Gene expression of central and peripheral renin-angiotensin system components upon dietary sodium intake in rats

Jo, Hak-Ryul; Yang, Eun-Kyoung; Lee, Won-Jung; Park, Keun-Yong; Kim, Hyeong-Jin; Park, Jaesik

doi:10.1016/s0167-0115(96)00119-x

Cited by 34 publications

(25 citation statements)

References 19 publications

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“…This contributes to NaCl and BP homeostasis. 36,37 Apparently, there is a counter-regulation in this model of CKD in which salt loading paradoxically enhances the intrarenal epithelial RAS, despite maintenance of a suppressed circulating RAS. This extends similar findings in rat models of salt-sensitive hypertension, 26,38 nephritis, 39 and reduced renal mass.…”

Section: Discussionmentioning

confidence: 91%

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A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Cao

Wang

et al. 2015

Journal of the American Society of Nephrology

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Salt intake promotes progression of CKD by uncertain mechanisms. We hypothesized that a salt-induced reno-cerebral reflex activates a renin-angiotensin axis to promote CKD. Sham-operated and 5/6-nephrectomized rats received a normal-salt (0.4%), low-salt (0.02%), or high-salt (4%) diet for 2 weeks. High salt in 5/6-nephrectomized rats increased renal NADPH oxidase, inflammation, BP, and albuminuria. Furthermore, high salt activated the intrarenal and cerebral, but not the systemic, renin-angiotensin axes and increased the activity of renal sympathetic nerves and neurons in the forebrain of these rats. Renal fibrosis was increased 2.2-fold by high versus low salt, but intracerebroventricular tempol, losartan, or clonidine reduced this fibrosis by 65%, 69%, or 59%, respectively, and renal denervation or deafferentation reduced this fibrosis by 43% or 38%, respectively (all P,0.05). Salt-induced fibrosis persisted after normalization of BP with hydralazine. These data suggest that the renal and cerebral renin-angiotensin axes are interlinked by a reno-cerebral reflex that is activated by salt and promotes oxidative stress, fibrosis, and progression of CKD independent of BP.

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Section: Discussionmentioning

confidence: 91%

“…36 All histologic analyses were performed by two pathologists who were blinded to the treatment of the animals. …”

Section: Evaluation Of Cerebral Neuronal Activationmentioning

confidence: 99%

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Cao

Wang

et al. 2015

Journal of the American Society of Nephrology

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“…To our knowledge, the few studies available concerning salt supplementation on both mRNA and protein expression of AT 1 R and AT 2 R are somewhat inconsistent. While lower AT 1 R protein expression (Nora et al 2000) and reduced number of AT 1 R binding sites (Douglas & Catt 1976) following high-salt intake have been described, other studies meanwhile have shown unaltered AT 1 R mRNA expression (Jo et al 1996, Schmid et al 1997. Only one study has reported an absence of effect of salt supplementation on AT 2 R protein expression in the rat adrenal gland (Nora et al 2000).…”

Section: Adrenal Changes Induced By Nacl Supplementationmentioning

confidence: 99%

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Bibeau¹,

Otis²,

St‐Louis³

et al. 2011

Journal of Endocrinology

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In low sodium-induced intrauterine growth restricted (IUGR) rat, foetal adrenal steroidogenesis as well as the adult reninangiotensin-aldosterone system (RAAS) is altered. The aim of the present study was to determine the expression of cytochrome P450 aldosterone synthase (P450aldo) and of angiotensin II receptor subtypes 1 (AT 1 R) and 2 (AT 2 R) in adult adrenal glands and whether this expression could be influenced by IUGR and by high-salt intake in a sex-specific manner. After 6 weeks of 0 . 9% NaCl supplementation, plasma renin activity, P450aldo expression and serum aldosterone levels were decreased in all groups. In males, IUGR induced an increase in AT 1 R, AT 2 R, and P450aldo levels, without changes in morphological appearance of the zona glomerulosa (ZG). By contrast, in females, IUGR had no effect on the expression of AT 1 R, but increased AT 2 R mRNA while decreasing protein expression of AT 2 R and P450aldo. In males, salt intake in IUGR rats reduced both AT 1 R mRNA and protein, while for AT 2 R, mRNA levels decreased whereas protein expression increased. In females, salt intake reduced ZG size in IUGR but had no affect on AT 1 R or AT 2 R expression in either group. These results indicate that, in response to IUGR and subsequently to salt intake, P450aldo, AT 1 R, and AT 2 R levels are differentially expressed in males and females. However, despite these adrenal changes, adult IUGR rats display adequate physiological and adrenal responses to high-salt intake, via RAAS inhibition, thus suggesting that extra-adrenal factors likely compensate for ZG alterations induced by IUGR.

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“…Elevated brain AngII binding sites have also been reported in spontaneously hypertensive fetal and newborn rats (47,48), and blockade of central RAS in adult spontaneously hypertensive rat can reverse their chronic hypertension (49). The underlying mechanisms and regulatory processes that lead to increased AT 1 receptor brain expression in 9% offspring are unknown but may involve a defect in nitric oxide pathway (27,50,51), positive feedback regulation by elevated brain AngII (52,53), and glucocorticoids (12,54,55).…”

Section: Table 2 Spectral Measurements Of Arterial Bpv In 9-to 12-wkmentioning

confidence: 99%

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

et al. 2004

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Intrauterine programming of hypertension is associated with evidence of increased renin-angiotensin system (RAS) activity. The current study was undertaken to investigate whether arterial baroreflex and blood pressure variability are altered in a model of in utero programming of hypertension secondary to isocaloric protein deprivation and whether activation of the RAS plays a role in this alteration. Pregnant Wistar rats were fed a normalprotein (18%) or low-protein (9%) diet during gestation, which had no effect on litter size, birth weight, or pup survival. Mean arterial blood pressure (MABP; 126 Ϯ 3 mm Hg 9% versus 108 Ϯ 4 mm Hg 18%; p Ͻ 0.05) and blood pressure variability were significantly greater in the adult offspring of the 9% protein-fed mothers. Arterial baroreflex control of heart rate, generated by graded i.v. infusion of phenylephrine and nitroprusside, was significantly shifted toward higher pressure; i.v. angiotensinconverting enzyme inhibitor normalized MABP and shifted the arterial baroreflex curve of the 9% offspring toward lower pressure without affecting the 18% offspring. For examining whether brain RAS is also involved in programming of hypertension, angiotensin-converting enzyme inhibitor and losartan (specific AT 1 receptor antagonist) were administered intracerebroventricularly; both significantly reduced MABP of the 9% but not the 18% offspring. Autoradiographic receptor binding studies demonstrated an increase in brain AT 1 expression in the subfornical organ and the vascular organ of the lamina terminalis in the 9% offspring. These data demonstrate a major tonic role of brain and peripheral RAS on hypertension associated with antenatal nutrient deprivation. Abbreviations ACE-I, angiotensin-converting enzyme inhibitor AngII, angiotensin II AP, area postrema BPV, blood pressure variability HR, heart rate ICV, intracerebroventricular MABP, mean arterial blood pressure MEPO, median preoptic nucleus NTS, nucleus of the solitary tract OVLT, vascular organ of the lamina terminalis PVH, paraventricular nucleus of the hypothalamus RAS, renin-angiotensin system SFO, subfornical organ Chronic cardiovascular diseases of adults can have their origins in fetal life. Epidemiologic studies reveal that hypertension, stroke, and coronary heart disease are inversely related to birth weight (1) and that this relationship is independent of genetic factors (2) and lifestyle (3). It has been suggested that a poor nutrient supply at a critical period of early development leads to permanent alterations in the programming of the developing cardiovascular structures or functions (4). This concept has been supported by animal studies demonstrating an association between nutritional deficit during fetal life and increased blood pressure in adulthood (5, 6).Experimental evidence suggests that activation of the reninangiotensin system (RAS) (7,8) is an important element of hypertension programmed during fetal life. Infants who are born with intrauterine growth restriction have increased plasma renin activity and r...

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Gene expression of central and peripheral renin-angiotensin system components upon dietary sodium intake in rats

Cited by 34 publications

References 19 publications

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Differential responses to salt supplementation in adult male and female rat adrenal glands following intrauterine growth restriction

Role of Brain and Peripheral Angiotensin II in Hypertension and Altered Arterial Baroreflex Programmed during Fetal Life in Rat

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