Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic locus identified has shown an association with DNA methylation at multiple nearby CpG sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.
In hypertensive emergency, there is evidence of direct damage to one or more organs. The most affected organs include the brain, kidney, heart and lungs, producing symptoms which may include confusion, drowsiness, chest pain and breathlessness. In hypertensive emergency, the blood pressure must be reduced more rapidly to stop ongoing organ damage, however, there is a lack of randomized controlled trial evidence for this approach.
A slow heart rate (bradycardia) can decrease the amount of blood pumped by the heart. The resting heart rate for a healthy adult is between 60 and 100 beats/minute. Bradycardia (resting heart rates slower than 60 beats/minute) does not always cause low blood pressure. In fact, some highly trained athletes can have resting heart rates in the 40s and 50s (beats per minute) without any symptoms. The slow heart rates are offset by more forceful contractions of the heart that pump more blood than in non-athletes. However, in many patients bradycardia can lead to low blood pressure, lightheadedness, dizziness, and even fainting.
3. Implement strategies to lower inflammation. Several cross-sectional and longitudinal studies connect high blood pressure with chronic inflammation, a driving force for nearly every disease on the planet. Lowering inflammation starts with what you put on your fork. Focus on anti-inflammatory foods like wild-caught seafood (rich in omega-3 fatty acids), freshly ground flax and chia seeds, spices like turmeric, and plenty of colorful plant foods. Good sleep, stress management, exercise, and the right nutrients can also help lower inflammation.
Hypertension with certain specific additional signs and symptoms may suggest secondary hypertension, i.e. hypertension due to an identifiable cause. For example, Cushing's syndrome frequently causes truncal obesity, glucose intolerance, moon face, a hump of fat behind the neck/shoulder (referred to as a buffalo hump), and purple abdominal stretch marks. Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis (RAS) may be associated with a localized abdominal bruit to the left or right of the midline (unilateral RAS), or in both locations (bilateral RAS). Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt ("paroxysmal") episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.
In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal. There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension. These individuals develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age. Whether this pattern is typical of all people who ultimately develop hypertension is disputed. The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles, although a reduction in the number or density of capillaries may also contribute.
Stress reduction techniques such as biofeedback or transcendental meditation may be considered as an add-on to other treatments to reduce hypertension, but do not have evidence for preventing cardiovascular disease on their own. Self-monitoring and appointment reminders might support the use of other strategies to improve blood pressure control, but need further evaluation.
This study is exploring whether use of losartan, a medicine commonly used to lower blood pressure, is effective at treating abnormal nighttime blood pressure in children and young adults who have sickle cell disease. To participate in this study, you or your child must be 5 to 25 years old and have high blood pressure and a certain type of sickle cell disease: hemoglobin SS or Sβ0 thalassemia. This study is located in Birmingham, Alabama.
Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol. 2017; pii: S0735-1097(17)41519-1. PMID: 29146535 www.ncbi.nlm.nih.gov/pubmed/29146535.