Key result
Acute administration of 1,25-dihydroxycholecalciferol caused a 15% decrease in cardiac output (P<.05) and a transient blood pressure increase in men with essential hypertension.
Why the study?
Does acute administration of 1,25-dihydroxycholecalciferol alter hemodynamics in patients with essential hypertension?
Does acute administration of 1,25-dihydroxycholecalciferol alter hemodynamics in patients with essential hypertension?
p-value: p=<.05
Acute administration of 1,25-dihydroxycholecalciferol causes a rapid decrease in cardiac output and transient blood pressure increase in patients with essential hypertension, suggesting enhanced cardiovascular responsiveness compared to healthy subjects.
Potential acute hemodynamic effects in hypertension warrant monitoring; leaves open chronic safety and mechanisms in larger trials.
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.
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Jespersen et al. (1998) studied Essential hypertension (n=27). 1,25-dihydroxycholecalciferol (1,25-D) vs. Placebo and healthy controls was evaluated on Cardiac output (p=<.05). Acute administration of 1,25-dihydroxycholecalciferol caused a 15% decrease in cardiac output (P<.05) and a transient blood pressure increase in men with essential hypertension.
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