1.
Pathophysiology of essential hypertension: an update.
Saxena, T, Ali, AO, Saxena, M
Expert review of cardiovascular therapy. 2018;(12):879-887
Abstract
Hypertension is caused by increased cardiac output and/or increased peripheral resistance. Areas covered: The various mechanisms affecting cardiac output/peripheral resistance involved in the development of essential hypertension are covered. These include genetics; sympathetic nervous system overactivity; renal mechanisms: excess sodium intake and pressure natriuresis; vascular mechanisms: endothelial cell dysfunction and the nitric oxide pathway; hormonal mechanisms: the renin-angiotensin-aldosterone system (RAAS); obesity, obstructive sleep apnea (OSA); insulin resistance and metabolic syndrome; uric acid; vitamin D; gender differences; racial, ethnic, and environmental factors; increased left ventricular ejection force and hypertension and its association with increased basal sympathetic activity - cortical connections. Expert commentary: Maximum association of hypertension is found with sympathetic overactivity which is directly or indirectly involved in different mechanisms of hypertension including RAAS, OSA, obesity, etc.. It is not overt sympathetic activity but disturbed basal sympathetic tone. Basal sympathetic tone arises from hypothalamus; possibly affected by cortical influences. Therefore, hypertension is not merely a disease of circulatory system alone. Its pathogenesis involves alteration in ANS (autonomic nervous system) and likely in cortical-hypothalamic connections. Assessment of ANS and cortical-hypothalamic connections may be required for better understanding of hypertension.
2.
Chapter 7 Investigations on the Relationship Between the Autonomic Nervous System and the Triggering of Malignant Hyperthermia: A State-of-the-Science Review.
Perry, SM
Annual review of nursing research. 2014;:135-54
Abstract
Early research in malignant hyperthermia (MH) focused on the autonomic nervous system (ANS) as a primary trigger of the syndrome. This hypothesis was based on the initial signs and symptoms of MH such as tachycardia, cardiac arrhythmias, hypertension, and signs of increased metabolism in patients who developed MH. Supporting these early links between MH and the ANS were case reports from anesthesia providers who reported that patients who subsequently developed MH after a nontriggering previous anesthetic had appeared unusually stressed prior to the surgical procedure in which they triggered. There is no disagreement in the scientific community that a primary disorder in MH lies in the inability to control myoplasmic calcium levels in skeletal muscles. However, considering the variability in genetic and clinical presentation, the timing of intraoperative triggering, and the unexplained phenomenon of nonanesthetic triggering, the identification of cofactors in MH triggering remains paramount. A careful review of existing research supports the hypothesis that the autonomic nervous system plays a significant role as a cofactor in the triggering and progression of an MH episode. If a differentiation can be made and a link can be demonstrated between abnormalities in receptor sensitivity for or release, reuptake, or metabolism of catecholamines in malignant hyperthermia susceptible individuals, we may be able to use these as additional markers/predictors of disease.