The Role of Renal Natriuretic and Depressor Systems in Insulin-Resistant Hypertensive Rats

Abstract

Insulin resistance and impairment of the renal depressor system have been thought to be involved in the development of essential hypertension. However, the relationship between insulin resistance and this system is still unclear. To clarify this relationship, we investigated the role of the renal depressor system in a rat model of insulin-resistant hypertension. Sprague-Dawley rats were fed a standard diet (control) or a fruc- important factor in the etiology and pathophysiology of essential hypertension (4, 5) and that compensating hyperinsulinemia leads to high blood pressure by several factors, such as prompted sodium reabsorption (6), stimulation of the sympathetic nervous system or renin-angiotensin system (7,8), and proliferation of vascular smooth muscle cells (1). Insulin resistance has also been reported in several animal models of hypertension, including spontaneously hypertensive rats and fructose-fed rats (FFR) (9). FFR become insulin-resistant due to a change in muscle fiber composition (10), peripheral vasoconstriction (11), or an increase in tumor necrosis factor-α (TNF-α) in skeletal muscle (12), and

Chronic Hyperinsulinemia Enhances Adrenergic Vasoconstriction and Decreases Calcitonin Gene-Related Peptide-Containing Nerve-Mediated Vasodilation in Pithed Rats

“…There have been many studies about the relation between insulin resistance and the reduction of endothelium-dependent vasodilation induced by ACh (26)(27)(28)(29). Recent studies have shown that insulin resistance and/or obesity is associated with a reduction of endothelial function (30)(31)(32). Furthermore, tumor necrosis factor-α (TNF-α), resistin and free fatty acid (FFA), which are secreted from large adiposities and cause worsening of insulin resistance and endothelium disorder, have been reported to be significantly increased in obese patients (33)(34)(35).…”

Effects of chronic fructose overload on renal dopaminergic system: alteration of urinary L-dopa/dopamine index correlates to hypertension and precedes kidney structural damage

“…El SDR constituye un sistema natriurético local que regula la excreción de sodio y los niveles de presión arterial(Aperia, 2000; Armando y col., 2011). Muchos estudios han establecido la existencia de una relación entre el estado de IR y el SDR en la patogénesis de la HTA(Carey, 2001;Hasegawa y col., 2006). Principalmente a través de la activación del receptor D 1 , la DA renal promueve la natriuresis mediante inhibición de diversos transportadores de sodio a nivel renal, siendo los más importantes la enzima Na + , K + -ATPasa de la membrana basolateral y el intercambiador NHE3 en la membrana apical de las células del TP (Armando y col., 2011; Salyer y col., 2011).…”

Impacts of High Fructose Diet and Chronic Exercise on Nitric Oxide Synthase and Oxidative Stress in Rat Kidney

“…Previous studies have reported the impact of an HFr on renal NOS expression in HFr-fed rats [ 12 , 13 , 15 ]. Nishimoto et al reported that an HFr (40% fructose) for 2 weeks decreased the eNOS expression in the renal medulla during high-salt diet (3% NaCl) intake, although the HFr did not affect the urinary NO x excretion [ 12 ].…”

“…Gordish et al reported that an HFr (20% fructose) for 2 weeks reduced the urinary NO x excretion caused by a high-salt diet (4% NaCl) by 40% [ 29 ]. Hasegawa et al reported that an HFr (60% fructose) for 6 weeks decreased the renal eNOS mRNA expression and the urinary NO x excretion in rats [ 13 ]. Prince et al reported that an HFr (10% fructose in drinking water) for 8 weeks decreased the renal nNOS protein expression but did not affect the renal eNOS protein expression [ 15 ].…”

“…HFrs also affect the renal nitric oxide (NO) system. An HFr decreases the renal expression of endothelial NO synthase (eNOS) protein caused by the dietary sodium load in a high-salt diet (3% NaCl) [ 12 ], and an HFr decreases the renal expression of eNOS mRNA [ 13 ] and urinary nitrate/nitrite (NO x ) excretion [ 13 , 14 ]. Additionally, the gene transfection of eNOS increases the eNOS expression and urinary NO x excretion and decreases blood pressure in HFr-fed rats [ 14 ].…”