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The new Chinese hypertension guideline comprehensively covers almost all major aspects in the management of hypertension. In this new guideline, hypertension remains defined as a systolic/diastolic blood pressure of at least 140/90 mm Hg. For risk assessment, a qualitative approach is used similarly as in previous Chinese guidelines according to the blood pressure level and the presence or absence of other risk factors, target organ damage, cardiovascular complications, and comorbid diseases. The therapeutic target is 140/90 mm Hg in general, and if tolerated, especially in high‐risk patients, can be more stringent, that is, 130/80 mm Hg. However, a less stringent target, that is, 150/90 mm Hg, is used in the younger (65‐79 years, if tolerated, 140/90 mm Hg) and older elderly (≥80 years). Five classes of antihypertensive drugs, including β‐blockers, can be used either in initial monotherapy or combination. The guideline also provided information on the management of hypertension in several special groups of patients and in the presence of secondary causes of hypertension. To implement the guideline recommendations, several nationwide hypertension control initiatives are being undertaken with new technology. The new technological platforms hopefully will help improve the management of hypertension and generate scientific evidence for future hypertension guidelines, including a possible Asian hypertension guideline in the near future.

It is unclear whether black patients with chronic kidney disease (CKD) vs those without CKD who take antihypertensive medication have an increased risk for apparent treatment-resistant hypertension (aTRH). The authors analyzed 1741 Jackson Heart Study participants without aTRH taking antihypertensive medication at baseline. aTRH was defined as uncontrolled blood pressure while taking three antihypertensive medication classes or taking four or more antihypertensive medication classes, regardless of blood pressure level. CKD was defined as an albumin to creatinine ratio ≥30 mg/g or estimated glomerular filtration rate

Objective: The purpose of this study was to compare the impact of achieving tight versus usual systolic blood pressure (SBP) control on stroke prevention through meta-analysis of randomized controlled trials. Methods: We searched PubMed and bibliographies of recent review articles. Relative risk with 95% confidence interval was used as a measure of the association between an active treatment group with achieved SBP

Purpose Endothelial damages are one of the most important causes of persistent hypertensive complications. The aim of our study was to discuss the relationship between the molecular markers of endothelial damage, thrombomodulin, and complications in hypertension. Methods A total 132 cases of hypertensive patients, including 13 patients with damage of target organs, were selected as research subjects. And grouping was based on different levels of blood pressure. The blood pressure and thrombomodulin levels were detected among all cases, and their drinking, smoking, and other medical records were tracked. Results Higher plasma concentration of thrombomodulin was demonstrated in subjects with hypertensive complications compared with without complications [24.5 (18.1,37.55) vs 12.1 (9.1,22.3) TU/mL, P = .001, respectively]. The optimum thrombomodulin cutoff value was determined to be more than 15.5 TU/mL, with a sensitivity of 92.3% and a specificity of 63%. With the increase in blood pressure level, thrombomodulin levels in three groups gradually raised [6.15(5.475,12.75) vs 9.75(7.725,13.35) vs 16.45 (10.125,23.725) TU/mL, P = .007, respectively]. Conclusion With the increase in blood pressure and the occurrence of complications, thrombomodulin showed an increasing trend, which was caused by an increase in the degree of endothelial injury. So, thrombomodulin may serve as a clinically meaningful marker of the progression of hypertension.

Thirty-seven patients with a supine systolic blood pressure greater than 160 and/or a diastolic blood pressure greater than 95 mmHg were enrolled in the study and treated for 6 months with prazosin and 6 months with metoprolol (in random order). Neither the systolic nor the diastolic blood pressures differed after the two types of treatment (median difference 0/0 mmHg). The mean and median differences in serum cholesterol, however, were 0.4 and 0.3 mmol/l respectively, which were 9 and 5% of the pretreatment values. The corresponding differences in the atherogenic index (in which cholesterol in high density lipoproteins is integrated) were 10 and 8% of the pretreatment values. This difference in the metabolic response to the two drugs at the same blood pressure level is most probably of importance in the long-term prevention of ischaemic heart disease, for which high levels of serum cholesterol and atherogenic index are major risk factors.

This paper describes a study of the degree of continuity in the drug treatment of hypertension. An analysis of antihypertensive drugs dispensed to 916 individuals during 1970-74 revealed that 22% of the men and 27% of the women were without treatment for 20-50% of their observation time. A closer examination of 46 patients under 60 years of age showed that between 2 and 20 physicians had been involved in the antihypertensive treatment of the individual patient. The time without treatment in this group of unselected patients varied between 0 and 77% of the observation time, the degree of discontinuity being insignificantly correlated to the resulting blood pressure level. Non-compliance was the cause for discontinuing a drug in at least every fifth case.

Cardiovascular disease (CVD) risk factors can be identified in children and tracked over time. We studied 519 children (mean age, 3.9 years) and reevaluated CVD risk factors 4 years later. Baseline and follow-up (FU) measures included height, weight, body mass index (BMI), blood pressure level, blood lipid values, and 24-hour dietary intake. Nutritional predictors of CVD risk factors (lipid levels and BMI) were identified using regression analysis at follow-up. Energy intake at baseline and FU, as well as increasing BMI over time, were directly associated with total cholesterol levels. Dietary intake of monounsaturated fat and dietary fiber were significant predictors of total cholesterol level at follow-up (inverse associations). Increasing BMI, waist circumference at FU, and intake of sucrose at FU were inversely associated with high-density lipoprotein cholesterol levels at FU. Waist circumference and BMI at FU were associated with higher triglyceride levels, while percent energy from monounsaturated fat was associated with lower values. This study provides further evidence that dietary intake influences CVD risk factors in childhood.

Regular aerobic exercise has the potential to induce several beneficial health effects, including a decrease in blood pressure level, especially in hypertensive patients and in subjects with high-normal blood pressure. However, it is also well documented that some people show more pronounced blood pressure responses to endurance training than others, despite identical training programs and similar initial blood pressure levels. This kind of variation is an example of normal biologic diversity and most likely originates from interactions with genetic factors. Data from genetic epidemiologic studies indicate that there is a genetic component that affects both resting blood pressure and blood pressure responses to acute exercise. Evidence from molecular genetic studies is scarce, but the first reports suggest that DNA sequence variation in the hypertension candidate genes, such as angiotensinogen, also modify blood pressure responses to endurance training. The current knowledge regarding the role of genetic factors in the modification of blood pressure responses to endurance training will be summarized and discussed.

We have studied a normal restriction fragment length polymorphism at the renin locus, detected with the restriction enzyme BglI in healthy Norwegians. No association with blood pressure level or variability was found. Thus, the normal genes detected by examination of this restriction fragment length polymorphism at the renin locus have neither "level gene" nor "variability gene" effects on normal blood pressure.

A five-year follow-up sample of 509 adult male and female Samoans experiencing modernization in American Samoa was studied to determine the relation between baseline biocultural factors and follow-up blood pressure level. Analyses were stratified by sex and baseline age: 18-44 and ≥45 years. Baseline factors in the predictive models included blood pressure level, sum of skinfolds, age, education level, and reported salt intake. This Samoan adult sample was characterized by high prevalence of overweight at all ages, continual fat gain, and high incidence of overweight in young adults over five years. Blood pressure levels were moderate in young adults considering the adiposity, although almost one-third of those ≥45 years of age were hypertensive. In young adults baseline adiposity was the most important predictor of follow-up blood pressure, whereas in older adults age itself was most important. As age increases, physiologic blood pressure regulation may become less labile due to long-term adiposity and salt intake and lead to persistent elevations of blood pressure.

Multi-unit recordings of muscle-nerve sympathetic activity (m.s.a) or skin-nerve sympathetic activity (s.s.a) were made in the left peroneal nerve of sixteen healthy volunteers during simulated diving by immersion of the face in a tub of water. The procedure was varied by the use of different water temperatures, by diving with snorkel breathing, by apnoea without diving, and by apnoea with a stream of air against the face instead of immersion in water. Diving for 12 s elicited a pronounced activation of m.s.a., the mean increase from control periods being 360%. The response was stronger with lower water temperatures. Immersion of the whole face evoked a stronger increase in m.s.a. than immersion of mouth and nose only. Diving without apnoea elicited a significant but weaker increase in m.s.a., whereas apnoea only for 12 s did not influence the sympathetic outflow. Cool air against the face during apnoea for 12 s was associated with a significant increase in m.s.a. The increase in m.s.a. usually occurred before the bradycardia. On emersion, m.s.a. ceased abruptly, whereas the bradycardia persisted for a few seconds. Mental arithmetic during diving did not change the m.s.a. response but reduced the bradycardia. M.s.a. increased despite increasing blood pressure levels. On emersion, m.s.a. did not reappear until the pre-diving blood pressure level was attained. S.s.a was inhibited on diving, with concomitant vasodilatation in the skin as recorded in the big toe. It is concluded that the response of m.s.a. to diving is initiated by a central 'pattern recognition' of an input from facial receptors, that this input and the effects of apnoea, acting by mutual reinforcement, maintain the strong sympathetic outflow, and that the mechanism releasing m.s.a. on diving overrides the normal blood pressure regulatory function of m.s.a. Diving exerts differentiated influence on different parts of the sympathetic nervous system, as illustrated by the inhibition of s.s.a.

The nervously mediated effect of angiotensin was studied in 13 rabbits by recording of renal and cervical sympathetic nerve activities, and was compared to results obtained with infusion of noradrenalin. I.v. infusion of angiotensin (0.5—3 μg/kg · min) raised the blood pressure, and initially reduced the normal rhythmical sympathetic activity. Whereas with noradrenalin the reduction of sympathetic nerve activity persisted, being determined by the blood pressure level, angiotensin shortly after the start of infusion was found to induce a non-rhythmical activity in the renal nerve. This activity was associated with a further rise of blood pressure. The non-rhythmical activity and the concomitant pressure rise were transient, and disappeared after a few minutes, in spite of continued infusion of angiotensin. This suggests that the nervously mediated effect, although capable of causing considerable transient increase of arterial blood pressure, is of minor importance for the blood pressure response to prolonged infusion of angiotensin in rabbits. The non-rhythmical sympathetic activity was not related to changes in baroreceptor activity, and was probably not caused by stimulation of chemoreceptors or sympathetic ganglions. Most likely, this effect of angiotensin was brought about by interaction with central sympathetic neurons.