Renal effects of atrial natriuretic peptide during dopa-decarboxylase inhibition in patients with essential hypertension

Summary

To assess whether intrarenal dopamine synthesis could contribute to the renal response to ANP in essential hypertension, the effects of α-human ANP influsion (50 ng·min⁻¹·kg⁻¹ b.w. for 30 min) on the urinary excretion of dopamine and sodium, urine flow rate and arterial pressure were evaluated in 7 patients with mild-moderate essential hypertension before (control period) and during DOPA-decarboxylase inhibition with carbidopa (carbidopa period).

In the control period, urinary dopamine excretion was 400 pg·min⁻¹ in baseline conditions and 340 pg·min⁻¹ during ANP infusion. Carbidopa significantly decreased urinary dopamine excretion both before (210 pg·min⁻¹) and during ANP (99 pg·min⁻¹). In contrast, carbidopa did not affect sodium excretion (control from 184 to 460 μEq·min⁻¹; carbidopa period from 140 to 390 μEq·min⁻¹) or urine flow rate (control from 5.35 to 11.21 ml·min⁻¹; carbidopa period from 4.29 to 11.54 ml·min⁻¹).

Arterial pressure fell significantly during ANP infusion in both periods, and no significant difference was observed between the two study days, i.e. in the absence of and during carbidopa administration.

We conclude that DOPA-decarboxylase inhibition does not influence the diuretic and natriuretic response to α-human ANP infusion in patients with essential hypertension.