Regulation of Parathyroid Hormone Secretion*

The ultrastructure of the rat parathyroid has been under study for more than 35 years, but controversies still exist, especially regarding structure-function relationships. The present review focuses on recent morphological parathyroid research on rats under normal conditions and in various states of disturbed calcium metabolism. To facilitate discussions on functional aspects, current biochemical data, particularly those dealing with the regulation of parathyroid hormone synthesis and release, are also considered. Our results from quantitative studies and from investigations employing serial sectioning form the basis for the discussions. A central issue is whether the parathyroid secretory cells undergo secretory cycles. Prompted by results obtained from improved fixation procedures and serial sectioning, we question the basis for the theory of secretory cycles. Since the rat parathyroid secretory cell is polar, a single section is not an appropriate sample for estimating functional activity and for comparing the structure and distribution of intracellular components of adjacent cells. The heterogeneity in ultrastructural appearance of intracellular vesicles calls for the use of specific markers in relating the structure of the vesicular compartment to intracellular processing of hormone. The importance of unbiased quantitative techniques is illustrated in discussions on cell number and size for estimating the response of the parathyroid gland to different functional states or disorders demanding changes in secretion of parathyroid hormone, e.g., hyper- and hypocalcemia.

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“…An effect of calcitriol independent of genomic activation has also been proposed (cf. Pocotte et al, 1991).…”

Section: Rat Parathyroids In Differentmentioning

confidence: 99%

Quantitative and three‐dimensional aspects of the rat parathyroid gland in normo‐, hypo‐, and hypercalcemia

Wernerson

Svensson

Reinholt

1995

Microscopy Res & Technique

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“…The secreted PTH then raises the calcium level in plasma by promoting the release of calcium from bone, reducing the calcium excretion by the kidneys, and increasing the calcium absorption by the small intestine. In turn, the increased calcium level inhibits PTH secretion from the parathyroid gland (Pocotte et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

Parathyroid hormone accelerates decompensation following left ventricular hypertrophy

et al. 2010

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Abbreviations: FS, fractional shortening; LVH, left ventricular hypertrophy; LVIDs, left ventricular internal dimension at systole; LVPWs, left ventricular posterior wall thickness at systole; PTH, parathyroid hormone; TAB, transverse aortic banding AbstractParathyroid hormone (PTH) treatment was previously shown to improve cardiac function after myocardial infarction by enhancing neovascularization and cell survival. In this study, pressure overload-induced left ventricular hypertrophy (LVH) was induced in mice by transverse aortic banding (TAB) for 2 weeks. We subsequently evaluated the effects of a 2-week treatment with PTH or saline on compensated LVH. After another 4 weeks, the hearts of the mice were analyzed by echocardiography, histology, and molecular biology. Echocardiography showed that hearts of the PTH-treated mice have more severe failing phenotypes than the saline-treated mice following TAB with a greater reduction in fractional shortening and left ventricular posterior wall thickness and with a greater increase in left ventricular internal dimension. Increases in the heart weight to body weight ratio and lung weight to body weight ratio following TAB were significantly exacerbated in PTH-treated mice compared to saline-treated mice. Molecular markers for heart failure, fibrosis, and angiogenesis were also altered in accordance with more severe heart failure in the PTH-treated mice compared to the saline-treated mice following TAB. In addition, the PTH-treated hearts were manifested with increased fibrosis accompanied by an enhanced SMAD2 phosphorylation. These data suggest that the PTH treatment may accelerate the process of decompensation of LV, leading to heart failure.

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“…Its rate of secretion is inversely proportional to the concentration of ionized calcium over the physiologic range of calcium values in ECF. 357,358 The relationship between extracellular ionized calcium and secretion of parathyroid hormone is governed by a calcium-sensing receptor protein, which is expressed on the surfaces of parathyroid and renal tubular cells. [359][360][361] The primary physiologic effect of PTH is to increase the concentration of ionized calcium in ECF.…”

Section: Pathophysiologymentioning

confidence: 99%