natriuresis


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natriuresis

 [na″tre-u-re´sis]
the excretion of sodium in the urine; see also salt wasting and salt-losing crisis (syndrome).

na·tri·u·re·sis

(nā'trē-yū-rē'sis),
Urinary excretion of sodium; commonly designates enhanced sodium excretion, which may occur in certain diseases or as a result of the administration of diuretic drugs.
[natrium + G. ouron, urine]

natriuresis

(nā′trə-yo͝o-rē′sĭs)
n.
Excretion of excessive amounts of sodium in the urine.

na′tri·u·ret′ic (-rĕt′ĭk) adj.

natriuresis

The excretion of sodium by the kidneys, which is controlled in large part by atrial natriuretic peptide (ANP). ANP may increase the glomerular filtration rate by binding to ANP receptors on glomerular mesangial cells, causing them to relax, thereby increasing the effective surface area available for filtration.

na·tri·u·re·sis

(nā'trē-yū-rē'sis)
Urinary excretion of sodium; commonly designates enhanced sodium excretion, which may occur in certain diseases or as a result of the administration of diuretic drugs.
[natrium + G. ouron, urine]

natriuresis

Excretion of sodium by the kidneys.
References in periodicals archive ?
There was also no significant difference in total natriuresis calculated according to the excreted volume (empagliflozin 83.3 mmol ([+ or -] 42) versus placebo 64.4 mmol ([+ or -] 41); treatment effect 8.54mmol/l (CI -14.19, 31.27), p = 0.5) however with an increase in the empagliflozin group towards the end of the observation period (Figure 2).
Llinas, "Mechanisms of pressure natriuresis," Current Hypertension Reports, vol.
In contrast, Wang observed that both rats and mice treated with L-NAME presented significant diuresis and natriuresis due to decreased ]v and renal tubular absorption of HC[O.sub.3.sup.-]([J.sub.HCO3]), indicating the stimulatory effect of NO on proximal tubular transport [52, 53].
The extract showed the highest natriuresis at 500 mg/kg (P<0.001), and the least was observed at 125 mg/kg.
Bradykinin [B.sub.2] and muscarinic receptors blockade prevents diuresis, natriuresis, kaliuresis, and chloride excretion induced by ES-EC
OSAS patients are characterized by a derangement in autonomic cardiovascular regulation.[sup][3] Sleep apnea patients often have nocturia, possibly because of increased plasma and urine levels of atrial natriuretic peptide, decreased antidiuretic hormone, and no normal decrease in nocturnal urinary output leading to increased natriuresis and diuresis.[sup][4] An increase in intra-abdominal pressure caused by intense inspiratory efforts against a closed upper airway has been implicated in the pathogenesis of enuresis.[sup][5]
Regarding the hormonal and renal systems, the changes are an increase in the excretion of urine (dieresis) and sodium in the urine (natriuresis) as well as enhanced atrial natriuretic peptide levels in the circulation.
3) Calcium channel blockers cause relaxation of the smooth muscle in arterial walls and may induce mild natriuresis and diuresis; they are also considered to have a neutral effect on glucose and insulin resistance.
These factors are associated with kidney hypertrophy, glomerular hyperfiltration, increased albumin excretion in the urine, increased diuresis, natriuresis, kaliuresis associated to changes in blood pressure, augmented risk for nephrolithiasis, alterations in the kidney morphology, interstitial fibrosis and increased production of oxygen-reactive species, with a consequent increase of oxidative stress.
We will examine whether sEH inhibition attenuates BP and improves renal autoregulation and pressure natriuresis in 2K1C hypertension.
Un estudio reciente senalo que la inhibicion de la endopeptidasa neutral (NEP), potencia el aumento en la excrecion de sodio en ausencia de un aumento en la tasa de filtracion glomerular o de aumento en el flujo sanguineo renal en respuesta a la ADM exogena, lo que indica que NEP induce natriuresis mediante la inhibicion de la reabsorcion tubular de sodio por atenuar el metabolismo de la ADM (11).
By inhibiting NEP, TD-0714 elevates the levels of these peptides, which may exert protective cardiac and renal effects including vasodilation, diuresis, natriuresis, reversal of maladaptive changes in heart, blood vessels and kidney, prevention of fibrosis, and prevention of end-organ damage.