Study of the rat adrenal renin-angiotensin system at a cellular level.

Chiou, Cho-Yen; Williams, G. H.; Kifor, Imre

doi:10.1172/jci118172

Cited by 15 publications

(9 citation statements)

References 22 publications

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“…Chinese hamster ovary (CHO) cells expressing mouse renin and human angiotensinogen served as positive and negative controls. Immunoblotting was performed as described 13,14 by use of anti-mouse renin antibody, biotinylated anti-mouse IgG (DAKO Corp), and streptavidinalkaline phosphatase (DAKO) at 1:500 dilutions. Alkaline phosphatase was detected by using the chromogen NBT/BCIP (Sigma).…”

Section: Cell Immunoblottingmentioning

confidence: 99%

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Elements of a Paracrine Tubular Renin-Angiotensin System Along the Entire Nephron

et al. 1999

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Abstract-The renin-angiotensin system is a major regulator of body sodium, predominantly through the actions of intrarenal angiotensin II of unclear origin. We show that polarized epithelium of the proximal tubule synthesizes and secretes angiotensinogen at its apical side and that the protein can be detected in urine as a function of dietary sodium. Furthermore, we demonstrate that renin is expressed and secreted in a restricted nephron segment, the connecting tubule, also in a sodium-dependent fashion. A paracrine renin-angiotensin system operating along the entire nephron may contribute to long-term arterial pressure regulation by integrating distant tubular sodium-reabsorbing functions.(Hypertension. 1999;34:1265-1274.)

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Section: Cell Immunoblottingmentioning

confidence: 99%

“…13,14 Cells isolated from microdissected arcades of CNT secreted renin ( Figure 5A). CHO cells express- ing mouse renin ( Figure 5B) and human angiotensinogen ( Figure 5C) served as positive and negative controls, respectively.…”

Section: Cnt Cells Secrete Reninmentioning

confidence: 99%

Elements of a Paracrine Tubular Renin-Angiotensin System Along the Entire Nephron

et al. 1999

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“…A shift has occurred in recent years from an emphasis on the function of the circulating renin-angiotensin system (RAS) to a focus on the local tissue RAS in the brain, heart, peripheral blood vessels, adrenal glands, and kidney (39). Sodium restriction has been found to increase adrenal renin activity and Aldo production in parallel (8) and to increase angiotensin II (ANG II) secretion from the zona glomerulosa cells (5). Nephrectomy has been shown to increase adrenal renin activity via increased serum potassium but to decrease plasma renin to undetectable levels (8,9).…”

mentioning

confidence: 99%

“…Nephrectomy has been shown to increase adrenal renin activity via increased serum potassium but to decrease plasma renin to undetectable levels (8,9). Although some studies have shown that adrenal ANG II may be important in Aldo production through a paracrine or autocrine effect (5,24), the function of the adrenal RAS in regulating adrenal function still awaits further study.…”

mentioning

confidence: 99%

Guanylyl cyclase/natriuretic peptide receptor-A gene disruption causes increased adrenal angiotensin II and aldosterone levels

Zhao

Vellaichamy²,

Somanna³

et al. 2007

American Journal of Physiology-Renal Physiology

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Disruption of the guanylyl cyclase-A/natriuretic peptide receptor-A (GC-A/NPRA) gene leads to elevated arterial blood pressure and congestive heart failure in mice lacking NPRA. This study was aimed at determining whether Npr1 (coding for GC-A/NPRA) gene copy number affects adrenal ANG II and aldosterone (Aldo) levels in a gene-dose-dependent manner in Npr1 gene-targeted mice. Adrenal ANG II and Aldo levels increased in 1-copy mice compared with 2-copy mice, but decreased in 3-copy and 4-copy mice. In contrast, renal ANG II levels decreased in 1-copy (25%), 3-copy (38%), and 4-copy (39%) mice compared with 2-copy mice. The low-salt diet stimulated adrenal ANG II and Aldo levels in 1-copy (20 and 2,441%), 2-copy (15 and 2,339%), 3-copy (20 and 424%), and 4-copy (31 and 486%) mice, respectively. The high-salt diet suppressed adrenal ANG II and Aldo levels in 1-copy (46 and 29%) and 2-copy (38 and 17%) mice. On the other hand, the low-salt diet stimulated renal ANG II levels in 1-copy (45%), 2-copy (45%), 3-copy (59%), and 4-copy (48%) mice. However, the high-salt diet suppressed renal ANG II levels in 1-copy (28%) and 2-copy (27%) mice. In conclusion, NPRA signaling antagonizes adrenal ANG II and Aldo levels in a gene-dose dependent manner. Increased adrenal ANG II and Aldo levels may play an important role in elevated arterial blood pressure and progressive hypertension, leading to renal and vascular injury in Npr1 gene-disrupted mice.

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“…ANG II increases aldosterone release within minutes from adrenal cells in vitro. Under sodium depletion, the same amount of ANG II elicits a greater increase of aldosterone production than under sodium load (6). The reasons for this long-term modulation of adrenal sensitivity to rapid stimulation are complex.…”

Section: Discussionmentioning

confidence: 99%

StAR expression and the long-term aldosterone response to high-potassium diet in Wistar-Kyoto and spontaneously hypertensive rats

Peters¹,

Teubner²,

Clausmeyer³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Study of the rat adrenal renin-angiotensin system at a cellular level.

Cited by 15 publications

References 22 publications

Elements of a Paracrine Tubular Renin-Angiotensin System Along the Entire Nephron

Elements of a Paracrine Tubular Renin-Angiotensin System Along the Entire Nephron

Guanylyl cyclase/natriuretic peptide receptor-A gene disruption causes increased adrenal angiotensin II and aldosterone levels

StAR expression and the long-term aldosterone response to high-potassium diet in Wistar-Kyoto and spontaneously hypertensive rats

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