Sympathetic nerve activity and

Niijima, A., Okui, T., Matsumura, Y., Yamano, T., Tsuroka, N., Kiso, Y., and Nagai, K. (2002). Effects of L-carnosine on renal sympathetic nerve activity and DOCA-salt hypertension in rats. Auton. Neurosci. 97, 99-102. 

Grossman E, Rea RF, Hoffman A, et al Yohimbine increases sympathetic nerve activity and norepinephrine spillover in normal volunteers. Am J Physiol 2601 (1 pt 2 R142-R147, 1991... 

Several drugs that interfere with the sympathetic nervous system inhibit the secretion of renin. Examples are clonidine and propranolol. Clonidine inhibits renin secretion by causing a centrally mediated reduction in renal sympathetic nerve activity, and it may also exert a direct intrarenal action. Propranolol and other 13-adrenoceptor-blocking drugs act by blocking the intrarenal and extrarenal 3 receptors involved in the neural control of renin secretion. 

Many investigators have shown heightened sympathetic nerve activity observed in plasma norepinephrine or microneurography in patients with ESRD in cross-sectional studies [20, 21], These observations show renal injury or ESRD is a consequence of hypertension and obesity, however, most of previous studies regarding the relationships between sympathetic nerve activity and renal function have investigated proteinuria or microalbuminuria as a maker for renal injury. Few investigations have simultaneously taken into account... 

The purpose of this article is to provide the current findings on the important, but not fully clarified topics, including the relationships between sympathetic nerve activity and renal injury in hypertension and obesity. To better understand the contribution of the sympathetic nervous system to the onset and the development of renal injury might prevent future ESRD especially in patients with obesity, hypertension and diabetes, and help theoretically rational treatments on those patients with renal injury. 

Sympathetic Nerve Activity and Abnormal Renal-Pressure Natriuresis in Hypertension (Figure 4)... 

The role of the sympathetic nervous system in renal injury, end-stage renal disease, and renovascular hypertension are discussed through a literature review accompanying sympathetic nerve mechanisms in hypertension and obesity. Relevant studies of sympathetic nerve activity and 32-adrenoceptor polymorphism might contribute to the onset and maintenance of renal injury in healthy subjects and in patients with chronic heart failure and cardiovascular events in ESRD patients. A better understanding of the relationships of sympathetic nerve activity with renal injury might help clinical implications (treatment) for renal injury in hypertensive patients and hypertension in patients with ESRD. Recently, the role of denervation of renal sympathetic nerve in refractory hypertension has been examined and showed its efficacy in humans. The outcome from the study have not been established, but a number of animal studies show theoretical benefits for those patients in the acute phase. Further studies are needed to clarify the relationships between the sympathetic nerve activity and renal injury. 

Caffeine consumption appears to have adverse cardiovascular effects including enhanced sympathetic nerve activity and increased pulse pressure and systolic pressure. 

Sympathetic nerve activity causes an increase in blood pressure through many mechanisms, including an increase in cardiac activity and vasoconstriction. Activation of the sympathetic system also causes the stimulation of Pi-adrenergic receptors on the renin-producing cells, which promotes renin release. 

An overall increase in sympathetic nerve activity includes an increase in sympathetic input to the kidneys. Consequently, resistance of the afferent arteriole increases, leading to a decrease in RBF. As discussed, this results in a decrease in PGC, GFR, and urine output. As such, the renal excretion of sodium and water is decreased. In other words, sodium and water are... 

Shen, J., Yao, J. F., Tanida, M., and Nagai, K. (2008). Regulation of sympathetic nerve activity by L-carnosine in mammalian white adipose tissue. Neurosci. Lett. 44,100-104. 

The injection of a vasoconstrictor, which causes an increase in mean arterial blood pressure, results in activation of the baroreceptors and increased neural input to the cardiovascular centers in the medulla oblongata. The reflex compensation for the drug-induced hypertension includes an increase in parasympathetic nerve activity and a decrease in sympathetic nerve activity. This combined alteration in neural firing reduces cardiac rate and force and the tone of vascular smooth muscle. As a consequence of the altered neural control of both the heart and the blood vessels, the rise in blood pressure induced by the drug is opposed and blunted. 

Thus, it seems that the lack of sympathetic nervous system inhibition produced by the vasodilators, which is advantageous in some ways, can also be a disadvantage in that reflex increases in sympathetic nerve activity will lead to hemodynamic changes that reduce the effectiveness of the drugs. Therefore, the vasodilators are generally inadequate as the sole therapy for hypertension. However, many of the factors that limit the usefulness of the vasodilators can be obviated when they are administered in combination with a -adrenoceptor antagonist, such as propranolol, and a diuretic. Propranolol reduces the cardiac stimulation that occurs in response to increases in sympathetic nervous activity, and the... 

The antihypertensive activity of clonidine can be ascribed solely to a decrease in the sympathetic activity transmitted from the brain to the peripheral vasculature. After clonidine administration, direct measurements of sympathetic nerve activity show that electrical discharge is reduced in a number of sympathetic nerves, including the cardiac, splanchnic, and cervical nerves. 

These are the agents which block the action of sympathetic nerve stimulation and circulating sympathomimetic amines on the beta adrenergic receptors. At the cellular level, they inhibit the activity of the membrane cAMP. The main effect is to reduce cardiac activity by diminishing (3 receptor stimulation in the heart. This decreases the rate and force of myocardial contraction of the heart, and decreases the rate of conduction of impulses through the conduction system. They are classified as in table 3.3.2. 

Early evidence that prejunctional histamine H3-receptors may modulate the sympathetic nerve activity on the heart was provided by Luo et al., (1991). These authors clearly stated that the selective H3-agonist (R)a-methylhistamine attenuates the inotropic response induced by transmural stimulation of the adrenergic nerve terminals in the isolated right atrium, without affecting basal contractile force of the preparation or the positive inotropic effect elicited by exogenous noradrenaline. The effect of (R)a-methylhistamine, which is not modified by Hi and H2-receptor blockade, was reversed by the specific H3-receptor antagonist thioperamide, at concentrations which do not influence the inhibitory activity mediated by other presynaptic receptors, like a2-adrenoceptors. 

Contrastingly, it was found that presynaptic histamine H3-receptor activation lowers the hypertensive effect evoked by nicotinic stimulation of sympathetic ganglia (Oudart et al., 1995), or by electrical stimulation of the spinal sympathetic nerves (Malinowska and Schlicker, 1991, Godlewski et al., 1997a). In spontaneously hypertensive rats, these receptors are probably activated by endogenous histamine, since thioperamide increases arterial pressure. Therefore, histamine H3-receptors appear to be operative in hypertension, where histamine could play a modulatory role in the control of sympathetic system hyperreactivity (Godlewski et al., 1997a). 

Seals, D. R., and Victor, R. G. (1991). Regulation of Muscle Sympathetic Nerve Activity During Exercise in Humans. Exerc Sport Sci Rev 19 313—49. 

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