236 B. E. C. NoRDiN 



growth hormone as described above, and the plasma phosphate is increased (Henne- 

 MAN et al., 1960) the implication is that tubular reabsorption of phosphate has 

 increased as Corvilain et al. (1962, 1964) have shown. This could be the result of 

 diminished parathyroid activity such as would be produced if growth hormone 

 tended to raise plasma calcium, as it did in one of Henneman's two cases. The early 

 literature (reviewed by Bauer and Aub, 1941) suggested in fact that pituitary 

 extract raised plasma calcium but it is hard to know how much credence to place in 

 those data now. 



If the effect of growth hormone in raising plasma phosphorus were a primary 

 one, it would be expected to depress plasma calcium and stimulate the parathyroids 

 in the manner suggested by Tornblom (1949). This would lead to a fall in urinary 

 calcium, Smith and Nordin (1964). Since the hormone raises urinary calcium, how- 

 ever, another explanation must be sought — either a rise in plasma calcium or a 

 diminution in parathyroid activity or both. Since a primary action of the hormone 

 is to stimulate new bone growth It presumably Increases the proportion of young to 

 old mineral in the skeleton so producing the increased miscible pool and decreased 

 24-hr. plasma specific activity reported by Haymovitz and Horwith (1964). Mac- 

 Gregor (1962) has suggested that the increased "solubility" of child bone might 

 explain the higher plasma phosphates in children. A similar explanation might be 

 applied to acromegaly. Young bone (probably octocalcium phosphate as suggested 

 by Brown and MacGregor [1965]) being more soluble than old allows the plasma 

 calcium to rise, thus diminishing parathyroid activity and allowing the plasma 

 phosphate to rise. Urinary calcium increases both because of the rise in plasma 

 calcium, however small (MacFadyen et al., 1965) and because of the fall in para- 

 thyroid activity (Kleeman et al., 1961). 



Thus to summarise the action of growth hormone on calcium metabolism it 

 appears that the hormone stimulates bone growth, raises plasma phosphate and 

 raises urinary calcium and increases tubular phosphate reabsorption. It may tend to 

 elevate plasma calcium but this is speculative. The evidence that it stimulates the 

 parathyroids and/or reduces kidney citrate is still Inconclusive, and Its effect on 

 calcium absorption is uncertain. 



Other hormones 



The association between Diabetes and Osteoporosis reported by Hernberg (1952) 

 is unexplained. Nielsen (1964) has shown that antidiuretic hormone increases the 

 excretion of calcium and suggests that it Inhibits renal tubular reabsorption of 

 calcium. PiTis et al. (1964) have reported that noradrenaline may precipitate tetany 

 in Man. Space and time do not permit me to pursue any of these trains of thought, 

 inviting though they seem to be. 



Conclusions 



It seems that it might be possible to Integrate our knowledge of the action of the 

 hormones on calcium metabolism by relating them all to the plasma calcium level. 

 The plasma and extracellular calcium form a pool through which all calcium traffic 

 as It were must pass. The calcium concentration in this pool Is governed by the 

 relation of blood to bone. Taking this as the starting point, it appears that the 

 following effects may just be discernible: 



