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

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Abstract
In order to elucidate a participation of intact parathyroid hormone (PTH(l-84)) in blood pressure (BP) and body fluid homeostasis, we studied fluctuations of PTH(l-84) during manipulations of BP in hyperparathyroid 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 values of PTH(l-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 patients with tertiary hyperparathyroidism (221-264ngl”1, p < 0.05), but not in dialysis patients without hypercalcaemia (126-174ngl−1, NS). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was positively correlated to the increase of serum PTH(l-84) in the healthy subjects (p = 0.619, n= 15, p < 0.05) and in the patients with primary hyperparathyroidism (p = 0.549, n = 18, p < 0.05). Noradrenaline induced BP elevation did not have a similar effect on PTH(l-84), and changes of PTH(l-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of angiotensin II, resulted in elevation of PTH(l-84) in controls, cirrhotics, patients with glomerulonephritis without the nephrotic syndrome, but not in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH(l-84) in healthy subjects (20-18ngl−1, p < 0.02), but not in patients with nephrotic syndrome and liver cirrhosis. Volume expansion induced by albumin infusion caused increased plasma levels of ANP, but PTH(l-84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(l-84), and PTH(l-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or changes in blood volume per se do not seem to influence PTH(l-84) levels.

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