The role of the tissue renin-angiotensin system in the response of the rat adrenal to exogenous angiotensin II

Vinson, G. P.; Teja, Ravi; Ho, MM; Hinson, J. P.; Puddefoot,

doi:10.1677/joe.0.1580153

Cited by 19 publications

(5 citation statements)

References 28 publications

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“…Studies using bisected whole adrenal gland showed that Cap inhibited the response of aldosterone to exogenous Ang II stimulation by preventing the conversion of aldosterone from its precursor. These data suggested that the adrenal could regulate Ang IIstimulated aldosterone synthesis and release through the local RAS, independently of the circulating RAS (47). Other studies further demonstrated the dissociation between the circulating RAS and the adrenal-specific RAS in regulating aldosterone production.…”

Section: Fig 7 Effect Of E 2 On Adrenal At 1 R Expression After Higmentioning

confidence: 83%

Estrogen Regulates Adrenal Angiotensin Type 1 Receptors by Modulating Adrenal Angiotensin Levels

Zheng

Sandberg

2003

Endocrinology

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Estrogen inhibits adrenal angiotensin type 1 receptor (AT(1)R) binding sites and attenuates the adrenal responsivity to angiotensin II (Ang II). Ang II modulates AT(1)R expression. Here, we determined if estrogen-induced down-regulation of adrenal AT(1)Rs involves modulation of adrenal Ang II. Female rats were ovariectomized (OVX) and injected with 17beta-estradiol benzoate (E(2); 40 micro g/kg) or vehicle for 7 d. Adrenal Ang II was separated from other angiotensin peptides by HPLC and measured by RIA. Scatchard analysis of radioligand binding curves showed that E(2) or captopril (Cap; 0.5 g/liter water) significantly reduced adrenal AT(1)R binding (maximum binding capacity) by 22% and 19%, respectively, compared with OVX (276 +/- 2.09 fmol/mg protein). E(2) and Cap lowered adrenal Ang II levels by 39% and 21%, respectively, compared with OVX (4.10 +/- 0.44 pmol/g). E(2) caused no further reductions in adrenal AT(1)R binding or in Ang II levels in Cap-treated OVX rats. High-dose Ang II infusion (1000 ng/kg.min) increased adrenal Ang II levels by 71% and lowered AT(1)R binding by 18%. Under these infusion conditions, E(2) did not reduce adrenal Ang II or AT(1)R binding. No differences in AT(1)R affinity (dissociation constant) were observed among groups. These data suggest that E(2) regulates the number of adrenal AT(1)R binding sites indirectly by modulating adrenal Ang II.

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Section: Fig 7 Effect Of E 2 On Adrenal At 1 R Expression After Higmentioning

confidence: 83%

Estrogen Regulates Adrenal Angiotensin Type 1 Receptors by Modulating Adrenal Angiotensin Levels

Zheng

Sandberg

2003

Endocrinology

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“…Many lines of in vitro evidence (obtained by the use of capsular zona glomerulosa strips, adrenal slices, or zona glomerulosa cell cultures) suggest that adrenal RAS controls aldosterone secretion. ACE inhibitors were found to lower either basal (20) or K ϩ -and ACTH-stimulated aldosterone output by rat zona glomerulosa (2,14,17,18,21) and basal aldosterone yield by cultured bovine (9) and human adrenal tissue (5), as well as by K ϩ -stimulated aldosterone release by human adrenocortical NCI-H295 cell line (8). A selective AT 1 receptor antagonist was reported to block both basal and agonist-stimulated aldosterone secretion from cultured bovine zona glomerulosa cells (7) and K ϩenhanced aldosterone production from the NCI-H295 cell line (8).…”

Section: Discussionmentioning

confidence: 98%

Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

Mazzocchi

Malendowicz²,

Markowska³

et al. 2000

American Journal of Physiology-Endocrinology and Metabolism

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This study examined the effect of the pharmacological manipulation of adrenal renin-angiotensin system (RAS) on aldosterone secretion from in situ perfused adrenals of rats kept on a normal diet and sodium restricted for 14 days. Neither the angiotensin-converting enzyme inhibitor captopril nor the nonselective angiotensin II receptor antagonist saralasin and the AT(1) receptor-selective antagonist losartan affected basal aldosterone output in normally fed rats. In contrast, they concentration dependently decreased aldosterone secretion in sodium-restricted animals, with maximal effective concentration ranging from 10(-7) to 10(-6) M. Captopril (10(-6) M), saralasin (10(-6) M), and losartan (10(-7) M) counteracted aldosterone response to 10 mM K(+) in sodium-restricted rats but not in normally fed animals. Collectively, these findings provide evidence that adrenal RAS plays a role in the regulation of aldosterone secretion, but only under conditions of prolonged stimulation of zona glomerulosa probably leading to overexpression of adrenal RAS.

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“…This local production of the bioactive peptides is not necessarily dependent on the local expression of all components of the local tissue RAS, since it is also possible to take up components from the circulation, such as renin. Furthermore, besides presence of Angiotensin II and Angiotensin (1–7), expression of AT1R, AT2R, and Mas-receptor human reproductive tissue is needed in order to mediate the local impact of the RAS for physiological and pathological processes, including follicle maturation, fine-tuning of the regulation of reproduction, angiogenesis as well as tumor cell proliferation (15–18). An influencing effect on cancer has been described for different tumor types already during the last two decades (19, 20).…”

Section: Introductionmentioning

confidence: 99%

Local Renin-Angiotensin System in the Reproductive System

Herr

Bekes²,

Wulff³

2013

Front. Endocrinol.

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The renin-angiotensin system (RAS) is well known as regulator of electrolytes and blood pressure. Besides this function, there are numerous studies supporting the idea of a local tissue RAS. This system controls the local activity of the different RAS family members, especially of the functional proteins Angiotensin II and Angiotensin (1–7). Those antagonistically acting proteins have been described to be expressed in different organ systems including the human reproductive tract. Therefore, this local RAS has been suspected to be involved in the control and regulation of physiological and pathological conditions in the female reproduction tract. This review of the available literature summarizes the physiological influence of the RAS on the follicular development, ovarian angiogenesis, and placental- and uterine function. In addition, in the second part the role of the RAS concerning ovarian- and endometrial cancer becomes elucidated. This section includes possible novel therapeutic strategies via inhibition of RAS-mediated tumor growth and angiogenesis. Looking at a very complex system of agonistic and antagonistic tissue factors, it may be supposed that the RAS in the female reproduction tract will be of rising scientific interest in the upcoming years.

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The role of the tissue renin-angiotensin system in the response of the rat adrenal to exogenous angiotensin II

Cited by 19 publications

References 28 publications

Estrogen Regulates Adrenal Angiotensin Type 1 Receptors by Modulating Adrenal Angiotensin Levels

Estrogen Regulates Adrenal Angiotensin Type 1 Receptors by Modulating Adrenal Angiotensin Levels

Role of adrenal renin-angiotensin system in the control of aldosterone secretion in sodium-restricted rats

Local Renin-Angiotensin System in the Reproductive System

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