PARATHYROID-HORMONE IN BLOOD-PRESSURE AND VOLUME HOMEOSTASIS IN HEALTHY-SUBJECTS, HYPERPARATHYROIDISM, LIVER-CIRRHOSIS AND GLOMERULONEPHRITIS - A POSSIBLE INTERACTION WITH ANGIOTENSIN-II AND ATRIAL-NATRIURETIC-PEPTIDE

In order to elucidate a participation of intact parathyroid hormone (P TH(1-84)) in blood pressure (BP) and body fluid homeostasis, we studie d fluctuations of PTH(1-84) during manipulations of BP in hyperparathy roid and healthy subjects, and during manipulations of blood volume in patients with glomerulonephritis or liver cirrhosis and in controls. Angiotensin II induced BP elevation was associated with increased valu es of PTH(1-84) both in healthy subjects (12-25 ngl(-1), medians, p < 0.01), in patients with primary hyperparathyroidism (94-125 ngl(-1), p < 0.01), in patients with low calcium due to end stage renal disease before requirement of dialysis (95-151 ngl(-1), p < 0.02), and in pati ents with tertiary hyperparathyroidism (221-264 ngl(-1), p < 0.05), bu t not in dialysis patients without hypercalcaemia (126-174 ngl(-1), NS ). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was posit ively correlated to the increase of serum PTH(1-84) in the healthy sub jects (rho = 0.619, n = 15, p < 0.05) and in the patients with primary hyperparathyroidism (rho = 0.549, n = 18, p < 0.05). Noradrenaline in duced BP elevation did not have a similar effect on PTH(1-84), and cha nges of PTH(1-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of an giotensin II, resulted in elevation of PTH(1-84) in controls, cirrhoti cs, patients with glomerulonephritis without the nephrotic syndrome, b ut in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH( 1-84) in healthy subjects (20-18 ngl(-1) p < 0.02), but not in patient s with nephrotic syndrome and liver cirrhosis. Volume expansion induce d by albumin infusion caused increased plasma levels of ANP, but PTH(1 -84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(1-84), and PTH(1-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or change s in blood volume per se do not seem to influence PTH(1-84) levels.