Renal physiology of the mouse

Meneton, Pierre; Ichikawa, Iekuni; Inagami, Tadashi; Schnermann, Jürgen

doi:10.1152/ajprenal.2000.278.3.f339

Cited by 116 publications

(101 citation statements)

References 56 publications

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“…13 However, we found that although anesthesia did increase PRC slightly, it was generally less than double, similar to the rat. 21 Previous reports of large increases may be because of the concurrent use of ketamine, 22 which we found induced transient hypotension and stimulated renin (unpublished observations, Beierwaltes, 1999).…”

Section: Discussionsupporting

confidence: 54%

“…In addition to the presence of a second renin gene, the renin angiotensin system in the mouse may be different from other species because of reported high levels of renin, low levels of substrate, 13 as well as considerable variations between strains. 13 The complexity posed by the presence or absence of a second renin gene is a critical element in designing any physiological study involving mice.…”

mentioning

confidence: 99%

“…13 The complexity posed by the presence or absence of a second renin gene is a critical element in designing any physiological study involving mice. We have compared wild-type mice with one or two renin genes using two common normal (nonmutant) strains: C-57BL/6J (C-57), which carries only Ren-1 c , and 129/SvJ (Sv-129), which has both Ren-1 d and Ren-2.…”

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confidence: 99%

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Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

et al. 2004

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Abstract-We compared the phenotype of two common mouse models, C-57BL/6J (C57), which carries only the Ren-1 c gene, and 129/SvJ (Sv-129), with both Ren 1 d and Ren-2. We hypothesized two renin gene Sv-129 would have increased blood pressure and the renin-angiotensin system would be more influential in regulating renal function compared with one renin gene mice. Sv-129 consistently had higher blood pressure than C-57, whether conscious (128 versus 108 mm Hg, PϽ0.001) or anesthetized (102 versus 88 mm Hg, PϽ0.001). Plasma renin concentration in both conscious and anesthetized C-57 mice was 3-to 4-fold higher than in Sv-129 (PϽ0.05), whereas renal cortical renin content was 2.5-fold higher (PϽ0.005). Renal blood flow and renal vascular resistance were the same in C-57 and Sv-129. Exogenous angiotensinogen produced identical pressor and renal vasoconstrictor responses in both strains. Blocking AT 1 receptors with losartan reduced blood pressure by 19 mm Hg in both strains. Nitric oxide synthase inhibition by L-NAME increased blood pressure by 29 mm Hg in C-57 and 35 mm Hg in Sv-129 mice, but the decrease in renal blood flow was 30% less in C-57 (PϽ0.025). We conclude that Sv-129 mice with two renin genes have higher blood pressure but lower plasma and renal renin than C-57 mice with one renin gene. Renin substrate may limit angiotensin II production in the mouse. In Sv-129, the influence of nitric oxide on renal but not systemic resistance may be exaggerated. Renin from Ren-2 may act independently of normal renin control mechanisms. Key Words: angiotensin Ⅲ angiotensinogen Ⅲ endothelium Ⅲ mouse Ⅲ nitric oxide Ⅲ nitric oxide synthase Ⅲ renin T he potent vasoconstrictor hormone angiotensin II (AngII) is the active product of the renin-angiotensin system. AngII is typically produced through the rate-limiting cleavage of the substrate angiotensinogen by the enzyme renin.

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Section: Discussionsupporting

confidence: 54%

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confidence: 99%

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Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

et al. 2004

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“…Specifically, the disappearance of ERβ immunoreactivity in the rat SON with dehydration and the increase in ERβ mRNA with hyponatremia suggests that the reported absence of ERβ expression in SON neurons of the mouse and guinea pig might reflect differences between these species and rats in the balance between positive and negative factors regulating ERβ under basal conditions. The higher basal plasma osmolality in mice (303−355 mOsm/kg) versus rats (280−295 mOsm/kg) [40] is consistent with this possibility. Additional ERβ regulatory candidates that might differ between species include gonadal and adrenal steroid hormones as well as the neurotransmitters carrying information about osmolality (glutamate, GABA, angiotensin) and blood volume (norepinephrine, ATP, neuropeptide Y, others?).…”

Section: Conclusion and Future Researchsupporting

confidence: 55%

Estrogen receptors: Their roles in regulation of vasopressin release for maintenance of fluid and electrolyte homeostasis

Sladek

Somponpun

2008

Frontiers in Neuroendocrinology

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Long standing interest in the impact of gonadal steroid hormones on fluid and electrolyte balance has led to a body of literature filled with conflicting reports about gender differences, the effects of gonadectomy, hormone replacement, and reproductive cycles on plasma vasopressin (VP), VP secretion, and VP gene expression. This reflects the complexity of gonadal steroid hormone actions in the body resulting from multiple sites of action that impact fluid and electrolyte balance (e.g. VP target organs, afferent pathways regulating the VP neurons, and the VP secreting neurons themselves). It also reflects involvement of multiple types of estrogen receptors (ER) in these diverse sites including ERs that act as transcription factors regulating gene expression (i.e. the classic ERα as well as the more recently discovered ERβ) and potentially G-protein coupled, membrane localized ERs that mediate rapid non-genomic actions of estrogen. Furthermore, altered expression of these receptors in physiologically diverse conditions of fluid and electrolyte balance contributes to the difficulty of using simplistic approaches such as gender comparisons, gonadectomy, and hormone replacement to assess the role of gonadal steroids in regulation of VP secretion for maintenance of fluid and electrolyte homeostasis. This review catalogs these inconsistencies and provides a frame work for understanding them by describing: 1) the effect of gonadal steroids on target organ responsiveness to VP; 2) the expression of multiple types of estrogen receptors in the VP neurons and in brain regions monitoring feedback signals from the periphery; and 3) the impact of dehydration and hyponatremia on expression of these receptors.

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“…As reviewed recently [33], the tail-cuff approach to determine arterial blood pressure requires certain precautions to reduce the stress of the animals, including appropriate training of the mice over multiple days and adequate prewarming to dilate the tail artery. The animals were placed in a heated chamber at an ambient temperature of 30°C for 15 min.…”

Section: Determination Of Plasma Volumementioning

confidence: 99%

Lack of the serum and glucocorticoid-inducible kinase SGK1 attenuates the volume retention after treatment with the PPARγ agonist pioglitazone

Artunc

Sandulache

Nasir

et al. 2008

Pflugers Arch - Eur J Physiol

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PPARγ-agonists enhance insulin sensitivity and improve glucose utilization in diabetic patients. Adverse effects of PPARγ-agonists include volume retention and edema formation. Recent observations pointed to the ability of PPARγ agonists to enhance transcription of the serum and glucocorticoid-inducible kinase SGK1, a kinase that is genomically upregulated by mineralocorticoids and stimulates various renal channels and transporters including the renal epithelial Na + channel ENaC. SGK1 has been proposed to mediate the volume retention after treatment with PPARγ agonists. To test this hypothesis, food containing the PPARγ agonist pioglitazone (0.02%, i.e., approximately 25 mg/kg bw/day) was administered to gene-targeted mice lacking SGK1 (sgk1 −/− , n=12) and their wild-type littermates (sgk1 +/+ , n=12). According to in situ hybridization, quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) and immunofluorescence, treatment with pioglitazone significantly increased renal SGK1 mRNA and protein expression in sgk1 +/+ mice. The treatment increased body weight significantly in both, sgk1 +/+ mice (+2.2±0.3 g) and sgk −/− mice (+1.3±0.2 g), and decreased hematocrit significantly in sgk1 +/+ mice (−6.5±1.0%) and sgk1 −/− mice (−3.1±0.6%). Both effects were significantly (p<0.05) more pronounced in sgk1 +/+ mice. According to Evans Blue

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Renal physiology of the mouse

Cited by 116 publications

References 56 publications

Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

Cardiovascular and Renal Phenotype in Mice With One or Two Renin Genes

Estrogen receptors: Their roles in regulation of vasopressin release for maintenance of fluid and electrolyte homeostasis

Lack of the serum and glucocorticoid-inducible kinase SGK1 attenuates the volume retention after treatment with the PPARγ agonist pioglitazone

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