The thyroid in the spontaneously hypertensive rat: A light and electron microscopic study

Abstract

The present study was undertaken to seek ultrastructural changes in the thyroid gland of the spontaneously hypertensive rat which would contribute to the understanding of previously reported abnormalities in thyroid function. Light and electron microscopic observations and measurements of plasma T3 and systolic blood pressure were recorded from a colony of Wistar Kyoto rats (WKY) and of spontaneously hypertensive rats (SHR). The systolic blood pressure of SHR was significantly higher than that of WKY but the plasma T3 levels of the two groups did not differ significantly. After administration of propylthiouracil (PTU), serum T3 levels and systolic pressure of both groups decreased. The size of the thyroid follicles in SHR was highly variable throughout the gland, and the colloid contained unevenly dense areas and cell debris. The follicular cells contained slightly dilated rough surfaced endoplasmic reticulum (ER) and numerous pleomorphic bodies of uneven density. After treatment with PTU, the vessels between the follicles of SHR did not become as dilated as those in WKY but the fine structure of follicular cells in SHR was similar to that of WKY and was characteristic of the typical thyroid response to PTU administration. We suggest that the thyroid in SHR does not respond adequately to the elevated TSH levels reported to be present in these animals, although it can respond to the highly elevated TSH levels which occur with PTU administration. This impairment most probably involves defects in synthesis and/or secretion of thyroid hormones in response to TSH stimulation.

Elevation of plasma immunoglobulin A in the spontaneously hypertensive rat.

“…These include lowered levels of plasma thyroxine and triiodothyronine, elevated plasma thyroid-stimulating hormone, consequent increased thyroid weight and radioiodine uptake, 50 and impairment of synthesis or secretion of thyroid hormones in response to thyroid-stimulating hormone. 51 It is also noteworthy that Takeichi et al 19 proposed that the natural thymocytotoxic autoantibody they observed in many SHR is an IgM molecule, as indicated by its elution pattern on gel filtration and sensitivity to reduction by 2-mercaptoethanol. These properties, however, are equally compatible with polymeric IgA, the major component of plasma IgA in SHR.…”