Central Nervous System Circuitry and Peripheral Neural Sympathetic Activity Responsible for Essential Hypertension

Abstract

Both clinical and experimental studies dealing with patients affected by idiopathic or essential hypertension (EH) are devoted to the great deal of physiological, pharmacological and pathological as well as therapeutical issues of EH. However, most articles devoted to EH do not refer to the central nervous system mechanisms underlying this disease and the channels which allow that these mechanisms are funneled to the peripheral autonomic nervous system and trigger this cardiovascular disorder. In the present review article we attempted to reach this target devoted to the central nervous system circuitry involved in the cardiovascular pathophysiology. We postulated that EH depends on the predominance of the binomial A5 noradrenergic (NA) nucleus + median raphe serotonergic (5-HT) nucleus over the (A6)-NA + dorsal raphe-5HT nuclei. This hypothesis receives additional support from our results obtained throughout the neuropharmacological therapy of this type of neurophysiological disorder. Our therapeutical strategy is addressed to enhance the activity of the (A6)-NA + dorsal raphe-5HT binomial circuitry.

Central Nervous System Plus Autonomic Nervous System Disorders Responsible for Gastrointestinal and Pancreatobiliary Diseases

“…Furthermore, considering that both CNS nuclei interchange inhibitory axons, alpha-2 agonists and/or antagonists are able to revert the physiological predominance of any of both systems. In addition, it is important to know that whereas the C1-Ad nuclei are positively correlated with the dorsal raphe (DR) serotonergic nucleus, the A5-NA nucleus parallels the activity of the median raphe (MR) serotonergic nucleus (MR-5HT) [103,104]. Finally, it should be known that both serotonergic nuclei interchange inhibitory axons.…”

“…Finally, it should be known that both serotonergic nuclei interchange inhibitory axons. Summarizing the above, it has been established that whereas the DR-5HT + C1-Ad hyperactivity is responsible for the uncoping stress syndrome, the MR-5HT + A5-NA binomial predominates in patients affected by endogenous depression as well as in patients affected by neural sympathetic overactivity (essential hypertension, hyperinsulinism, rheumatoid arthritis, and all TH-1 autoimmune diseases) [3,24,[101][102][103][104][105]. At the gastrointestinal level, patients with reflux esophagitis [81,82] Figs.…”

Central Nervous System Circuitries Underlying Two Types of Peripheral Autonomic Nervous System Disorders~!2008-04-24~!2008-09-26~!2008-12-05~!

“…Finally, the above tests have been carried out during both relapsing and remission periods. The information derived from that research work has allowed us to understand the pathophysiological mechanisms which underlie most type of diseases: gastrointestinal, cardiovascular, endocrinological, neurological, psychiatric and others; and in addition, to be the first to demonstrate the neuroautonomic profiles which *Address correspondence to this author at the Departments of Neurophysiology, Neurochemistry, Neuropharmacology and Neuroimmunology, Instituto de Medicina Experimental, Faculty of Medicine, Universidad Central de Venezuela, Caracas, Venezuela; E-mail: flechin@movistar.net.ve underlie psychosis [20][21][22][23], endogenous depression [4,24], hyperinsulinism [8, [24][25][26][27][28][29][30][31], biliary dyskinesia [32][33][34], ulcerative colitis [35], infertility [26,36], duodenal ulcer and gastritis [37,38], irritable bowel syndrome [39][40][41][42][43], Crohn's diseases [44,45], pancreatitis [45][46][47][48], essential hypertension [6, 49,50], thrombocytopenic purpura [51], polycythemia vera [52], myasthenia gravis [53], reactive hypoglycemia [8], cardiovascular and pulmonary disorders [53]<...>…”

Effect of Tianeptine on Glucose Tolerance with Insulin Secretion in Human: Potential Anti-Diabetic Effect of the Drug

“…With respect to the above, it should be known that the C1(Ad) nuclei interchanges inhibitory axons with A5(NA) pontomedullary nucleus, responsible for neural sympathetic activity [45,46] thus, the disappearance of the activity of the former, triggered by tianeptine minimized the peripheral adrenal sympathetic drive and favored the absolute predominance of the neural sympathetic activity registered in the present study. With respect to the latter, exhaustive evidence has demonstrated that insulin crosses the blood brain barrier and excites the A5(NA) nucleus responsible for the activity of sympathetic nerves [9,[47][48][49]. It is well known that at CNS level, tianeptine triggers the absolute disappearance of 5-HT from synaptic clefts.…”