Programming Hypertension—Animal Models

Denton, Kate M.; Kett, Michelle M; Dodic, Miodrag

doi:10.1007/0-387-32632-4_9

Cited by 10 publications

(8 citation statements)

References 132 publications

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“…Possible explanations for these disparities include lack of catch-up growth as observed in our model (65) or may reflect stress induced by the method employed to measure arterial pressure (25,26). Indeed, intra-arterial pressure measurement in acutely instrumented rats, as employed in the current study, may be associated with a degree of stress (12,25). Nevertheless, in the current study, there were clear differences in blood pressure with age, and it appeared that control females were protected against the age-related increase in arterial pressure observed in males, but that IUGR females were not.…”

Section: Enhanced Age-related Increase In Arterial Pressure In Growthmentioning

confidence: 63%

Accelerated age-related decline in renal and vascular function in female rats following early-life growth restriction

Black

Lim

Zimanyi

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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Many studies report sexual dimorphism in the fetal programming of adult disease. We hypothesized that there would be differences in the age-related decline in renal function between male and female intrauterine growth-restricted rats. Early-life growth restriction was induced in rat offspring by administering a low-protein diet (LPD; 8.7% casein) to dams during pregnancy and lactation. Control dams were fed a normal-protein diet (NPD; 20% casein). Mean arterial pressure (MAP) and renal structure and function were assessed in 32- and 100-wk-old offspring. Mesenteric artery function was examined at 100 wk using myography. At 3 days of age, body weight was ∼24% lower (P < 0.0001) in LPD offspring; this difference was still apparent at 32 wk but not at 100 wk of age. MAP was not different between the male NPD and LPD groups at either age. However, MAP was greater in LPD females compared with NPD females at 100 wk of age (∼10 mmHg; P < 0.001). Glomerular filtration rate declined with age in the NPD male, LPD male and LPD female offspring (∼45%, all P < 0.05), but not in NPD female offspring. Mesenteric arteries in the aged LPD females had reduced sensitivity to nitric oxide donors compared with their NPD counterparts, suggesting that vascular dysfunction may contribute to the increased risk of disease in aged females. In conclusion, females growth-restricted in early life were no longer protected from an age-related decline in renal and arterial function, and this was associated with increased arterial pressure without evidence of renal structural damage.

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Section: Enhanced Age-related Increase In Arterial Pressure In Growthmentioning

confidence: 63%

Accelerated age-related decline in renal and vascular function in female rats following early-life growth restriction

Black

Lim

Zimanyi

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Conversely, programmed hypertension has been demonstrated in the absence of changes in birth weight or decreased nephron number in a number of animal models, including maternal overfeeding, maternal hypertension, and maternal water restriction (16,25,70,72), demonstrating that hypertension can also be programmed independently of a reduction in nephron number. Previously, we suggested potential mechanisms whereby this may occur, including alteration in the renin-angiotensin system, renal sympathetic innervation, and tubular transport mechanisms in the kidney (26).…”

Section: Mechanisms Leading To Formation Of a Low Nephron Endowmentmentioning

confidence: 99%

“…This is an area requiring further research. and hypertension may be simply coincident, and it is possible that compensatory changes in tubular function and/or renal hormonal systems must occur concomitantly for hypertension to develop (26). Furthermore, a reduced nephron number has been documented in the absence of hypertension (29,51,112) with or without changes in birth weight.…”

Section: Mechanisms Leading To Formation Of a Low Nephron Endowmentmentioning

confidence: 99%

Developmental programming of a reduced nephron endowment: more than just a baby's birth weight

Moritz¹,

Singh²,

Probyn³

et al. 2009

American Journal of Physiology-Renal Physiology

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“…The idea that a reduction in nephron number leads to the development of hypertension is well established [7]. However, programmed nephron deficit has also been described in the absence of hypertension [8], which has led to the suggestion that concomitant changes in renal function must occur in order for hypertension to develop [9]. A major candidate is the intrarenal renin-angiotensin system, which displays altered activity in several models of developmental programming [10,11].…”

Section: Introductionmentioning

confidence: 99%

Segmental sodium reabsorption by the renal tubule in prenatally programmed hypertension in the rat

Alwasel

Ashton

2011

Pediatr Nephrol

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Hypertension and renal dysfunction can be programmed in the rat by prenatal exposure to a low-protein (LP) diet. Expression of the renal thick ascending limb (TAL) sodium transporter NKCC2 is up-regulated, which has been predicted to result in greater sodium reabsorption. However, we have shown that LP rats excrete more not less sodium. The aim of this study was to determine whether the increased abundance of sodium:potassium:chloride (Na(+):K(+):2Cl(-)) co-transporter (NKCC2) leads to enhanced sodium uptake by the TAL. Pregnant Wistar rats were fed a control (18%) or LP (9%) diet. Amiloride (AM), bendroflumethiazide (BF), and furosemide (FUR) were administered acutely to male offspring at 4 weeks of age. Fractional excretion of sodium (FE(Na)) was significantly greater in vehicle-infused LP rats (3.0 ± 0.3%) compared with controls (1.7 ± 0.5, P < 0.01). FE(Na) by the LP proximal tubule did not differ from controls, whereas FE(Na) by the distal tubule was significantly greater (P < 0.01). These differences were abolished by the administration of AM + BF (equivalent to the outflow from the TAL) and AM + BF + FUR (equivalent to the outflow from the proximal tubule), suggesting that the increase in NKCC2 expression was not functional. However, during acute salt loading, the LP rat pressure natriuresis curve was shifted rightward, implying that raised systemic blood pressure is required to match urinary sodium excretion with dietary intake. These data suggest that renal sodium handling is impaired in the LP rat but that this is not due to increased NKCC2 expression.

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Programming Hypertension—Animal Models

Cited by 10 publications

References 132 publications

Accelerated age-related decline in renal and vascular function in female rats following early-life growth restriction

Accelerated age-related decline in renal and vascular function in female rats following early-life growth restriction

Developmental programming of a reduced nephron endowment: more than just a baby's birth weight

Segmental sodium reabsorption by the renal tubule in prenatally programmed hypertension in the rat

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