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Hypertension adds to the burden of healthcare problems in the United States. It affects thousands of Americans. According to Magellan Medicaid Administration (2013), every third American has symptoms of hypertension, which greatly increases the risks of developing cardiovascular disease. The current state of pharmacology displays the growing commitment to developing and implementing new classes of drugs that will help to meet the blood pressure target of 140/90 mm Hg in patients (Magellan Medicaid Administration, 2013). Unfortunately, the potential of many pharmacological agents in treating hypertension is either underestimated or poorly understood. Given the profound role played by the sympathetic nervous system in the development of hypertension, central sympatholytic drugs should occupy a better place in hypertension therapy.
Significance of central sympatholytic drugs should be considered in terms of the role the sympathetic nervous system plays in the development of hypertension and cardiovascular disease. Sorota (2014) writes that the sympathetic nervous system is a critical element of all human mechanisms and functions involved in stress adaptation, physical activity, and energy utilization. The system regulates metabolism, temperature, and hemodynamics (Sorota, 2014). Its activation leads to an increase in cardiac contractility, heart rate, salt retention, peripheral resistance, and water retention (Sorota, 2014). It is posible to assume that the sympathetic nervous system is one of the principal drivers of high blood pressure in humans, and it has profound impact on heart and vasculature.
Central sympatholytic drugs are intended to regulate the sympathetic nervous system in ways that reduce the symptoms of hypertension. They were first introduced in the 1960s (Vongpatanasin, Kario, Atlas, & Victor, 2011). The very first sympatholytic drug, ɑ-Methyldopa, was developed to function as a false neurotransmitter. The second-generation alternative, Clonidine, displays a vasoconstrictor effect by stimulating ɑ2-adrenergic receptor (Vongpatanasin et al., 2011). It activates the production of ɑ-methylnorepinephrine that lowers blood pressure (Vongpatanasin et al., 2011). Moreover, central sympatholytic drugs also activate I1 receptors located in the human brain stem, which increase the blood pressure lowering effects of norepinephrine (Vongpatanasin et al., 2011). Such drugs have proved to reduce the muscle sympathetic nerve activity that greatly contributes to the development of hypertension and cardiovascular disease (Hausberg & Grassi, 2004).
While the mechanism of action sounds quite complicated, the pharmacological effects of central sympatholytic drugs on patients can be easily explained. Basically, such drugs reduce the scope of sympathetic activity in the human organism. It is not a secret that increased sympathetic outflow is responsible for numerous functional changes in arteries and myocardium (Hausberg & Grassi, 2004). Sympatholytics reduce sympathetic nerve activity, which is responsible for arterial stiffening, cardiac hypertrophy, and chronic renal failure (Hausberg & Grassi, 2004). Poyhonen-Alho et al. (2008) have also shown that these pharmacological agents can have anti-inflammatory properties, which are particularly helpful for postmenopausal women with hypertension and overweight. Simultaneously, the exact nature of central sympatholytic drugs and their implications for hypertension therapy require further analysis.
Sympatholytic drugs represent a second-line option in hypertension therapy. They also generate an increased professional interest. Magellan Medicaid Administration (2013) refers to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure, which recommends using sympatholytics for patients, who are sensitive to new drugs. Still, their use is limited due to numerous adverse effects they have on the central nervous system, including dizziness and drowsiness (Hausberg & Grassi, 2004). Thus, even though central sympatholytic drugs promise to alleviate the symptoms of hypertension in adult patients, their benefits should be treated with caution. Sympatholytics should occupy a better place in hypertension therapy but only after risks of their adverse health outcomes are minimized.