Значения термина renal sodium на английском

However, whether T cells contribute to renal sodium retention and salt-sensitive hypertension is unknown.

Controlled mandatory ventilation with positive end-expiratory pressure (PEEP) reduces renal sodium excretion.

This study hypothesized that ENaC contributes to the increase in renal sodium reabsorption following a meal.

Context: A genetic variant in alpha-adducin has been associated with renal sodium reabsorption and salt-sensitive hypertension.

Thus, disruption of the D3 receptor increases renal renin production and produces renal sodium retention and renin-dependent hypertension.

Abnormalities in renal sodium reabsorption may be involved in the development and maintenance of experimental and clinical hypertension.

Sodium regulating hormones remained unaffected by desmopressin, indicating a possible direct effect of the agent on renal sodium handling.

The present study aimed to elucidate the role of Na, K-ATPase inhibitor in renal sodium metabolism in essential hypertension.

The onset of hypertension in spontaneously hypertensive rats (SHRs) is preceded by defects in renal sodium excretion.

Consequences of this neurohumoral activation with arterial uderfilling include renal sodium and water retention and an increase in peripheral vascular resistance.

However, the functional significance of ATRAP in renal sodium handling and blood pressure regulation under pathological stimuli is not fully resolved.

The impaired renal sodium handling in primary hypertension and salt sensitivity may be caused by aberrant counter-regulatory natriuretic and anti-natriuretic pathways.

Background: Nitric oxide (NO) is an important regulator of renal sodium transport and participates in the control of natriuresis and diuresis.

The aim of this study was to determine the effect of NO depletion on renal sodium handling in a model of diet-induced obesity hypertension.

To assess renal sodium handling under non-steady-state conditions, we infused 2 L normal saline intravenously over a 2-hour period.

Conclusions: These results demonstrated that distal tubule-dominant enhancement of ATRAP inhibits pathological renal sodium reabsorption and blood pressure elevation in response to HS loading.