title: Effects of PTH(1-34) on blood pressure, renal function, and hormones in essential hypertension: the altered pattern of reactivity may counteract raised blood pressure.
abstract: As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.
authors.affiliation: Department of Medicine and Nephrology B, Herlev Hospital, University of Copenhagen, Denmark.
authors.forename: B
authors.initials: B
authors.lastname: Jespersen
authors.forename: A
authors.initials: A
authors.lastname: Randløv
authors.forename: J
authors.initials: J
authors.lastname: Abrahamsen
authors.forename: N
authors.initials: N
authors.lastname: Fogh-Andersen
authors.forename: I L
authors.initials: IL
authors.lastname: Kanstrup
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000187:drug effects*; D001834:Body Water / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002302:Cardiac Output / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007668:Kidney / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D011674:Pulse; D012964:Sodium / Q000378:metabolism; D019379:Teriparatide / Q000494:pharmacology*; D001613:beta 2-Microglobulin / Q000652:urine
chemical_list: D001613:beta 2-Microglobulin; D019379:Teriparatide; D012964:Sodium; D002118:Calcium