Thyroid hormone stimulates renin synthesis in rats without involving the sympathetic nervous system

Kobori, Hiroyuki; Ichihara, Atsuhiro; Suzuki, Hiromichi; Miyashita, Yutaka; Hayashi, Matsuhiko; Saruta, Takao

doi:10.1152/ajpendo.1997.272.2.e227

Cited by 41 publications

(56 citation statements)

References 27 publications

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“…Although the sensitivity of renin release to -adrenergic stimulation is impaired by thyroidectomy in adult rats (Bouhnik et al 1981), the thyroid hormones can influence the activity of the renin-angiotensin system independent of the sympathetic nervous system (Kobori et al 1997). Therefore, in the present study, tissue ACE concentrations may have been affected by changes in substrate availability induced by the thyroid hormones.…”

Section: Discussionmentioning

confidence: 66%

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: 66%

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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“…Plasma levels of components of the circulating RAS were determined as described previously (8). Total renin content and the AngI and AngII levels in renal cortex that was harvested from the kidneys were determined as previously reported (9,10).…”

Section: Rasmentioning

confidence: 99%

Contribution of Nonproteolytically Activated Prorenin in Glomeruli to Hypertensive Renal Damage

Ichihara¹,

Kaneshiro²,

Takemitsu³

et al. 2006

Journal of the American Society of Nephrology

132

128

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Prorenin is activated without proteolysis by binding of prorenin receptor to the pentameric "handle region" (HR) of prorenin prosegment. It was hypothesized that such activation occurs in the kidneys of hypertensive rats and causes tissue reninangiotensin system (RAS) activation and end-organ damage. Because the HR's binding to its binding protein made the adjacent tetrameric "gate region" (GR) accessible to its specific antibody, immunohistochemistry of the GR was performed to test the hypothesis. Methods also were devised specifically to inhibit the nonproteolytic activation by the decapeptide corresponding to the HR as a decoy. Immunohistochemistry of the GR demonstrated that the majority of nonproteolytically activated prorenin is present in podocytes of the kidneys from stroke-prone spontaneously hypertensive rats, in which activation of renal tissue RAS, proteinuria, and glomerulosclerosis occurred. Continuous subcutaneous administration of the HR decoy peptide completely inhibited both nonproteolytic activation of tissue prorenin and activation of tissue RAS without affecting circulating RAS or arterial pressure and significantly attenuated the development and progression of proteinuria and glomerulosclerosis. These studies clearly demonstrated that nonproteolytic activation of prorenin in glomeruli is critically involved in renal tissue RAS activation, leading to renal damage in hypertensive animals.

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“…Body weight (BW) was checked daily. Rats were divided into control and hyperthyroid (Hyper) groups by daily intraperitoneal injections of saline vehicle or thyroxine (0·1 µg/g) for 4 weeks as described previously (Kobori et al 1997a). Hyperthyroid rats were then treated with daily intraperitoneal administration of saline vehicle (Hyper+Vehicle), 5 µg/g losartan (Hyper+Los), or 10 µg/g nicardipine (Hyper+Nic) for 4 weeks as described previously (Kobori et al 1997b).…”

Section: Preparation Of Animalsmentioning

confidence: 99%

“…The first portion of the kidney was used to measure the renal renin level as described previously (Kobori et al 1997a). In brief, the kidney was thawed and homogenized with a Polytron (Kinematica, Littau, Switzerland) in 10 ml buffer containing 2·6 mmol/l EDTA, 1·6 mmol/l dimercaprol, 3·4 mmol/l 8-hydroxyquinoline sulfate, 0·2 mmol/l phenylmethylsulfonyl fluoride, and 5 mmol/l ammonium acetate.…”

Section: Hormone Measurements In Renal Tissuementioning

confidence: 99%

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Mechanism of hyperthyroidism-induced renal hypertrophy in rats

Kobori

Ichihara²,

Miyashita³

et al. 1998

Journal of Endocrinology

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It is well known that renal hypertrophy is induced by hyperthyroidism; however, the mechanism is not fully understood. We recently reported that cardiac hypertrophy in hyperthyroidism is mediated by enhanced cardiac expression of renin mRNA. The present study addresses the hypothesis that renal hypertrophy in hyperthyroidism is mediated by amplification of renal expression of renin mRNA. Twenty Sprague-Dawley rats were divided into control (n=5) and hyperthyroid groups by daily intraperitoneal injections of saline vehicle or thyroxine. The hyperthyroid group was subdivided further into hyperthyroid-vehicle (n=5), hyperthyroid-losartan (n=5), and hyperthyroid-nicardipine (n=5) groups by daily intraperitoneal injections of saline vehicle, losartan, or nicardipine. All rats were killed at 4 weeks, and the blood and kidneys were collected. The kidney-to-body weight ratio increased in the hyperthyroid groups (+34%). Radioimmunoassays and reverse transcriptase-polymerase chain reaction revealed increased renal renin (+91%) and angiotensin II (+65%) levels and enhanced renal renin mRNA expression (+113%) in the hyperthyroid groups. Losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced renal hypertrophy. These results suggest that thyroid hormone activates the intrarenal reninangiotensin system via enhancement of renal renin mRNA expression, which then leads to renal hypertrophy.

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Thyroid hormone stimulates renin synthesis in rats without involving the sympathetic nervous system

Cited by 41 publications

References 27 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

Contribution of Nonproteolytically Activated Prorenin in Glomeruli to Hypertensive Renal Damage

Mechanism of hyperthyroidism-induced renal hypertrophy in rats

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