Effect of the parathyroid hormone—Calcium system on functional activity of the hypothalamus-neurohypophysis complex

Abstract

The effect of single and repeated parenteral administration of parathyroid hormone on the protein synthesis in neurosecretory cells of the supraoptic nucleus and on the blood vasopressin content is studied. The hormone enhances the synthesis of RNA in the supraoptic nucleus and the blood vasopressin content, particularly after a single administration.Key Words: parathyroid hormone; calcium; vasopressin; RNA; hypothalamus; neurohypophysis Although the effect of parathyroid hormone (PTH) on various organs and systems has been extensively studied, the central mechanisms of its action so far remain obscure. In parathyroidectomized animals, functional activity of the hypothalamic supraoptic nucleus (SON) and vasopressin (VP) content are changed, which may result from the PTH deficiency and related processes [1,6]. In the present study we examined the direct effects of PTH on protein synthesis in the SON cells, and, consequently, on the synthesis and release of VP. MATERIALS AND METHODSExperiments were performed on male albino rats weighing 120-200 g. The rats were divided into three groups: group 1 were intact controls, group 2 consisted of rats receiving daily intravenous injections of PTH in a dose of 0.5 U/100 g body weight for 7 days, and group 3 included rats given the same dose of PTH in a single injection. The animals of group Department of Normal Physiology, M. Geratsi State Medical University, Yerevan 3 were decapitated 30 min postinjection. The frontal hypothalamic area was fLxed in formalin. Serial frontal paraffin sections were processed by routine morphological and histochemical methods (staining with hematoxylin and eosin and the method of Einarson with the RNA-specific dye halocyanide-chromium alum). The RNA content in the neurosecretory cells of SON was measured by the single-wave method in a LYuMAM-I2 apparatus ()~=550 nm, probe diameter 0.1 mm) and expressed in arbitrary optical units. Serum Ca 2 § content was determined spectrophotometrically. The content of ionized calcium was measured with a Kone-Microlit ion-selective analyzer, inorganic phosphorus was measured using Bio-LabTest kits, and the VP content was determined in a radioimmunoassay with Buhlmann-Laboratories kits. The results were analyzed using Student's t test. RESULTSChronic administration of PTH elevated serum content of ionized Ca 2 § and lowered that of phosphorus (Table 1). The RNA content in neurosecretory cells of the SON increased from 0.95+0.03 to 1.38+0.01

Parathyroid Hormone, Cognitive Function and Dementia: A Systematic Review

“…Arterial stiffness and endothelial dysfunction have been observed in patients with primary hyperparathyroidism and may result in cognitive impairment [ 47 ]. PTH crosses the blood-brain barrier and PTH excess in animal models has been linked to enhanced release of vasopressin and vasoconstriction [ 48 ]. Additionally, hypoperfusion in several cortical regions involved in memory and learning has been observed in patients with primary hyperparathyroidism compared to controls [ 3 ].…”

Age-related increases in parathyroid hormone may be antecedent to both osteoporosis and dementia

“…Based on our findings, we suggest that control of PTH levels may be important for protecting against age-induced dementia. PTH's potential involvement with dementia may be explained in the following way: PTH has been shown to cross the blood-brain barrier [ 26 ]. PTH has been considered a candidate risk factor for senile dementia because sustained high levels of PTH in the brain may cause degeneration of specific brain regions due to Ca(2+) overloading [ 27 , 28 ].…”

The Vitamin D, Ionised Calcium and Parathyroid Hormone Axis of Cerebral Capillary Function: Therapeutic Considerations for Vascular-Based Neurodegenerative Disorders

“…Several lines of evidence also suggest that PTH may directly affect neurovascular integrity independent of vitamin D homeostasis. PTH has been shown to cross the BBB and an exaggerated level of PTH within CSF appears to cause neuronal degeneration due to cellular iCa overloading [ 33 , 34 ]. In clinical studies, increased levels of PTH have been reported as an independent risk factor of age-related cognitive decline [ 35 , 36 ].…”