Etiology of hypertension new discovery

To middle-aged people, the increased blood pressure often, and even lead to heart and circulatory system diseases. However, what causes hypertension, or people so far only superficial knowledge. For example, we all know that, in most cases of hypertension are due to hardening of the blood vessels, vascular cross-sectional area decreases caused. However, why would vascular sclerosis this issue, it does not seem clear. Recently, German Technical University of Munich Drug Institute’s scientists have been made to answer, and their research results published in the March issue of “Nature” magazine.

They found the body in the name of IRAG discovered a protein, this protein can make vascular softened, thus increasing vascular cross-sectional area to reduce blood pressure. However, once the IRAG disrupts the function of vascular not be its role, has begun to harden. To the University Hoffman (Hofman) headed by Professor researchers found that protein can hinder IRAG vascular muscle cells in the release of calcium, and calcium content reduced, it will cause the blood vessels to soften. They also found that, in addition to renal arteries as a result of tightening of hypertension, the other causes of hypertension are thus formed. Therefore, they believe that this discovery will contribute to the future development of new prevention and treatment of hypertension drugs.

However, you should not have this new found that the treatment of hypertension can be easily handled, Professor Professor Hoffman said, usually from a new discovery really started to research into new drugs, need at least 10 hours, so, for us, or attention should be paid to physical activity and health is being strokes.

Renovascular hypertension pathology

Renovascular hypertension due to ischemia caused renin - angiotensin - aldosterone axis and the activation. The renal perfusion due to a decrease in the release of renin, renin angiotensin reasons prompted into angiotensin Ⅰ, angiotensin Ⅰ the conversion of angiotensin-converting-enzyme angiotensin Ⅱ. Angiotensin Ⅱ is a strong Vasoconstrictor, angiotensin Ⅱ (A Ⅱ) can also stimulate the adrenal gland secretion of aldosterone, which have sodium retention.
Renal artery occlusive disease incidence can be unilateral or bilateral, or occurred in patients with kidney alone, because different types of renal vascular hypertension pathophysiology not the same. In the renal mode (renal, a clamp-type kidney), renal ischemia Shuinazhuliu lead to the release of renin, but normal contralateral kidney will pressure sodium row of the diuretic, so that patients actually negative sodium balance, has further increased the renin release. Kidney in a single mode (single kidney, renal clamp-type), not the impact of the contralateral kidney, thereby preventing the loss of sodium, extracellular fluid volume increase in the number of blood renin inhibition activity, such patients with high blood pressure main is caused by excessive fluid. Patients with renal artery stenosis with a similar situation.

Pathophysiological mechanism of hypertension

Essential hypertension is a kind of interaction of multiple factors leading to disease, including such factors as changes in gene structure and the function of the mechanism of change and the environment, and other factors. Most of the studies show that hypertension is a multi-gene genetic diseases, there are many candidate genes in the study.
From the point of view of physiology, and pathogenesis of essential hypertension in the final mechanism of peripheral blood would lead to increased tension. These include the pathogenesis of sympathetic activity increased renin - angiotensin system changes, nitric oxide and endothelin-such as the imbalance of vasoactive cells cationic changes, and so on, these are the current research. Many environmental factors, such as salt intake, depression and obesity and hypertension are also relevant.

Correct blood pressure measurement?

We now are widely used blood pressure measurement method is the application of vascular compression sleeve bring pressure methods. Inflatable, once the cuff pressure over artery systolic pressure, pressure vessel was closed, blood flow was blocked, the distal vascular artery pulsatility heard on the sound. Deflated later, when the cuff pressure within the artery systolic pressure below Vascular open, restore blood flow, arterial pulse generated sound, the sound heard artery pulsatility (auscultation audio), which is the pressure within the cuff pressure. Continue to deflated when the cuff pressure lower than diastolic blood pressure, blood vessels completely unobstructed, blood flow was no longer blocked artery pulsatility sound disappeared, at the cuff, which is the diastolic pressure. DBP to children artery pulsatility tone suddenly changed hours to determine more accurately the pressure. Because blood pressure measurement by many external factors, so the correct blood pressure measurement to perform the following tasks:

(1) choose a suitable device: general is the most commonly used mercury sphygmomanometer, the barometer of the device and electronic sphygmomanometer also commonly used. Sphygmomanometer cuff width of the upper arm should be able to cover the length of 2 / 3, the length of the cuff at the same time the need to arm circumference of the 2 / 3. If it is too narrow cuff blood pressure measured at the high cuff too long, measured blood pressure was lower.

(2) choose a suitable pressure environment: Patients should be in a quiet, temperature appropriate environment rest 5-10 minutes, with the sleeves of the arms should not be unduly fettered avoid under stress such as bladder filling or smoking, Daohan, a cup of coffee after manometry.

(3) the pressure to choose the correct steps: Patients admitted seat, the arm should be measured exposed, palms upward Horizontal, in the heart of the elbow, arm and upper torso was 45. Kok, with the lower edge of the cuff before elbow gap spacing of 2-3 cm, inflatable to disappear after torsion arterial pulse with 4.0 kPa (30 mm Hg), this was the largest inflatable level. If high pressure will be the result of high systolic blood pressure. If inflation reached 40.0 kPa (300 mm Hg) level, which will lead to “Airbag Inflators hypertension.” Then gradually deflated and a speed of 0.27 kPa (2 mm Hg) / sec, for the first auscultation audio systolic blood pressure, pulse tone for the disappearance of diastolic blood pressure (the old system units blood pressure reading should be accurate to 2 mm Hg). Inflatable oppression time not too long, it could easily lead to the false impression of elevated blood pressure.

Insulin resistance is also cause hypertension

Insulin resistance is obesity and hypertension risk factors one by oral glucose tolerance test and insulin release test of the indirect indicators of insulin sensitivity compared with EICT law, about 10 ~ 20% of the patients missed in the conditions do not EICT units available insulin area under the curve, fasting glucose and fasting insulin product countdown, as two better insulin sensitivity of the indirect indicators of renal vascular hypertension does not exist obvious insulin resistance, the insulin resistance that is the primary in hypertension, and blood pressure secondary to increased insulin resistance in patients with essential hypertension and abnormal metabolism of the other closely related to the merger of insulin resistance in patients with essential hypertension incidence of salt sensitivity, blood lipids and blood uric acid levels than those without insulin resistance in patients with hypertension, that insulin resistance may be the root cause of the abnormal metabolism.

The study is the first demonstration of insulin resistance in patients with essential hypertension and heart, brain and kidney damage in the three organs process, that is, without insulin resistance in hypertension → hypertensive patients with insulin resistance Ⅱ → hypertensive patients with type 2 diabetes. The study also found that perindopril and amlodipine in addition to relief, but also improve insulin sensitivity, and no effect of nifedipine.

The etiology and pathology of hypertension

The etiology and pathogenesis of the disease has not yet fully appreciate principle. Through years of observational study, compared recognized with the following factors: (1) Age: Statistics found over 40 years of age suffering from hypertension and more than 40 people under the age of 3.5 times (2) job and the Environment: Where a high degree of attention concentrated, excessive tension in the mental work or work environment are susceptible to the irritation of hypertension; (3) Family genetic: Statistics found that 50 percent of hypertension patients have family history, it is felt that the genetic and (4) too much salt: Some people carried out of a trial, more than five grams of salt a day compared with less than 5 grams of the large proportion of hypertension (5) Obesity: overweight, hypertension than the normal high incidence of 2-6 times (6) Smoking: The experiment proved that the smoke of nicotine on the role of vascular endothelial injury there can lead to atherosclerosis, hypertension occurred.
Blood pressure and cardiac ejection peripheral resistance the result of the interaction, the two rely on each other to maintain balance if the blood pressure for some factors that balance will be destroyed in high blood pressure, such as the movement of the central nervous central vascular dysfunction, resulting in vascular systolic and diastolic dysfunction, and also because of renin - excessive secretion of angiotensin can make systemic arterial spasm small, the long, small arterial oxygen vacancy occurred Hyalinized, fibrous tissue and endometrial fibroelastosis, a small artery sclerosis, advanced by ischemia and hypoxia can be an important organ dysfunction occurred.

The biochemical mechanism of genetic hypertension

The biochemical mechanism of genetic hypertension

The current biochemical research results support the following Hypertension is a genetic disease:

(1) transmembrane cation transporter defect: blood pressure in patients with essential hypertension and “normal” children of sodium, potassium ion membrane transporter inhibition, leading to intracellular sodium and calcium ion concentration increased, from the vascular smooth muscle contraction, was increased.

(2) Sympathetic media metabolic deficiencies: the plasma of patients with essential hypertension infants phenol-amine B hydroxylase and dopamine content of genetic activity increased, leading to cardiac hypertrophy, the vascular smooth muscle contraction.

(3) renal function and endocrine dysfunction: patients with essential hypertension reduced glomerular filtration rate, renal vascular hormone on the vasoconstrictor response to increased reserves decreased renal function, such as sensitive to salt boost.

(4) abnormal arterial smooth muscle calcium pool: cells in patients with essential hypertension increased calcium channel, resulting in calcium flow increased intracellular calcium ion concentration increased, from the vascular smooth muscle contraction, increased peripheral resistance, elevated blood pressure.

Discover new mechanism of hypertension

Technical University of Munich, Germany, Professor Hoffman on March 13 announced to the media, he led a research team had found a can of protein vascular muscle relaxation TRAG-Prot ein. The discovery will allow people to further understand the pathogenesis of hypertension, and find a treatment for cardiovascular diseases laid the foundation for new methods.
Professor Hoffman explained that hypertension was mainly due to the vascular wall excessive calcium in the muscle cells, leading to hardening caused by the vascular wall. The team found that this protein can prevent calcium in the blood vessel wall cells in free. But if such obstacles in the function of proteins, vascular relaxation of the wall will lose a result of high blood pressure, which led to coronary heart disease. Pathogenesis of Hypertension This applies to most types of hypertension, renal artery stenosis only causes such as disease except for a small number of hypertension. Therefore, as long as control of this protein can be effective in preventing hypertension.
Professor Hoffman said, the study results published in the United Kingdom recently published in the “Nature” magazine. But this will be found for it will take several years of the time, which must be a lot of animal experiments.

Nephropathy patients with urine testing knowledge

Stay in urine tests should be noted:
Urine collection time: any time from the conventional urine testing can be done inspections. General kidney patients before and after results are to observe all provisions of the first to get up by the early morning urine censorship.
Submitted urine: 5 ~ 10 ml general, as measured Nibichong can not be less than 50 ml.
Stay urine specimens should take urine samples: the first part from the urine abandoned, in an Chongdiao remain in the anterior urethral meatus and bacteria, and then collecting urine samples submitted.
Care should be taken not to bring non-urine composition of urine: If women do not mix with Leucorrhea and menstrual blood, not mixing with men, such as prostatic fluid.

Nephrotic syndrome diagnosis

Blood tests of urinary protein as a positive, more than 1.030,24 Nibichong hour urinary protein greater than 150 mg, plasma protein grams less than 6.0%, below the 3.0% albumin grams per litre of blood cholesterol check Moore more than 6.7 cents, kidney function tests suggested that dysfunction. Blood, blood viscosity, serum complement the determination of changes in the fundus examination, the determination of thyroid function, the diagnosis of the disease and understanding of the progress of the disease to a certain extent help.