Regulation of ACE gene expression and plasma levels during rat postnatal development

Costerousse, Olivier; Allegrini, J; Huang, Hongzhang; Bounhik, J.; Alhenc-Gélas, François

doi:10.1152/ajpendo.1994.267.5.e745

Cited by 39 publications

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“…In neonatal rats, plasma, pulmonary and duodenal ACE concentrations, and pulmonary ACE mRNA abundance, are reduced by maternal administration of anti-thyroid drugs over the perinatal period (Jimenez et al 1990, Costerousse et al 1994. In addition, the ontogenic increments in plasma and pulmonary ACE observed immediately after birth are suppressed by hypothyroidism induced by drug treatment (Jimenez et al 1990, Costerousse et al 1994. Administration of T 3 to adult rats has been shown to increase renal and plasma ACE levels but, in contrast, it causes a reduction in ACE concentration in the lungs (Michel et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Effects of thyroid hormones on pulmonary and renal angiotensin-converting enzyme concentrations in fetal sheep near term

Forhead¹,

Fowden²

2002

Journal of Endocrinology

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In the sheep fetus, pulmonary and renal concentrations of angiotensin-converting enzyme (ACE) increase towards term in parallel with the prepartum surges in plasma cortisol and tri-iodothyronine (T 3 ). The ontogenic change in pulmonary ACE has been shown to be induced, at least in part, by cortisol but the role of the thyroid hormones is unknown. Therefore, this study investigated the effects of thyroid hormones on tissue ACE concentration in fetal sheep during late gestation. Pulmonary and renal ACE concentrations were measured in sheep fetuses after experimental manipulation of thyroid hormone status by fetal thyroidectomy and exogenous hormone infusion. In intact fetuses, pulmonary and renal ACE concentrations increased between 127-132 and 142-145 days of gestation (term 145 2 days), coincident with the prepartum rises in plasma cortisol and T 3 . The ontogenic increment in pulmonary ACE concentration was abolished when the prepartum surge in T 3 , but not cortisol, was prevented by fetal thyroidectomy. At 143-145 days, ACE concentration in the lungs and kidneys of the thyroidectomised fetuses were both lower than those in the intact fetuses. In intact fetuses at 127-132 days, pulmonary ACE was upregulated by intravenous infusions of either cortisol (2-3 mg/kg per day) or T 3 (8-12 µg/kg per day) for 5 days. Renal ACE was unaffected by cortisol or T 3 infusion. Therefore, thyroid hormones have an important role in the developmental control of pulmonary and renal ACE concentration in the sheep fetus towards term. In addition, the prepartum rise in plasma T 3 appears to mediate, in part, the maturational effect of cortisol on pulmonary ACE concentration.

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Section: Discussionmentioning

confidence: 99%

Effects of thyroid hormones on pulmonary and renal angiotensin-converting enzyme concentrations in fetal sheep near term

Forhead¹,

Fowden²

2002

Journal of Endocrinology

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“…33 Forty micrograms of total lung RNA was used for Northern blotting. 34 RNA blots were probed with TR31 rat ACE cDNA 35 labeled with ␣-32 P-dCTP. Prehybridization, hybridization, and washing were performed in standard conditions.…”

Section: Analysis Of Lung Ace Mrna By Northern Blotmentioning

confidence: 99%

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Challah

Villard

Philippe

et al. 1998

ATVB

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Abstract-Two normotensive strains of rat, the Lou and Brown Norway (BN) strains, have contrasting levels of plasma angiotensin-converting enzyme (ACE). To investigate the degree of genetic determination of ACE expression, a polymorphic marker of the ACE gene was analyzed in inbred rats of the two strains. The two inbred strains were shown to bear different alleles for a polymorphic marker at the ACE gene. The segregation of the alleles of this marker and the plasma ACE levels were studied in a group of F2 rats issued from a cross between Lou and BN rats. The degree of genetic determination of plasma ACE activity was estimated to be 94% in the F2 cohort. The ACE locus accounts for 74% of total plasma ACE variance. ACE activity and mRNA expression in lungs were also genetically determined. The difference observed in ACE mRNA accumulation in the lungs between the two strains was due to a difference in the transcriptional rate of the ACE gene, as shown in nuclear run-on experiments. No differences were observed in arterial blood pressure of homozygous F2 progeny. In these animals, ACE genotype did not interfere with the pressor or the depressor responses to ACE-dependent vasoactive peptides. There was a significant effect of strain on constitutive or inducible membrane or soluble ACE activity in primary cultures of vascular cells. Neointima formation in the carotid artery 14 days after balloon injury was also influenced by the genotype in F2 homozygous progeny, whereas the medial area was not. These results demonstrate that there is a close relationship between the genetically determined ACE expression and the inducibility of the ACE gene. The degree of genetic determination of ACE expression in inbred rat strains offers a unique opportunity to study the interaction between genetic and environmental determinants of ACE expression and its involvement in response to experimental cardiovascular and renal injury. (Arterioscler Thromb Vasc Biol. 1998;18:235-243.)

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“…However, controversies still exist regarding the physiological mechanism responsible for sodium appetite, since genetic expression, synthesis and release of the components of the renin-angiotensin-aldosterone system are reduced in hypothyroidism (3,(5)(6)(7)(8)(9). Moreover, angiotensin II receptor density is altered in hypothyroidism.…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

Ventura

Olivares

Passos

et al. 2001

Braz J Med Biol Res

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Rats rendered hypothyroid by treatment with methimazole develop an exaggerated sodium appetite. We investigated here the capacity of hypothyroid rats (N = 12 for each group) to respond to a low dose of captopril added to the ration, a paradigm which induces an increase in angiotensin II synthesis in cerebral areas that regulate sodium appetite by increasing the availability of circulating angiotensin I. In addition, we determined the influence of aldosterone in hypothyroid rats during the expression of spontaneous sodium appetite and after captopril treatment. Captopril significantly increased (P<0.05) the daily intake of 1.8% NaCl (in ml/100 g body weight) in hypothyroid rats after 36 days of methimazole administration (day 36: 9.2 ± 0.7 vs day 32: 2.8 ± 0.6 ml, on the 4th day after captopril treatment). After the discontinuation of captopril treatment, daily 1.8% NaCl intake reached values ranging from 10.0 ± 0.9 to 13.9 ± 1.0 ml, 48 to 60 days after treatment with methimazole. Aldosterone treatment significantly reduced (P<0.05) saline intake before (7.3 ± 1.6 vs day 0, 14.4 ± 1.3 ml) and after captopril treatment. Our results demonstrate that, although hypothyroid rats develop a deficiency in the production of all components of the renin-angiotensin-aldosterone system, their capacity to synthesize angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8% NaCl intake during aldosterone treatment suggests that sodium retention reduces both spontaneous and captopril-induced salt appetite. Key wordsPrevious studies have shown a reduction in NaCl aversion in hypothyroid rats with urinary sodium loss and an increase in sodium appetite in different experimental models (1-4). However, controversies still exist regarding the physiological mechanism responsible for sodium appetite, since genetic expression, synthesis and release of the components of the renin-angiotensin-aldosterone system are reduced in hypothyroidism (3,(5)(6)(7)(8)(9). Moreover, angiotensin II receptor density is altered in hypothyroidism. An increase in

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Regulation of ACE gene expression and plasma levels during rat postnatal development

Cited by 39 publications

References 0 publications

Effects of thyroid hormones on pulmonary and renal angiotensin-converting enzyme concentrations in fetal sheep near term

Effects of thyroid hormones on pulmonary and renal angiotensin-converting enzyme concentrations in fetal sheep near term

Angiotensin I-Converting Enzyme Genotype Influences Arterial Response to Injury in Normotensive Rats

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

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