Abstract
Salt sensitivity of blood pressure (BP) is speculated to be a characteristic in obesity-induced hypertension. To elucidate the influence of obesity on salt-sensitive hypertension, we examined the effect of fat loading on BP, renal damage, and their progression induced by salt excess in Dahl salt-sensitive (S) rats. High fat (HF: 45% fat diet: 8 weeks) diet increased BP with greater weight gain and visceral fat accumulation than low fat (10% fat) diet. In HF-fed rats, plasma glucose, plasma insulin, and urinary catecholamine increased, and urinary protein tended to be elevated. Moreover, excessive salt (8% salt diet: 8 weeks)-induced hypertension and proteinuria was accelerated in HF-fed rats. Therefore, fat loading increased BP in Dahl S rats possibly through insulin-resistance and sympathetic excitation. Moreover, fat loading accelerated salt-induced BP elevation and renal damage, suggesting excessive intake of both fat and salt, such as a civilized diet, exert the synergic harmful effects.
Highlights
It has been believed that obesity is one of the factors that accentuate blood pressure (BP) response to excessive salt [1]
Body weight was increased during the treatment in both groups of rats, but after 6 weeks of the treatment, it was significantly (P < 0.05) higher in high fat (HF)-fed Dahl S rats compared with LFfed rats (Figure 1A)
Because visceral fat accumulation preceded body weight gain to a rise in BP, accumulation of visceral fat rather than body weight gain may play an important role in the rise in BP
Summary
It has been believed that obesity is one of the factors that accentuate blood pressure (BP) response to excessive salt [1]. Long-term high fat (HF) intake caused greater saltinduced BP rise associated with body weight gain in rats [2]. Salt reduction decreased BP more significantly in obese subjects than in nonobese ones and weight loss suppressed a salt-induced rise in BP [3]. We have demonstrated that salt loading decreased the glucose infusion rate during the hyperinsulinemic euglycemic clamp study and insulin-induced 2-deoxy glucose uptake into isolated soleus muscle in Dahl salt-sensitive (S) rats, an animal model of salt-sensitive hypertension [5]. In patients with essential hypertension, BP rise with salt loading was positively correlated with steady-state plasma glucose during high salt intake [7]. Insulin resistance may contribute to hypertension in Dahl S rats, because a high sucrose diet increased BP in Dahl S rats, which was reversed by troglitazone [8]. Insulin resistance may be a common background between obesity- and salt-induced hypertension
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