Key result
Borderline essential hypertension is linked to higher daytime urinary noradrenaline and dopamine excretion.
Why the study?
An opposite modulatory influence of renal noradrenergic and dopaminergic activities on sodium excretion was suggested but not fully characterized in borderline essential hypertension.
Does saline infusion alter urinary noradrenaline and dopamine excretion differently in patients with borderline versus established essential hypertension?
Observational (n=28)
Does saline infusion alter urinary noradrenaline and dopamine excretion differently in patients with borderline versus established essential hypertension?
Patients with borderline essential hypertension exhibit increased basal urinary dopamine, possibly as a compensatory mechanism for defective sodium excretion, while maintaining normal sympathetic modulation in response to volume loading.
Answers are grounded in this paper and cite their sources.
Does not support catecholamine monitoring in borderline hypertension; hypothesis-generating for sympathetic activity and needs prospective validation.
An opposite modulatory influence of renal noradrenergic and dopaminergic activities on sodium excretion has been suggested. In this study urinary noradrenaline (UNA) and dopamine (UDA) excretion were evaluated in patients with borderline essential hypertension (BH; n = 9) and in patients with established essential hypertension (EH; n = 11) as well as in normal subjects (NT, n = 8), during normal sodium and potassium intake. Measurements were performed on fractionated urine collections on two separate days: on the first day under basal conditions and on the second day after saline infusion (SAL), 2L/2h, i.v. In BH, basal UNA and UDA were higher with respect to NT and EH. The difference was significant (p less than 0.05) in urine collected between 8 and 14 h. In all three groups, SAL induced a significant decrease in UNA and a significant increase in UDA; the decrease in UNA after SAL was significantly lower in EH in respect to BH and NT. In conclusion, the increased UDA in BH may represent a compensatory mechanism to a defect in sodium excretion, possibly due to elevated renal and/or systemic noradrenergic activity; the normal response to volume and salt loading suggests that the physiological modulation of sympathetic tone is still preserved in BH.
No takes yet. Share an insight, caveat, or question.
Castellano et al. (1986) conducted an observational in Borderline essential hypertension (n=28). Borderline essential hypertension vs. Established essential hypertension and normal subjects was evaluated on Basal urinary noradrenaline (UNA) and dopamine (UDA) excretion (p=<0.05).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: