Abstract
In essential hypertension, peripheral sympathetic nerve activity is generally thought to be increased regardless of salt sensitivity or insensitivity. Recent reports suggest that the cause may be abnormal central nervous system enhancement. However, other several reports have shown that a central sympathetic inhibitory system, the neuronal nitric oxide synthase system, may be strongly enhanced in salt-sensitive hypertensive Dahl rats, an animal model of salt-sensitive hypertension. These two facts lead to questions what happens finally in peripheral sympathetic activity and what is the relationship between sympathetic nerves and hypertension. In this review, we will show evidences for enhancement of central sympathetic inhibitory system, putative cause for up-regulation of central neuronal nitric oxide synthase system, and a role of its function, then lastly we consider the relationship between hypertension and sympathetic nerves in a rat model, with a focus on salt-sensitive hypertension.
Highlights
Essential hypertension accounts for about 90% of all cases of hypertension, and both salt-sensitive and salt-insensitive cases are thought to exist [1,2]
In Dahl hypertensive rats, the sympathetic center becomes pathophysiologically hyper-reactive, concomitant with compensatory upregulated activity in nNOS neuron-mediated inhibitory systems of the central sympathetic center, which results in almost same activity in resting peripheral sympathetic nerve of hypertensive Dahl rats as that of normotensive Dahl rats
The enhancement of the central inhibitory system caused by high blood pressure per se produces reduction in arterial pressure, indicating that the sympathetic control system seems to be operated in order to counter-attack hypertension, the other part of the sympathetic center becomes pathophysiologically enhanced
Summary
Essential hypertension accounts for about 90% of all cases of hypertension, and both salt-sensitive and salt-insensitive cases are thought to exist [1,2]. Na+ ion transport abnormalities in the choroid of salt-sensitive hypertensive Dahl rats have been indicated, and elevation of the Na+ ion concentration in cerebrospinal fluid activates the renin-angiotensin system in the brain This is reported to cause abnormal excitement of sympathetic nerve centers [31]. When S-methyl-L-thiocitrulline (SMTC), an inhibitor with high specificity, was administered intraventricularly to rats in the same unanesthetized, unrestrained state, a similar rise was seen in resting peripheral sympathetic nerve activity as well as in blood pressure [39] (Figure 2). These results suggest the following: 1) central neurons with nNOS enzyme activity comprise a central inhibitory system of blood.
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