Abstract

Objective: Alterations in sodium and water intake-excretion balance are currently admitted as a relevant factor in arterial hypertension development. Hyaluronic acid metabolism in renal medullary has been proved to play a relevant role in the regulation of water resorption by the collecting duct, and hyaluronidase excretion in urine has been found to be inversely related to hydration status. Thus, the aim of our study was to assess urinary hyaluronidase activity in response to water loading in hypertensive and normotensive subjects with and without familial predisposition to hypertension. Design and method: Eighty-six adult Caucasian men underwent a water loading test consisting of oral administration of 15-20 ml of water/kg body weight over 40-45 min. Urinary hyaluronidase activity was assessed by turbidimetric assay at baseline and every 60 min for 4 hours. The study cohort included 21 hypertensive patients (HT) and 65 normotensive offsprings of normotensive (NT neg, n = 29) and hypertensive subjects (NT pos, n = 36). Results: Urinary hyaluronidase activity decreased in response to water loading in all groups, attaining the lowest levels at 60 and 120 min. However, while at baseline and after 240 min hyaluronidase activity was similar for all subjects, between 60 and 180 min NT pos subjects maintained significantly highest levels than both NT neg and HT patients (p<0.0001 and p<0.001 at 120 min, respectively). Conclusions: Consistent with previous findings, our results show that hyaluronidase activity in urine is inversely correlated with hydration status as we observed in all studied groups in response to water loading. However, while baseline levels did not differ between groups, the decrease in hyaluronidase activity was significantly lower in the subgroup of subjects having a family history of hypertension. Since hyaluronidase activity in the renal medullary has been postulated to be associated with ADH metabolism, individuals genetically predisposed to hypertension might exhibit increased renal sensitivity to ADH action resulting in alterations in the management of water loading by the vasopressinergic system that could precede and contribute to hypertension development.

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