Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An estimated 70-87% of patients who suffer from posttraumatic stress disorder (PTSD) experience sleep disruption. These patients have distressing dreams or nightmares in which the traumatic event is reexperienced, and they also have difficulty in falling or staying asleep. Selective serotonin reuptake inhibitors are the treatment of choice for PTSD, but with the exception of fluvoxamine, they are often ineffective or only partially effective for sleep problems. Sedative-hypnotics may be helpful in the short term but are associated with tolerance and addiction potential. In the central nervous system, alpha(1)-adrenergic receptors are known to be important in both the startle and sleep responses. Stimulation of these receptors may contribute to PTSD-related trauma-content nightmares. Prazosin, a highly lipophilic alpha(1)-adrenergic receptor blocker that is traditionally used to treat hypertension and benign prostatic hyperplasia, has been shown to decrease the occurrence of trauma nightmares in both combat veterans and patients with non-combat-related PTSD. The available data, although mostly from open-label trials, suggest that this agent also improves sleep quality and patients' sense of wellbeing and ability to function in daily activities. The optimum dose is unknown; however, a dose-related response appears to be evident. Clinicians should monitor for orthostatic hypotension, usually seen early in therapy, when prazosin is started in patients with PTSD.
 ...
PMID:Prazosin for the treatment of posttraumatic stress disorder sleep disturbances. 1844 62

A 42-year-old right-handed man with major depression, posttraumatic stress disorder, gastroesophageal reflux disease, and hypertension received 7 treatments of right unilateral electroconvulsive therapy, with the only complications being elevated blood pressure up to 180/120 mm Hg and agitation upon awakening. During eighth treatment, he experienced blood pressures as high as 210/130 mm Hg with severe agitation upon awakening from anesthesia followed by pulmonary edema. Pulmonary edema is rarely seen as a complication in electroconvulsive therapy, but if the airway becomes obstructed or there is excessive sympathetic discharge during the procedure, pulmonary edema may be more likely to occur.
 ...
PMID:Pulmonary edema after electroconvulsive therapy. 1861 64

The clinical literature increasingly indicates that cardiovascular risk factors and cardiovascular disease (CVD) are more common among individuals with posttraumatic stress disorder (PTSD). Depression also poses a risk for CVD and is often comorbid with PTSD. Research to date has not established whether PTSD is associated with additional CVD risk beyond the risks associated with comorbid depression. The authors examined relationships of lifetime PTSD and depression with high blood pressure in data from the US National Comorbidity Survey. They divided participants into 4 mutually exclusive diagnostic groups: (1) PTSD history and no depression history, (2) PTSD and depression history, (3) depression history and no PTSD history, and (4) no history of mental disorder. Hypertension prevalence was higher for the PTSD, no depression and PTSD plus depression groups compared with the depression only and no mental disorder groups. PTSD appears to be related to hypertension independent of depression. This may partially explain elevated rates of CVD in PTSD patients.
 ...
PMID:Hypertension in relation to posttraumatic stress disorder and depression in the US National Comorbidity Survey. 1906 71

The gradual emergence of symptoms following exposure to traumatic events has presented a major conceptual challenge to psychiatry. The mechanism that causes the progressive escalation of symptoms with the passage of time leading to delayed onset post-traumatic stress disorder (PTSD) involves the process of sensitization and kindling. The development of traumatic memories at the time of stress exposure represents a major vulnerability through repeated environmental triggering of the increasing dysregulation of an individual's neurobiology. An increasing body of evidence demonstrates how the increased allostatic load associated with PTSD is associated with a significant body of physical morbidity in the form of chronic musculoskeletal pain, hypertension, hyperlipidaemia, obesity and cardiovascular disease. This increasing body of literature suggests that the effects of traumatic stress need to be considered as a major environmental challenge that places individual's physical and psychological health equally at risk. This broader perspective has important implications for developing treatments that address the underlying dysregulation of cortical arousal and neurohormonal abnormalities following exposure to traumatic stress.
 ...
PMID:The long-term costs of traumatic stress: intertwined physical and psychological consequences. 2014 46

Persistent pain, disability, and depression are hallmarks for chronic pain. While disparities based upon race, gender, and class are documented, little is known about pain disparities in minority men. This investigation examines black (6.2%) and white (93.8%) men (N = 1650) presenting for initial assessment at a tertiary care pain center. Racial comparisons utilized analysis of variance; all variables of interest were then placed in a theoretical model using path analysis. The model included race, age, education, neighborhood income, marital status, litigation, substance use, and high blood pressure as predictors and pain, depression, affective distress, posttraumatic stress disorder (PTSD), and disability as outcomes. Black race was associated with lower neighborhood income, education and marriage rates, and higher rates of litigation and high blood pressure. Black men also had higher pain (affective and miscellaneous), disability, and depression. Path analysis found black race was a direct predictor of greater pain, and through pain, was an indirect predictor of depression, affective distress, PTSD, and disability. Path analysis confirmed the complexity of relationships and supported using techniques to understand these relationships. Our data highlight disparities in the pain experience for black men. They also elucidate potential mechanisms through which disparities work in vulnerable and understudied populations.
 ...
PMID:The impact of chronic pain on the health of black and white men. 2043 39

In hypertension, there is an autonomic imbalance in which sympathetic activity dominates over parasympathetic control. Parasympathetic activity to the heart originates from cardiac vagal neurons located in the nucleus ambiguus. Presympathetic neurons that project to sympathetic neurons in the spinal cord are located in the ventral brainstem in close proximity to cardiac vagal neurons, and many of these presympathetic neurons are catecholaminergic. In addition to their projection to the spinal cord, many of these presympathetic neurons have axon collaterals that arborize into neighboring cardiorespiratory locations and likely release norepinephrine onto nearby neurons. Activation of alpha(2)-adrenergic receptors in the central nervous system evokes a diverse range of physiological effects, including reducing blood pressure. This study tests whether clonidine, an alpha(2)-adrenergic receptor agonist, alters excitatory glutamatergic, and/or inhibitory GABAergic or glycinergic synaptic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. Cardiac vagal neurons were identified in an in vitro brainstem slice preparation, and synaptic events were recording using whole cell voltage clamp methodologies. Clonidine significantly inhibited GABAergic neurotransmission but had no effect on glycinergic or glutamatergic pathways to cardiac vagal neurons. This diminished inhibitory GABAergic neurotransmission to cardiac vagal neurons would increase parasympathetic activity to the heart, decreasing heart rate and blood pressure. The results presented here provide a cellular substrate for the clinical use of clonidine as a treatment for hypertension as well as a role in alleviating posttraumatic stress disorder by evoking an increase in parasympathetic cardiac vagal activity, and a decrease in heart rate and blood pressure.
 ...
PMID:Clonidine, an alpha2-receptor agonist, diminishes GABAergic neurotransmission to cardiac vagal neurons in the nucleus ambiguus. 2055 74

Studies on various medical conditions have shown that poor health is associated with lower parasympathetic tone. People with epilepsy appear to have decreased parasympathetic tone, with a greater decrease in those with intractable seizures than in those with well-controlled epilepsy. Slow breathing exercises have been shown to increase parasympathetic tone in healthy volunteers. Slow breathing exercises have been shown to improve a number of medical conditions including asthma, hypertension, anxiety states, and posttraumatic stress disorder. We hypothesize that slow breathing exercises in people with epilepsy can lead to an increase in parasympathetic tone and an accompanying reduction in seizure frequency. The slow breathing exercises, probably through baroreceptors, chemoreceptors, and pulmonary stretch receptors, affect cortical activity and hence seizure thresholds. It is also possible that slow breathing exercises might reduce seizure frequency by reducing anxiety. The hypothesis can be tested by employing devices and protocols that have been used to reduce breathing rates and have been shown to improve health outcomes in other medical conditions.
 ...
PMID:Can slow breathing exercises improve seizure control in people with refractory epilepsy? A hypothesis. 2063 Aug 7

Norepinephrine receptors have been studied in emotion, memory, and attention. However, the role of alpha1-adrenergic receptors in fear conditioning, a major model of emotional learning, is poorly understood. We examined the effect of terazosin, an alpha1-adrenergic receptor antagonist, on cued fear conditioning. Systemic or intra-lateral amygdala terazosin delivered before conditioning enhanced short- and long-term memory. Terazosin delivered after conditioning did not affect consolidation. In vitro, terazosin impaired lateral amygdala inhibitory postsynaptic currents leading to facilitation of excitatory postsynaptic currents and long-term potentiation. Since alpha1 blockers are prescribed for hypertension and post-traumatic stress disorder, these results may have important clinical implications.
 ...
PMID:Antagonism of lateral amygdala alpha1-adrenergic receptors facilitates fear conditioning and long-term potentiation. 2087 Jul 45

Poor adaptation to stress, alterations in cerebrovascular function and excessive brain inflammation play critical roles in the pathophysiology of many psychiatric and neurological disorders such as major depression, schizophrenia, post traumatic stress disorder, Parkinson's and Alzheimer's diseases and traumatic brain injury. Treatment for these highly prevalent and devastating conditions is at present very limited and many times inefficient, and the search for novel therapeutic options is of major importance. Recently, attention has been focused on the role of a brain regulatory peptide, Angiotensin II, and in the translational value of the blockade of its physiological AT(1) receptors. In addition to its well-known cardiovascular effects, Angiotensin II, through AT(1) receptor stimulation, is a pleiotropic brain modulatory factor involved in the control of the reaction to stress, in the regulation of cerebrovascular flow and the response to inflammation. Excessive brain AT(1) receptor activity is associated with exaggerated sympathetic and hormonal response to stress, vulnerability to cerebrovascular ischemia and brain inflammation, processes leading to neuronal injury. In animal models, inhibition of brain AT(1) receptor activity with systemically administered Angiotensin II receptor blockers is neuroprotective; it reduces exaggerated stress responses and anxiety, prevents stress-induced gastric ulcerations, decreases vulnerability to ischemia and stroke, reverses chronic cerebrovascular inflammation, and reduces acute inflammatory responses produced by bacterial endotoxin. These effects protect neurons from injury and contribute to increase the lifespan. Angiotensin II receptor blockers are compounds with a good margin of safety widely used in the treatment of hypertension and their anti-inflammatory and vascular protective effects contribute to reduce renal and cardiovascular failure. Inhibition of brain AT(1) receptors in humans is also neuroprotective, reducing the incidence of stroke, improving cognition and decreasing the progression of Alzheimer's disease. Blockade of AT(1) receptors offers a novel and safe therapeutic approach for the treatment of illnesses of increasing prevalence and socioeconomic impact, such as mood disorders and neurodegenerative diseases of the brain.
 ...
PMID:Blockade of brain angiotensin II AT1 receptors ameliorates stress, anxiety, brain inflammation and ischemia: Therapeutic implications. 2103 50

Brain inflammation has a critical role in the pathophysiology of brain diseases of high prevalence and economic impact, such as major depression, schizophrenia, post-traumatic stress disorder, Parkinson's and Alzheimer's disease, and traumatic brain injury. Our results demonstrate that systemic administration of the centrally acting angiotensin II AT(1) receptor blocker (ARB) candesartan to normotensive rats decreases the acute brain inflammatory response to administration of the bacterial endotoxin lipopolysaccharide (LPS), a model of brain inflammation. The broad anti-inflammatory effects of candesartan were seen across the entire inflammatory cascade, including decreased production and release to the circulation of centrally acting proinflammatory cytokines, repression of nuclear transcription factors activation in the brain, reduction of gene expression of brain proinflammatory cytokines, cytokine and prostanoid receptors, adhesion molecules, proinflammatory inducible enzymes, and reduced microglia activation. These effects are widespread, occurring not only in well-known brain target areas for circulating proinflammatory factors and LPS, that is, hypothalamic paraventricular nucleus and the subfornical organ, but also in the prefrontal cortex, hippocampus, and amygdala. Candesartan reduced the associated anorexic effects, and ameliorated associated body weight loss and anxiety. Direct anti-inflammatory effects of candesartan were also documented in cultured rat microglia, cerebellar granule cells, and cerebral microvascular endothelial cells. ARBs are widely used in the treatment of hypertension and stroke, and their anti-inflammatory effects contribute to reduce renal and cardiac failure. Our results indicate that these compounds may offer a novel and safe therapeutic approach for the treatment of brain disorders.
 ...
PMID:Angiotensin II AT1 receptor blockade ameliorates brain inflammation. 2115 Sep 13


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>