Altered renal response to enhanced endogenous 5-hydroxytryptamine after tryptophan administration in essential hypertension

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1. To examine the pathophysiological significance of 5-hydroxytryptamine (serotonin) in essential hypertension, we compared the renal response to intrarenally formed 5-hydroxytryptamine by oral dosing with its precursor, L-tryptophan (2 g), in nine patients with essential hypertension and in six subjects with normotension. 2. Before tryptophan administration, urinary excretion of 5-hydroxytryptamine was significantly higher in the hypertensive group than in the normotensive group (66 ± 8 versus 36 ± 6 ng/min, P < 0.05), whereas renal plasma flow and glomerular filtration rate did not differ between the two groups. After dosing with tryptophan, urinary excretion of 5-hydroxytryptamine significantly increased to the same plateau level in both groups (366 ± 55 ng/min in the hypertensive group and 365 ± 64 ng/min in the normotensive group). Significant and equivalent decreases in renal plasma flow were observed in the early phase after tryptophan administration in both groups (−8.5 ± 3.4% in the hypertensive group and −8.2 ± 1.7% in the normotensive group). Thereafter, renal plasma flow increased to above the baseline value in normotensive subjects, whereas this late vasodilatation was absent in the hypertensive group. Glomerular filtration rate significantly decreased at the time of the fall in renal plasma flow in the normotensive group (106.8 ± 7.8 to 92.7 ± 8.5 ml min−1 1.73 m−2, P < 0.05), whereas it remained unchanged in the hypertensive group (108.2 ± 6.2 to 110.4 ± 6.3 ml min−1 1.73 m−2, not significant). Consequently, the filtration fraction did not change in normotensive subjects (0.21 ± 0.01 versus 0.19 ± 0.01, not significant), but it increased significantly in the hypertensive group (0.22 ± 0.01 versus 0.26 ± 0.02, P < 0.05). A similar sustained antidiuresis was also observed after tryptophan administration in both groups. In addition, the above-described renal functional changes were not accompanied by any significant changes in systemic blood pressure, the renin-angiotensin-aldosterone system, adrenergic activity or plasma 5-hydroxytryptamine concentration in either group. 3. Our data show that in essential hypertension there is a baseline overproduction of renal 5-hydroxytryptamine, which may contribute to a reduction in renal excretory capability. The altered renal response to tryptophan found in essential hypertension may be partly related to the exaggerated efferent arteriolar constriction induced by endogenously formed 5-hydroxytryptamine.

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