Association between ADD1 Gly460Trp Polymorphism and Essential Hypertension in Han Chinese

Essential hypertension (EH) is an important worldwide public health issue which contributes to the burden of heart disease, stroke and kidney failure and premature mortality and disability. It disproportionately affects populations in low- and middle-income countries where health systems are weak. EH is a complex disorder resulting from genetic and environmental factors, as well as their interactions. 

 

Essential Hypertension

Approximately 20-60% of the blood pressure variability in general population is heritable. Human ADD1 gene, located on chromosome 4p16.3, encodes one of adducin subunits (α-adducin). Adducin modulates the surface expression of multiple transporters and ion pumps, and thus regulates cellular signal transduction and cytolemma ion transport. Human and animal model studies have found that ADD1 gene is a candidate gene for EH. Read More>>>>>>>>>>>

Who is the Patient with Suspected White Coat Hypertension?

White coat hypertension (WCH) is the situation in which an individual has high blood pressure (BP) in the medical office (BP >140/90) and normal BP outside the office (BP <135/85). Masked hypertension (MHT) is the opposite of WCH, i.e., a situation in which a person has normal BP in the office and high BP outside of it. 

White Coat Hypertension

The overall prevalence of WCH is approximately 15%. However, in extreme situations, as in the case of suspected resistant hypertension, the prevalence of WCH reaches 40%. Among the many indications of Ambulatory Blood Pressure Monitoring (ABPM), the main one is to assess patients with suspected WCH , being also indicated to evaluate the white coat effect on hypertensive patients using antihypertensive drugs, whose BP levels measured in the office remain high despite anti-hypertensive therapy. As the white-coat effect is common among the elderly, this is a group where this assessment is often indicated. Read more>>>>>>>>>>

Determination of Ghrelin’s Role in the Pathogenesis of Pregnancy Induced Hypertension

Pregnancy induced hypertension (PIH) is a disease of an unclear etiology that complicates 2-3 % of pregnancies. PIH is a critical cause of perinatal mortality of pregnant women and neonates and a major cause of in trauterine growth retardation and of iatrogenic prematurity. PIH is a multiorgan complication; its main causes result from the interaction of the mother’s immunological system with trophoblast antigens. 

Pregnancy Induced Hypertension

The ethiopathogenesis of pregnancy induced hypertension remains to be elucidated. A crucial risk factor of pregnancy induced hypertension is obesity. Relationships between hypertension and obesity are well documented, ultimately involving excessive retention of sodium by the kidneys, insulin resistance, and chronic stimulation of the sympathetic system, leading to vessel remodelling. Read more>>>>>>

Role of Dietary Components in Modulating Hypertension

Hypertension is estimated by the Centers for Disease Control and Prevention to affect approximately 30% of adults in theUnited States. It is a significant factor in the pathogenesis of a number of diseases, including obesity, cardiovascular disease, and stroke. 

Hypertension itself can be caused by unhealthy lifestyle habits like alcoholism, drug addiction, smoking, high stress, or obesity, and certain non-modifiable attributes like age, gender, hereditary and genetic constitution, and racial or ethnic disparities. Hypertension to an extent correlates to the prevailing socioeconomic and geographical characteristics of a region, as well as to individual behavioral factors, and can pose a significant public health concern in populations defined by economic hardship, poverty, reduced health care access, low health literacy, and lack of resources due to geographic isolation.  Read more>>>>>>>>>>>>>>

Twelve Month Follow-Up Audit of Nigerian Hypertensives on Back Titration

The question of whether pharmacotherapy for systemic arterial hypertension should be life-long has continued to agitate the mind of care givers and patients alike. Whereas it is possible in some cases to reduce dose or discontinue drug(s) outright, relapse of high blood pressure is known to occur after some time. 

All the same, the attitude of step down or outright discontinuation of anti-hypertensive pharmacotherapy appears to be safe provided close monitoring continued. In an audit of hypertension care in a specialized care facility, the author observed that some patients remained controlled despite self-imposed drug holidays or physician initiated dose reduction following therapy induced hypotensive features. Some earlier workers had called for future studies to shed light on how long and intensively hypertensives could be treated before discontinuation of therapy can be embarked upon.  Read more>>>>>>>>>>>>

Can the Intensive Blood Pressure Control in Diabetes Reduce Left Ventricular Hypertrophy ?

Left ventricular hypertrophy (LVH) is a common complication of hypertension and has been associated with higher risk for targetorgan damage. 

Insulin resistance and type2 diabetes mellitus (DM), myocardial infarction(MI), cardiomyopathy, coronaryartery disease( CAD) is reported to be associated LVH. LVH is a maladaptive response to chronic pressure overload and an important risk factor for atrial fibrillation, diastolic and systolic heart failure, and sudden death in patients with hypertension. Echocardiographic assessment of LVH has a high specificity and sensitivity (≥ 80%). The presence of LV hypertrophy is often considered when LV mass >116 g/m2 for men (M) and >104 g/m2 for women (W), or >125 g/m2 for M and W. Read more>>>>>>>>>>>

Cilnidipine, An L-/N-Type Calcium Channel Blocker, Changes the Circulating Angiotensin?(1-7)/Angiotensin II Ratio

Angiotensin-converting enzyme (ACE) 2 is a newly recognized ACE homolog within the renin-angiotensin system (RAS) that is produced and secreted by a variety of cell types. Although ACE2 may act onseveral substrates, it exhibits high catalytic efficiency, specifically for the hydrolysis of angiotensin (Ang) II to the vasodilator and growth inhibitor heptapeptide Ang-(1-7). 

Previous reports have suggested that Ang-(1-7) exerts vasodilatory effects through a combination of ACE inhibition and angiotensin type 1 receptor (AT1R) blockade. Taken together, these studies suggest that the regulation of Ang-(1-7) production by ACE2 may be an important component of not only blood pressure control but also vascular remodeling because Ang-(1-7) opposes the actions of Ang II in both cases. According to this novel concept, the final functional effects of the RAS may reflect a balance between the ACE-Ang II-AT1R arm and the ACE2-Ang-(1-7)- Mas receptor arm. Read more>>>>>>>>>>>>>>