Adenosine is part of a group of substances that act as endogenous modulators, involved in the regulation of physiological activity in many organs and tissues. Currently, this substance is extensively studied for therapeutic purposes, specifically those related to cardiovascular control. It is known that the nucleus of the solitary tract (NTS) is one of the most important neural centers related to cardiovascular control mediating instant adjustments of heart rate and blood pressure in various behavioral situations, thus in maintaining body homeostasis. Adenosine, within the NTS, acts as a potent modulator of hemodynamic activity of the sympathetic nervous system. The activation of its receptors directly influences the action of other neurotransmitters and receptors, exhibiting a powerful modulatory action on cardiovascular control. It is also known that adenosine receptors are increased in the NTS of spontaneously hypertensive rats (SHR), suggesting a role of this nucleoside on the genesis of hypertension. Nitric oxide (NO) also plays an important role in cardiovascular control within the NTS by acting as a hypotensive agent. It is also known that NO synthesis is altered in the NTS of SHR, suggesting an important contribution of this molecule on blood pressure control and the development of hypertension. The relationship between NO and adenosine in the peripheral system is already well established in the literature. It is known that adenosine stimulates NO production. However, this interaction within the NTS is not well explored. Thus, the objective of our work is to analyze in vivo the effect of knockdown of adenosine receptors, A1R and A2AR, on the mRNA of the enzyme neuronal nitric oxide synthase (nNOS) in normotensive (WKY) and hypertensive (SHR) rats.
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