Oral carbidopa has no effect on the renal response to angiotensin II in normal man

Abstract

1. The effect of inhibition of intrarenal dopamine synthesis by carbidopa on the renal response to angiotensin II infusion was studied in six healthy salt-loaded volunteers. 2. Subjects received an infusion of angiotensin II at two doses (0.5 and 1.0 ng min-1 kg-1) on two occasions. Before one study they took a single dose of carbidopa (100 mg) by mouth. 3. The plasma concentrations of angiotensin II produced by the infusion were similar on both study days. Angiotensin II infusion reduced urinary dopamine excretion on the control day. Urinary dopamine excretion was undetectable at all times after carbidopa, but carbidopa did not change the basal excretion rate of sodium. Despite inhibition of renal dopamine synthesis, the reductions in both absolute and fractional sodium excretion during the angiotensin II infusion were not different from those seen in the control study. 4. The reductions in glomerular filtration rate and effective renal plasma flow which occurred during angiotensin II infusion were not modified by pretreatment with carbidopa. 5. The renal response to angiotensin II is not modulated either wholly or in part by endogenous intrarenal dopamine levels. The fall in urinary dopamine excretion which occurs during angiotensin II infusion is consistent with a modulatory role for tubular reabsorptive capacity in the regulation of proximal tubular dopamine synthesis.

The antinatriuretic action of gamma‐L‐glutamyl‐5‐hydroxy‐L‐tryptophan is dependent on its decarboxylation to 5‐hydroxytryptamine in normal man.

“…In the present study, a single 100 mg dose of carbidopa, an extracerebral LAAD inhibitor, suppressed dopamine and 5-HT excretion to below the levels of detection of the assays indicating effective inhibition of renal LAAD. We did not observe a significant effect of carbidopa on urinary sodium excretion during saline infusion in agreement with most previous studies [13][14][15]. Carbidopa substantially reduced the increment in urinary 5-HT excretion that followed administration of glu-5-HTP.…”

Neuroendocrine Factors Influencing Polydipsia in Psychiatric Patients: An Hypothesis

“…Many of these were acute studies in normal volunteers, and dietary sodium in take had an effect on the response in some studies. Dopaminergic control of A-II function was not con fIrmed in a study in which carbidopa-induced inhibi tion of dopamine synthesis had no effect on the renal response to A-II (Eadington et al 1991). However, the subjects in this study were sodium replete, not sodium depleted, as in the studies mentioned earlier.…”