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.

A role for vitamin D in the pathophysiology of essential hypertension has frequently been suggested, but acute direct effects on blood pressure, cardiac output, renal hemodynamics, or hormones have not previously been demonstrated. The rapid effects of 1,25-dihydroxycholecalciferol (1,25-D) were assessed over 120 min after a bolus injection (0.02 microg/kg body weight) in eight men with essential hypertension and in nine healthy men. A placebo group of 10 healthy men was also included. Ionized calcium was monitored closely during the study, and was kept constant with a clamping technique. In the hypertensive patients, a transient increase in blood pressure and a reciprocal fall in cardiac output measured by a CO2 rebreathing technique (-15%, P < .05) were observed after 1,25-D injection. In the control group, both blood pressure and cardiac output remained unchanged. The glomerular filtration rate, effective renal plasma flow, and urinary sodium and water excretions were unchanged in both groups. Plasma levels of atrial natriuretic peptide at baseline were higher in the hypertensive patients than in the control subjects (P < .02); plasma levels of renin, aldosterone, norepinephrine, endothelin, and parathyroid hormone(1-84) were similar in the two groups. None of these hormones was affected during the observation time after the injection of 1,25-D. In conclusion, acute administration of 1,25-D caused a fast and likely nongenomic-mediated decrease in cardiac output in patients with essential hypertension, which together with a transient BP increase implies a 1,25-D-induced increase in total peripheral resistance. These data suggest an enhanced cardiovascular responsiveness to 1,25-D in hypertensive compared to healthy normotensive subjects.

No abstract