure-natriuresis. Mean arterial pressure was determined in conscious 4-week-old SHRs and Wistar-Kyoto rats via previously implanted aortic catheters. Structurally based hindlimb vascular resistance properties were assessed in 2-and 4-week-old SHRs and Wistar-Kyoto rats. Renal interstitial hydrostatic pressure was measured after short-term manipulations of renal arterial pressure (RAP) in 4-week-old, anesthetized rats. Although mean arterial pressure in conscious SHRs (113Ϯ5 mmHg) and Wistar-Kyoto rats (110Ϯ6 mmHg) was not significantly different at 4 weeks of age, SHRs at 2 and 4 weeks of age already had increases in structurally based vascular resistance properties of Ϸ30% above age-and weight-matched Wistar-Kyoto rats. Furthermore, the acute RAP-renal interstitial hydrostatic pressure relationship was found to be linear in both strains, and the temporal coupling of the stimulus to response was rapid; that is, renal interstitial hydrostatic pressure responses to changes in RAP were Ͻ2 s. Although the slope of the RAP-renal interstitial hydrostatic pressure relationship was not significantly different between strains, the relationship was significantly shifted (18%) to higher RAPs in SHRs. These results suggest that alterations in both vascular structure and renal function in young SHRs occur before elevations in mean arterial pressure. A lthough the factors responsible for the initiation and development of genetic hypertension have been extensively studied in the spontaneously hypertensive rat (SHR), the basis and time course for blood pressure elevation remain enigmatic. Specifically, what remains controversial is whether the 2 most widely studied processes, vascular abnormalities and renal dysfunction, lead to increases in arterial pressure or vice versa.Since the 1970s, 1 it has been well established that vascular abnormalities, such as increases in vascular resistance, vascular reactivity to vasoconstrictors, and media:lumen ratio, are associated with hypertension in the adult SHR.1-3 Despite the number of studies describing vascular morphometric and histological differences in young SHRs, 4-9 evidence linking blood pressure elevations with vascular structural and functional changes remains unresolved in the neonatal and weaning SHRs. The hypothesis that vascular structural changes antecede and initiate a rise in arterial pressure has been disputed for 2 main reasons, the presence 8,10-13 or lack 4-7,9,14,15 of blood pressure elevation in studies of young SHRs and substantial differences be...

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“…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.…”

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Retinal Vessel Diameters and Risk of Hypertension

Ikram

Witteman²,

Vingerling³

et al. 2006

Hypertension

294

129

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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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Structural and reactivity alterations of the renal vasculature of spontaneously hypertensive rats prior to and during established hypertension.

Cited by 92 publications

References 23 publications

The penis is not protected — in hypertension there are vascular changes in the penis which are similar to those in other vascular beds

The penis is not protected — in hypertension there are vascular changes in the penis which are similar to those in other vascular beds

Altered Vascular Resistance Properties and Acute Pressure-Natriuresis Mechanism in Neonatal and Weaning Spontaneously Hypertensive Rats

Retinal Vessel Diameters and Risk of Hypertension

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