Impairment of renal compensatory hypertrophy by hypothyroidism in the rat

Stephan, Frank; Reville, P; Laharpe, F. De; Köll-Back, M H

doi:10.1016/0024-3205(82)90278-8

Cited by 24 publications

(14 citation statements)

References 14 publications

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“…In this study, we did not examine the mitotic index or DNA content. When we take the above discussion into consideration, we think that our results are consistent with the previous studies by Bradley et al (1974) and Stephan et al (1982). Bradley et al (1974) may have observed an ANG IIinduced rise in the mitotic index, and Stephan et al (1982) may have observed an ANG II-induced rise in the DNA content.…”

Section: Discussionsupporting

confidence: 92%

“…One such change, renal hypertrophy, has been described in hyperthyroid animals (Nakamura et al 1964, Katz & Lindheimer 1973, Bradley et al 1974, Stephan et al 1982, Garcia del Rio et al 1997. Bradley et al (1974) reported that in vivo thyroxine-induced renal hypertrophy is associated with a rise in the mitotic index, and Stephan et al (1982) indicated that renal hypertrophy is enhanced by thyroxine with a rise in the DNA content. However, the precise mechanism is not fully understood.…”

Section: Introductionmentioning

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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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Mechanism of hyperthyroidism-induced renal hypertrophy in rats

Kobori

Ichihara²,

Miyashita³

et al. 1998

Journal of Endocrinology

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“…Notably, a decrease urinary acidification with increased sodium and bicarbonate excretion rates has been reported in hypothyroid rats (63). In experimental animal models with hyperthyroidism, renal tubules are hypertrophic and hyperplastic (64). Thus, the tubular mass and kidney weight are increased.…”

Section: Thyroid Disorders and Tubular Functionmentioning

confidence: 97%

“…Hypothyroidism is associated with a decrease in transporter function and the opposite occurs (7) decreased (7) Peripheral vascular resistance decreased (7) increased (7) RAS activity increased (17) decreased (17) RBF increased (49) decreased (48,49) Glomerular vasoconstriction decreased (53) increased (50,51) Glomerular surface area increased (48) decreased (26) Tubulo-glomerular feedback increased (54) increased (49) Filtration pressure increased (53) decreased (48) GFR increased (11,12) decreased (8-10) Proteinuria increased (7) increased (7) Activity of tubular ion transport increased (65,66) decreased (56,59) Tubular mass increased (64) decreased (49) Urine concentrating ability decreased (68, 69) decreased (48) CO = cardiac output; GFR = glomerular filtration rate; RAS = renin-angiotensin system; RBF = renal blood flow.…”

Section: Thyroid Disorders and Tubular Functionmentioning

confidence: 99%

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

et al. 2014

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Thyroid hormones may directly affect the kidney and altered kidney function may also contribute to thyroid disorders. The renal manifestations of thyroid disorders are based on hemodynamic alterations or/and to direct effects of thyroid hormones. The renin-angiotensin system plays a crucial role in the cross-talk between the thyroid and the kidney. Hypothyroidism may be accompanied by an increase of serum creatinine and reduction of glomerular filtration rate (GFR), whereas hyperthyroidism may increase GFR. Treatment of thyroid disorders may lead to normalization of GFR. Primary and subclinical hypothyroidism and low triiodothyronine (T3) syndrome are common features in patients with chronic kidney disease (CKD). In addition low levels of thyroid hormones may predict a higher risk of cardiovascular and overall mortality in patients with end-stage renal disease. The causal nature of this correlation remains uncertain. In this review, special emphasis is given to the thyroid pathophysiology, its impact on kidney function and CKD and the interpretation of laboratorial findings of thyroid dysfunction in CKD.

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“…The kidney-to-body weight ratio is decreased by hypothyroidism and increased by hyperthyroidism (Stephan et al 1982, García del Río et al 1997, while hypothyroidism impairs renal compensatory hypertrophy in rats (Stephan et al 1982, Andrade et al 1992. Bradley et al (1974) reported that T 4 -induced renal hypertrophy in vivo is associated with a rise in the mitotic index, and Stephan et al (1982) found an increase in DNA content. The mechanism is not fully understood, but participation of the RAS has been proposed, because AII is known to have potent cell proliferation effects in several tissues in vitro (Gill et al 1977) and in vivo (Casellas et al 1997).…”

Section: Renal Hypertrophymentioning

confidence: 99%

The renin–angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations

Vargas¹,

Rodríguez-Gómez²,

Vargas-Tendero³

et al. 2011

Journal of Endocrinology

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Thyroid disorders are among the most common endocrine diseases and affect virtually all physiological systems, with an especially marked impact on cardiovascular and renal systems. This review summarizes the effects of thyroid hormones on the renin-angiotensin system (RAS) and the participation of the RAS in the cardiovascular and renal manifestations of thyroid disorders. Thyroid hormones are important regulators of cardiac and renal mass, vascular function, renal sodium handling, and consequently blood pressure (BP). The RAS acts globally to control cardiovascular and renal functions, while RAS components act systemically and locally in individual organs. Various authors have implicated the systemic and local RAS in the mediation of functional and structural changes in cardiovascular and renal tissues due to abnormal thyroid hormone levels. This review analyzes the influence of thyroid hormones on RAS components and discusses the role of the RAS in BP, cardiac mass, vascular function, and renal abnormalities in thyroid disorders.

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Impairment of renal compensatory hypertrophy by hypothyroidism in the rat

Cited by 24 publications

References 14 publications

Mechanism of hyperthyroidism-induced renal hypertrophy in rats

Mechanism of hyperthyroidism-induced renal hypertrophy in rats

The Thyroid and the Kidney: A Complex Interplay in Health and Disease

The renin–angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations

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