Abnormal Thyroid Function in Spontaneously Hypertensive Rats

Abstract

Thyroid weight, thyroidal radioiodide uptake, and cyclic AMP-dependent protein kinase activity of a thyroid supernatant fraction were increased significantly in spontaneously hypertensive rats (SHR), apparently because of increased secretion of pituitary TSH. However, the thyroids of SHR did not make supernormal amounts of thyroxine (T4), and thyroidal radioiodine release was apparently impaired. In the SHR, proteolytic enzyme activity was less than normal and the thyroglobulin was more resistant to normal proteolytic enzyme than was control thyroglobulin. Presumably because of these abnormalities, plasma T4 was significantly lower than normal, but triiodothyronine (T4) was normal, as a result of compensatory processes occurring in T3 synthesis and hydrolysis of thyroglobulin. T4 and T3 were less effective in depressing pituitary TSH synthesis and secretion in SHR than in controls, possibly because of an abnormal setting of the "hormostat." Although the hypothalamic content of TRH was normal in SHR, the exact site of the abnormality in the "hormostat" is not delineated in the present study.

Altered Postnatal Expression of Insulin-Like Growth Factor-I (IGF-I) and Type X Collagen Preceding the Perthes' Disease–Like Lesion of a Rat Model

“…(1,2) We used SHRs (Charles River Japan, Yokohama, Japan) as the disease models of epiphyseal osteonecrosis and WKRs (Charles River Japan) as normal control animals. Rats at postnatal weeks 1,2,3,4,5,6,8,10,12,14,18, and 60 were perfusion-fixed with 4% paraformaldehyde, 0.2% picric acid, and 0.5% glutaraldehyde in 0.1 M phosphate buffer (PB, pH 7.4) after an intraperitoneal injection of sodium pentobarbitone (50 mg/kg body weight). Hindlimbs were immediately excised and immersion-fixed with 2% paraformaldehyde and 0.2% picric acid overnight.…”

“…(2)(3)(4) Vascular damage may occur secondary to the hypertension and may lead to a disturbance of epiphyseal vascularization. However, the early postnatal epiphysis consists of the avascular cartilage (weeks [1][2][3][4][5], and it appears unlikely that the hypertension directly causes the abnormal IGF-I expression. In turn, disorders of the endocrine system other than that of the vasomotor system play an important role in causing the hypertension in SHRs.…”

“…In turn, disorders of the endocrine system other than that of the vasomotor system play an important role in causing the hypertension in SHRs. (3,4) Thus, delayed IGF-I expression and the subsequent delay in type X collagen expression may occur independently of the hypertension.…”

“…(2,3,4) It has been also shown that osteonecrosis occurs frequently in the proximal epiphysis of the femur. (5) The findings obtained from a series of the previous studies are summarized as follows: Osteonecrosis of the femoral epiphysis occurs naturally; osteonecrosis occurs during 7-13 weeks after birth; and osteonecrosis is repaired by invasion of the granulation tissue and does not undergo recurrent necrosis.…”

Osteonecrosis of the femoral head of growing, spontaneously hypertensive rats

“…Disorders of endocrine systems other than the autonomic nervous system play an important role in the pathogenesis of hypertension in SHRs (Kojima et al 1976, Braley et al 1983, Moll et al 1975, Nosaka 1968, Tsuchiyama et al 1972. Moreover, it was suggested recently that an osteoporotic bone disorder and abnormality of calcium metabolism are also present (Izawa et al 1985, Lucas et al 1986).…”