Cluster Headaches
Alexander R. Toftness in Incredible Consequences of Brain Injury, 2023
We don't yet know exactly what triggers the pain, but one current avenue of research is on a particular kind of vasodilator called calcitonin gene-related peptide, which can be found in the hypothalamus (Carmine Belin et al., 2020). A vasodilator is a chemical that widens blood vessels. It may be this widening, along with neuroinflammation causing additional swelling, that causes the pain behind the person's eye. Infusing calcitonin gene-related peptides into a person who is currently experiencing an active cluster can trigger a headache but infusing them during their remission period does not trigger such an attack (Vollesen et al., 2018). It has also been shown that there are places in a person's genetic code that make them vulnerable to cluster headaches, and those genes seem to be associated with neuroinflammation (O'Connor et al., 2021). Indeed, cluster headaches run in families, where relatives are more likely to experience attacks (Waung et al., 2020).
ENZOGENOL Pine Bark Extract
Dilip Ghosh, Pulok K. Mukherjee in Natural Medicines, 2019
Atherosclerosis is the process of hardening of arterial blood vessel walls and narrowing of the arteries, which may eventually result in cardiovascular diseases (CVD) such as coronary thrombosis, myocardial infarction and stroke. Many complex steps have to occur for this progressive disease to initiate and develop to the stage were atherosclerotic changes of the blood vessels can be diagnosed. These steps involve inflammatory mediators and the immune system, and begin with the interaction of vascular endothelial cells and circulating leukocytes. Leukocytes adhere to the inside of the inflamed vessel wall and transmigrate through the endothelial cell layer into the extracellular matrix. These processes involve several key molecules including the pro-inflammatory cytokine tumour necrosis factor alpha (TNF-α), adhesion factors vascular cell adhesion molecule-1 (VCAM-1), intercellular cell adhesion molecule-1 (ICAM-1) and E-selectin, and the matrix-degrading metalloproteinase 9 (MMP-9) required for monocyte penetration into the vessel wall.
Low magnesium plays a central role in high blood pressure
Kupetsky A. Erine in Magnesium, 2019
Hypertension is associated with stroke and heart disease and continually strains the heart, blood vessels, and kidneys. Hypertension is referred to as the “silent killer,” because it may often go unnoticed, even over the span of years.2 In 2013, about 77.9 million U.S. adults had hypertension.3 The incidence of hypertension continues to rise. From 1999 to 2009, high blood pressure among the U.S. population rose by 17.1% and deaths attributed to hypertension rose by 43.6%.3 Consumption of a mostly “Western diet,” which comprises processed foods that are generally low in both Mg and potassium, may contribute to difficulty in controlling hypertension.4–6 Physicians can play an important role in helping their patients prevent and treat high blood pressure, and knowledge of Mg research in this area is key to the success of both.
Qiqilian ameliorates vascular endothelial dysfunction by inhibiting NLRP3-ASC inflammasome activation in vivo and in vitro
Published in Pharmaceutical Biology, 2023
Yuan Luo, Zhenyuan Tan, Yun Ye, Xiaocong Ma, Guihua Yue
Hypertension is a prevalent cardiovascular disease. Globally, the number of patients with hypertension aged 30–79 has doubled to 1.28 billion since 1990 (NCD-RisC 2021). In patients with hypertension, the continuous increase in arterial pressure damages the blood vessels and impairs the function of many target organs, including the heart, kidneys, and brain, eventually increasing the risk of diseases such as cardiac hypertrophy, cerebral hemorrhage, and atherosclerosis. High blood pressure causes a longer disease course and substantial harm, making it a leading cause of premature death worldwide. The vascular endothelium is the largest endocrine and paracrine organ with crucial and diverse physiological functions. The dysfunction of vascular endothelium owing to organic damage may result in the onset and progression of hypertension. Furthermore, hypertension can cause endothelial damage, thus creating a vicious cycle. Vascular remodelling refers to the adaptive functional and structural alterations that occur in blood vessels in response to the changes in the internal and external environment (Baumbach and Heistad 1989). Vascular remodeling-related disease is regulated by the renin–angiotensin system, inflammatory response, and redox regulation (Whiteford et al. 2016). As a chronic inflammatory condition, the onset and progression of hypertension are also associated with immune hyperactivation and the release of inflammatory mediators in vivo (Vanhoutte et al. 2009).
Targeting VCAM-1: a therapeutic opportunity for vascular damage
Published in Expert Opinion on Therapeutic Targets, 2023
Mayarling F Troncoso, Magda C Díaz-Vesga, Fernanda Sanhueza-Olivares, Jaime A Riquelme, Marioly Müller, Luis Garrido, Luigi Gabrielli, Mario Chiong, Ramon Corbalan, Pablo F Castro, Sergio Lavandero
The cardiovascular system includes the heart and blood vessels that pump and deliver blood throughout the body. Blood vessels are structured in three layers: the tunica intima, media, and adventitia. The tunica intima, or inner layer, comprises endothelial cells (EC) in contact with the blood. The tunica media or medial layer is formed mainly by vascular smooth muscle cells (VSMC) and the extracellular matrix, such as collagen and elastin, that regulates vascular tone and the integrity of vessels. In capillaries, the medial layer does not contain VSMC, but pericytes form a thin wall that facilitates the transport of blood components [3]. The adventitia layer, or outer layer, comprises fibroblasts, nerves, and small arteries (Vasa vasorum) that deliver nutrients to this layer [4].
Factors associated with blood pressure variation in sickle cell disease patients: a systematic review and meta-analyses
Published in Expert Review of Hematology, 2022
Arthemon Nguweneza, Chandré Oosterwyk, Kambe Banda, Victoria Nembaware, Gaston Mazandu, Andre P Kengne, Ambroise Wonkam
SCD patients show substantial heterogeneity in the presentation and clinical course of the disease [2]. Typically, the pathobiology of SCD is a vicious cycle of four major processes. First, under deoxygenation conditions, HbS molecules polymerize to form bundles. The polymer bundles form long fibers that impair the erythrocyte membrane, leading to erythrocyte sickling. Second, the normally freely flowing cytosol of the erythrocyte becomes viscous making the cell much less deformable. This leads to the blockage of blood vessels, disrupting the blood supply, referred to as vaso-occlusion. Thirdly, the polymer bundles also promote hemolysis causing chronic anemia with Hb levels ranging from 6 to 11 g/dl. The severity of this anemia is dependent on primary genotype and genetic modifiers of fetal hemoglobin levels, the strongest known modifier of the SCD clinical expression. Patients with higher rates of hemolysis are more likely to develop vascular injury and multi-organ dysfunction. Finally, hemolysis by-products such as erythrocyte damage-associated molecular patterns (eDAMPS) along with ischemia-reperfusion injury caused by vaso-oclussion, promote sterile inflammation and oxidative stress. These events further amplify vaso-occlusion through a feedback loop by promoting adhesion of neutrophils, platelets, and endothelial cells. These molecular, cellular, and biophysical processes work in synergy to promote acute and chronic pain, ischemic reperfusion injury, and infarctions of vital organs, such as spleen, heart, kidneys, liver, muscle, brain, lung, and bone.