[Hormonal interactions of parathormone and calcium metabolism].
The possible hormonal interactions of parathormone and extracellular calcium level with other endocrine systems were studied. Primary hyperparathyroidism was used first as a clinical model, in which hypercalcemia and normocalcemia occurs before and after surgery, respectively. An increased activity of renin-aldosterone system related to parathormone was found in hyperparathyroidism, and surgery resulted in a small decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the cessation of the secondary hyperaldosteronism. The role of a relative hyperinsulinism, occurring in hyperparathyroidism, in the pathogenesis of hypertension was not proved. The basal and stimulated secretion of thyreotrophin, the basal growth hormone level, and the stimulated prolactin secretion increased after surgery. Follicle stimulating hormone and luteinizing hormone secretions remained unchanged. The results suggest that extracellular calcium may reversibly modify the secretion of certain anterior pituitary hormones and their stimulus-induced responses. In the second disease, growth hormone deficiency syndrome, studied, long-term growth hormone replacement therapy results in significant but transient changes in bone metabolism: calcium-, alkaline phosphatase-, and phosphate levels increase until 6 to 18 months as compared to the initial values; then these parameters decrease to the baseline level. Parathormone decreases until the first year then returns to the baseline level. Osteocalcin shows similar temporary changes. In spite of the above transient changes, osteodensity increases after 12 months of treatment, and further improvement can be seen after 18 and 24 months, i.e. GH treatment exerts a biphasic effect on bones; resorption increases first followed by an increase in formation. Based on the above results, it can be concluded that both parathormone and extracellular calcium are able to influence the secretion of certain hormones; and--as it is shown in growth hormone replacement therapy--other hormones may cause certain effect on them, too. The better understanding of these interactions may result in a better understanding of the pathomechanism of certain diseases and the improvement of their treatment.
Kovács
László
L
Országos Gyógyintézeti Központ, Belgyógyászati Osztály, Budapest.
D000293:Adolescent; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D015519:Bone Density; D001862:Bone Resorption; D002118:Calcium / Q000097:blood* / Q000378:metabolism; D004334:Drug Administration Schedule; D005260:Female; D006728:Hormones / Q000097:blood* / Q000378:metabolism; D019382:Human Growth Hormone / Q000008:administration & dosage* / Q000097:blood / Q000172:deficiency*; D006801:Humans; D006934:Hypercalcemia / Q000097:blood / Q000209:etiology; D006961:Hyperparathyroidism / Q000097:blood* / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D006973:Hypertension / Q000097:blood / Q000209:etiology; D007328:Insulin / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010281:Parathyroid Hormone / Q000097:blood* / Q000378:metabolism; D010908:Pituitary Hormones, Anterior / Q000097:blood; D012083:Renin / Q000097:blood; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome
D001786:Blood Glucose; D006728:Hormones; D007328:Insulin; D010281:Parathyroid Hormone; D010908:Pituitary Hormones, Anterior; D015675:Osteocalcin; D019382:Human Growth Hormone; D000450:Aldosterone; D012083:Renin; D002118:Calcium