Guanethidine sympathetic blockade: its value in reimplantation surgery.

levels to normal, although we cannot exclude the possibility that prednisone, administered for immunosuppression, may have contributed to the decrease in plasma p-MSH concentration. The way that the kidney influences r-MSH metabolism is uncertain. Since the patients on haemodialysis who retain their kidneys pass little urine the difference in plasma p-MSH levels between those with kidneys and those without suggests that the kidney regulates r-MSH metabolism by a non-excretory mechanism. which showed that significant amounts of P-MSH were excreted in the urine only when plasma levels rose to well above the levels of chronic renal failure. There are two possible non-excretory mechanisms: the kidney may influence p-MSH secretion or control its metabolism. The difference in plasma F-MSH levels between patients with kidneys and those without kidneys excludes the possibility of a pituitary stimulator elaborated by the diseased kidney or a metabolite retained in the blood despite dialysis. It does not exclude, however, the possibility of a retained stimulator that is normally destroyed by the kidney. An alternative hypothesis is that the kidney normally produces a factor that inhibits 3-MSH secretion by the pituitary. Production of this factor would progressively decrease in chronic renal failure, resulting in a greater secretion of pituitary 3-MSH. This and pituitary stimulation seem unlikely, especially since the increased p-MSH secretion would generally be associated with an increased secretion of ACTH,4 and this has not been found in CRF.' Thus the most probable explanation is that the kidney is the major site of r-MSH metabolism, and impairment of this metabolism leads to increased plasma p-MSH levels in CRF. The exact nature of immunoreactive f-MSH is unknown in CRF although it appears to be lipotrophin in normal people.' 2 The RP6 membrane is permeable to molecules with a molecular weight of less than 10 000. Thus substances with a molecular weight of less than 5000 should show an arteriovenous difference during dialysis. The findings in table II suggest that the hormone must have a molecular weight well above 5000 and is therefore unlikely to be the 22-amino-acid synthetic human r-MSH, which has a molecular weight of about 2500. Thus our findings suggest that the immunoreactive r-MSH of chronic renal failure is a lipotrophin. The function of this hormone is not known in man, although lipotrophin and MSH peptides are sebotrophic in the rat.5 6 As the present evidence suggests that 3-MSH is metabolished by the kidney the possibility …