Effects of enalapril and sodium depletion on the renin-angiotensin system in hydronephrotic mice

Zhang, Yanling ZhangY.; Wu, Junyan; Wang, Xuechun WangX.; Morgan, Trefor

doi:10.1139/y09-037

Cited by 5 publications

(15 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…At 4 weeks after the operation, the left kidney was hydronephrotic. 20,21 At this time the following studies were performed. The control group (n¼10) were fed regular mouse diet.…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

“…Briefly, a blood sample (20 ml) was taken from the left and right renal veins and from the abdominal aorta. [20][21][22] Plasma was separated from each blood sample by microcentrifuge. After blood sampling, the mouse was immediately killed.…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

“…22 Measurement of plasma renin concentration (PRC) and tissue renin concentration (TRC) PRC was measured in the blood from the aorta and renal veins using a radioimmunoassay described previously. [20][21][22] The renin value was expressed in Goldblatt units (1 GU¼0.42 mg of angiotensin I formation) per milliliter of plasma. The ½ kidneys removed from each mouse were weighed and homogenized in 1 ml buffer.…”

Section: Measurement Of Blood Pressure (Bp)mentioning

confidence: 99%

“…The dot-blot hybridization for measuring renin mRNA in the total RNA sample was carried out as described previously. [20][21][22] To analyze the value of renin mRNA between kidneys, the results from the renin signal were expressed relative to a value of 100 U in the control kidney. The mRNA was then referred back to the tissue weight of the sample, as described previously.…”

Section: Measurement Of Renin Mrna In the Kidneymentioning

confidence: 99%

“…The mRNA was then referred back to the tissue weight of the sample, as described previously. [20][21][22] …”

Section: Measurement Of Renin Mrna In the Kidneymentioning

confidence: 99%

See 4 more Smart Citations

Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

Zhang

et al. 2010

Hypertens Res

Self Cite

View full text Add to dashboard Cite

We previously reported that sodium depletion increased renin secretion from the normal kidney in mice. We postulated that the combined procedures of sodium depletion and b-adrenoceptor blockade would affect the activity of the renin-angiotensin system. To test this hypothesis, we investigated the interaction of low sodium intake (LSI) and propranolol (PRO) on renin synthesis and secretion. To prevent the influence of tubule flow on renin secretion, mice with a left hydronephrotic kidney were used. LSI increased plasma renin concentration (PRC) 5.6-fold in the right renal vein (Po0.01). There was no net increase of PRC in the left renal vein. Tissue renin concentration (TRC) was elevated 3.6-fold and 1.3-fold in the right and left kidneys (Po0.01), respectively. After administration of PRO, PRC decreased by 34% in the right renal vein and 47% in the aorta (Po0.05); TRC was reduced by 37.5% in the right and 29.3% in the hydronephrotic kidneys (Po0.05). The combination of LSI and PRO increased PRC 3.4-fold and 1.8-fold in the right (Po0.01) and left renal veins (Po0.05), respectively. TRC increased 3.4-fold in the right (Po0.01) but only 61% in the left kidneys (Po0.05). The pattern in change of renin mRNA levels was similar to TRC but the absolute amount was smaller. There were correlations between PRC and renin mRNA, and between TRC and renin mRNA in both kidneys (Po0.001). Thus, LSI increased renin synthesis in both kidneys. However, there was no apparent renin secretion in the hydronephrotic kidney. PRO treatment suppressed renin synthesis and renin secretion, irrespective of hydronephrosis and LSI. The macula densa is critical for renin secretion under all of the circumstances studied.

show abstract

“…At 4 weeks after the operation, the left kidney was hydronephrotic. 20,21 At this time the following studies were performed. The control group (n¼10) were fed regular mouse diet.…”

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Section: Animals and Experimental Protocolmentioning

confidence: 99%

Section: Measurement Of Blood Pressure (Bp)mentioning

confidence: 99%

Section: Measurement Of Renin Mrna In the Kidneymentioning

confidence: 99%

“…The mRNA was then referred back to the tissue weight of the sample, as described previously. [20][21][22] …”

Section: Measurement Of Renin Mrna In the Kidneymentioning

confidence: 99%

See 3 more Smart Citations

Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

Zhang

et al. 2010

Hypertens Res

Self Cite

View full text Add to dashboard Cite

show abstract

Salt feedback on the renin-angiotensin-aldosterone system

Schweda

2014

Pflugers Arch - Eur J Physiol

View full text Add to dashboard Cite

The renin-angiotensin-aldosterone system (RAAS) is a central element in the control of the salt and water balance of the body and arterial blood pressure. The activity of the RAAS is controlled by the protease renin, which is released from renal juxtaglomerular epithelioid cells (JGE cells) into the circulation. Renin release is regulated by a complex interplay of several locally acting hormones or mechanisms and longer feedback loops one of which involves salt intake. Acute NaCl loads or longer lasting high salt intakes suppress plasma renin activity, whereas reductions in NaCl intake stimulate it. Because the activation of the RAAS conserves the salt content of the body, a classical feedback loop between salt intake/body salt content and renin is established. Despite of its important role for body fluid homeostasis, the precise signaling pathways connecting salt intake with the synthesis and release of renin are only incompletely understood. Four putative controllers of the salt-dependent regulation of the RAAS have been suggested: (1) the macula densa mechanism which adjusts renin release in response to changes in the renal tubular salt concentration; (2) salt-dependent changes in the arterial blood pressure; (3) circulating salt-dependent hormones, particularly the atrial natriuretic peptide (ANP); and (4) renal sympathetic nervous activity, which is regulated by extracellular volume and arterial blood pressure. In this review, the role of these known controllers of the RAAS will be discussed with special emphasis on their relative contributions to the salt-dependent regulation of the RAAS at different time frames.

show abstract

Angiotensin II regulates brain (pro)renin receptor expression through activation of cAMP response element-binding protein

Liu

Hammond

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

We reported that brain (pro)renin receptor (PRR) expression levels are elevated in DOCA-salt-induced hypertension; however, the underlying mechanism remained unknown. To address whether ANG II type 1 receptor (AT 1R) signaling is involved in this regulation, we implanted a DOCA pellet and supplied 0.9% saline as the drinking solution to C57BL/6J mice. Sham pellet-implanted mice that were provided regular drinking water served as controls. Concurrently, mice were intracerebroventricularly infused with the AT 1R blocker losartan, angiotensin-converting-enzyme inhibitor captopril, or artificial cerebrospinal fluid for 3 wk. Intracerebroventricular infusion of losartan or captopril attenuated DOCA-salt-induced PRR mRNA elevation in the paraventricular nucleus of the hypothalamus, suggesting a role for ANG II/AT 1R signaling in regulating PRR expression during DOCAsalt hypertension. To test which ANG II/AT 1R downstream transcription factors were involved in PRR regulation, we treated Neuro-2A cells with ANG II with or without CREB (cAMP response elementbinding protein) or AP-1 (activator protein-1) inhibitors, or CREB siRNA. CREB and AP-1 inhibitors, as well as CREB knockdown abolished ANG II-induced increases in PRR levels. ANG II also induced PRR upregulation in primary cultured neurons. Chromatin immunoprecipitation assays revealed that ANG II treatment increased CREB binding to the endogenous PRR promoter in both cultured neurons and hypothalamic tissues of DOCA-salt hypertensive mice. This increase in CREB activity was reversed by AT 1R blockade. Collectively, these findings indicate that ANG II acts via AT 1R to upregulate PRR expression both in cultured cells and in DOCA-salt hypertensive mice by increasing CREB binding to the PRR promoter.(pro)renin receptor; CAMP response element-binding protein; central nervous system; renin-angiotensin system; salt-sensitive hypertension THE BRAIN RENIN-ANGIOTENSIN system (RAS) plays an essential role in neurogenic hypertension (4, 21). The (pro)renin receptor (PRR) is a newly discovered component of the RAS that is highly expressed in the brain (16,26). Binding of renin to the PRR increases the catalytic activity of renin by approximately fourfold to fivefold. Prorenin also gains enzymatic activity by binding to the PRR (24). Binding of renin or prorenin to the PRR also directly initiates an intracellular signaling pathway independent of ANG II that increases the synthesis of profibrotic molecules, including plasminogen activator inhibitor-1, fibronectin, collagen, and transforming growth factor-␤ (10, 25, 26).We and others have reported that the PRR is upregulated in the central nervous system (CNS) in different hypertensive models, including spontaneously hypertensive rats (SHR) (27) and human renin-angiotensinogen (RA) double-transgenic hypertensive mice (16). Knocking down PRR in the brain through virus-mediated introduction of small hairpin (inhibitory) RNA against the PRR (PRR-shRNA) attenuates hypertension in both SHR and RA mice. We also recently reported that PR...

show abstract

Effects of enalapril and sodium depletion on the renin-angiotensin system in hydronephrotic mice

Cited by 5 publications

References 28 publications

Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

Effect of low sodium intake and β-blockade on renin synthesis and secretion in mice with unilateral ureteral ligation

Salt feedback on the renin-angiotensin-aldosterone system

Angiotensin II regulates brain (pro)renin receptor expression through activation of cAMP response element-binding protein

Contact Info

Product

Resources

About