Alpha2-adrenoceptor and adenosine A1 receptor within the nucleus tractus solitarii in hypertension development

- We review alpha2-adrenoceptor and A1 adenosine receptor within the nucleus tractus solitarii.
- Alterations in receptor distribution and function are discussed in rat models of hypertension.
- Opposing alterations in the binding of these receptors co-localizes to specific NTS subnuclei.
- Alpha2-adrenoceptor has an altered sensitivity and regiospecificity of number and affinity.
- Altered cross-talk between these receptor systems may be important to hypertension development.

Alpha2-adrenoceptor and A1 adenosine receptor systems within the nucleus tractus solitarii (NTS) play an important role in cardiovascular control. Deregulation of these systems may result in an elevated sympathetic tone, one of the root causes of neurogenic hypertension. The dorsomedial/dorsolateral and subpostremal NTS subnuclei of spontaneously hypertensive rats (SHR) show density changes in both receptors, even at 15 days of age, prior to the onset of hypertension. In addition, adenosine A1 receptors have been specifically reported to modulate alpha2-adrenoceptors in several brain regions, including the NTS, via a PLC-dependent pathway involving cross regulation between sympathetic neurons and astrocytes. The physiological cross talk between these receptor systems is also deregulated in SHR suggesting that alpha2-adrenoceptor and A1 adenosine receptor might be germane to the development of hypertension. In this review, we will focus on these systems within the NTS during development, pointing out some interesting modulations in processes, and chemical changes within specific subnuclei of NTS circuitry, that might have implications for neurogenic hypertension.