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The United Kingdom has successfully implemented a salt reduction programme. We carried out a comprehensive analysis of the programme with an aim of providing a step-by-step guide of developing and implementing a national salt reduction strategy, which other countries could follow. The key components include (1) setting up an action group with strong leadership and scientific credibility; (2) determining salt intake by measuring 24-h urinary sodium, identifying the sources of salt by dietary record; (3) setting a target for population salt intake and developing a salt reduction strategy; (4) setting progressively lower salt targets for different categories of food, with a clear time frame for the industry to achieve; (5) working with the industry to reformulate food with less salt; (6) engaging and recruiting of ministerial support and potential threat of regulation by the Department of Health (DH); (7) clear nutritional labelling; (8) consumer awareness campaign; and (9) monitoring progress by (a) frequent surveys and media publicity of salt content in food, including naming and shaming, (b) repeated 24-h urinary sodium at 3-5 year intervals. Since the salt reduction programme started in 2003/2004, significant progress has been made as demonstrated by the reductions in salt content in many processed food and a 15% reduction in 24-h urinary sodium over 7 years (from 9.5 to 8.1 g per day, P<0.05). The UK salt reduction programme reduced the population's salt intake by gradual reformulation on a voluntary basis. Several countries are following the United Kingdom's lead. The challenge now is to engage other countries with appropriate local modifications. A reduction in salt intake worldwide will result in major public health improvements and cost savings. [ABSTRACT FROM AUTHOR]

To study the relationship between pre-dialysis plasma sodium and blood pressure (BP), we performed an audit of patients who were on stable haemodialysis at St Bartholomew's and The Royal London Hospital from 1 June 2009 to 15 June 2010. There were 651 patients with 7445 dialysis sessions where both plasma biochemistry and BP were measured before haemodialysis. We found a significant association between plasma sodium and both systolic and diastolic BP. A 1 mmol l−1 increase in plasma sodium was related to 0.65/0.36 mm Hg increase in BP (P<0.001 for both systolic and diastolic BP) after adjusting for potential confounding factors, including weight gain between dialyses and plasma albumin, both of which are crude indices of extracellular fluid volume. A separate analysis excluding individuals who were on BP treatment showed a similar relationship, with a 1-mmol l−1 increase in plasma sodium associated with 0.82/0.56 mm Hg increase in BP (P<0.001 for both, N=177). These results provide further support for the accumulating evidence that plasma sodium has an important role in regulating BP, which may be independent of extracellular volume. Our findings in conjunction with other evidence suggest that small changes in plasma sodium could be an important mechanism for the beneficial effects of lower dialysate sodium and lower salt intake on BP in haemodialysis patients. [ABSTRACT FROM AUTHOR]

High dietary salt is a major contributor to increased blood pressure, the leading risk for death worldwide. In several countries, national programmes to reduce dietary salt have been implemented with leadership and involvement of hypertension experts. Other hypertension experts may be interested in assisting or leading a national programme to reduce dietary salt, however, may not have the experience or training to do so. The article is based on the experiences of three hypertension experts who have led the development of national dietary salt reduction programmes in the United Kingdom, Australia and Canada. The article advises developing leadership and a coalition, conducting a nation-specific environmental scan of facilitators and barriers, estimating the national health and financial costs of high dietary salt and the benefits of reducing salt intake, obtaining core documents to provide the scientific rational for the programme, developing a policy statement to outline the required actions to be undertaken, engaging government and industry, using media to gain public support, overcoming industry supported opposition and sustaining the effort long term. Resources and potential sources for international collaboration are provided as well as caveats for developing the programme within the specific nations' context and overall effort to improve health. Developing and leading a national salt reduction programme is a major commitment, however, reducing dietary salt is estimated to be one of the most effective strategies to improve a nation's health. [ABSTRACT FROM AUTHOR]

Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. Raised blood pressure (BP), cholesterol and smoking, are the major risk factors. Among these, raised BP is the most important cause, accounting for 62% of strokes and 49% of coronary heart disease. Importantly, the risk is throughout the range of BP, starting at systolic 115 mm Hg. There is strong evidence that our current consumption of salt is the major factor increasing BP and thereby CVD. Furthermore, a high salt diet may have direct harmful effects independent of its effect on BP, for example, increasing the risk of stroke, left ventricular hypertrophy and renal disease. Increasing evidence also suggests that salt intake is related to obesity through soft drink consumption, associated with renal stones and osteoporosis and is probably a major cause of stomach cancer. In most developed countries, a reduction in salt intake can be achieved by a gradual and sustained reduction in the amount of salt added to food by the food industry. In other countries where most of the salt consumed comes from salt added during cooking or from sauces, a public health campaign is needed to encourage consumers to use less salt. Several countries have already reduced salt intake, for example, Japan (1960–1970), Finland (1975 onwards) and now the United Kingdom. The challenge is to spread this out to all other countries. A modest reduction in population salt intake worldwide will result in a major improvement in public health.Journal of Human Hypertension (2009) 23, 363–384; doi:10.1038/jhh.2008.144; published online 25 December 2008 [ABSTRACT FROM AUTHOR]

To study the relationship between salt intake and blood pressure in children and adolescents, we analysed the data of a large cross-sectional study (the National Diet and Nutrition Survey for young people), which was carried out in Great Britain in 1997 in a nationally representative sample of children aged between 4 and 18 years. A total of 1658 participants had both salt intake and blood pressure recorded. Salt intake was assessed by a 7-day dietary record. The average salt intake, which did not include salt added in cooking or at the table, was 4.7±0.2 g/day at the age of 4 years. With increasing age, there was an increase in salt intake, and by the age of 18 years, salt intake was 6.8±0.2 g/day. There was a significant association of salt intake with systolic blood pressure as well as with pulse pressure after adjusting for age, sex, body mass index and dietary potassium intake. An increase of 1 g/day in salt intake was related to an increase of 0.4 mm Hg in systolic and 0.6 mm Hg in pulse pressure. The magnitude of the association with systolic blood pressure is very similar to that observed in a recent meta-analysis of controlled trials where salt intake was reduced. The consistent finding of our present analysis of a random sample of free-living individuals with that from controlled salt reduction trials provides further support for a reduction in salt intake in children and adolescents.Journal of Human Hypertension (2008) 22, 4–11; doi:10.1038/sj.jhh.1002268; published online 6 September 2007 [ABSTRACT FROM AUTHOR]

Increased consumption of fruit and vegetables has been shown to be associated with a reduced risk of coronary heart disease (CHD) in many epidemiological studies, however, the extent of the association is uncertain. We quantitatively assessed the relation between fruit and vegetable intake and incidence of CHD by carrying out a meta-analysis of cohort studies. Studies were included if they reported relative risks (RRs) and corresponding 95% confidence interval (CI) of CHD with respect to frequency of fruit and vegetable intake. Twelve studies, consisting of 13 independent cohorts, met the inclusion criteria. There were 278 459 individuals (9143 CHD events) with a median follow-up of 11 years. Compared with individuals who had less than 3 servings/day of fruit and vegetables, the pooled RR of CHD was 0.93 (95% CI: 0.86–1.00, P=0.06) for those with 3–5 servings/day and 0.83 (0.77–0.89, P<0.0001) for those with more than 5 servings/day. Subgroup analyses showed that both fruits and vegetables had a significant protective effect on CHD. Our meta-analysis of prospective cohort studies demonstrates that increased consumption of fruit and vegetables from less than 3 to more than 5 servings/day is related to a 17% reduction in CHD risk, whereas increased intake to 3–5 servings/day is associated with a smaller and borderline significant reduction in CHD risk. These results provide strong support for the recommendations to consume more than 5 servings/day of fruit and vegetables.Journal of Human Hypertension (2007) 21, 717–728; doi:10.1038/sj.jhh.1002212; published online 19 April 2007 [ABSTRACT FROM AUTHOR]

Prospective comparisons of different drug classes have shown that differences in blood pressure control, rather than differences between drug classes, have the overriding influence on overall outcome. The same studies have also reinforced the need, in the majority of patients, to use combinations of drugs in order to achieve the target of < 140/85 mmHg. By contrast, most patients in routine practice receive single agents and consequently fail to achieve target blood pressure. This failure reflects in part the emphasis in individual studies and subsequent guidelines on comparison of individual drugs. In this article we show how the consistency of both theory and a broad range of evidence permits a didactic approach to combination therapy. Our advice is based on the growing recognition that essential hypertension and its treatment fall into two main categories. Younger Caucasians usually have renin-dependent hypertension that responds well to angiotensin-converting-enzyme inhibition or angiotensin receptor blockade (A) or β blockade (B). Most other patients have Iow-renin hypertension that responds better to calcium channel blockade (C) or diuretics (D). These latter drugs activate the renin system rendering patients responsive to the addition of renin suppressive therapy. Coincidence of the initials of these main drug classes with the first four letters of the alphabet permits an AB/CD rule, according to which recommended combinations are one drug from each of the 'AB' and 'CD' categories of drugs. However, the diabetogenic potential of the older 'B' and 'D' classes leads us to advise against combining 'B' and 'D' in older patients, and to recommend 'A' + 'C' + 'D' as standard triple therapy for resistant hypertension. [ABSTRACT FROM AUTHOR]

Two recent meta-analyses of randomised salt reduction trials have concluded that there is little purpose in reducing salt intake in the general population. However, the authors, as with other previous meta-analyses, included trials of very short duration (eg 1 week or less) and trials of acute salt loading followed by abrupt reductions to very Iow salt intake (eg from 20 to less than 1g of salt/day). These acute salt loading and salt depletion experiments are known to increase sympathetic tone, and with salt depletion cause a rise in renin release and, thereby, plasma angiotensin II. These trials are not appropriate, therefore, for helping to inform public health policy, which is for a more modest reduction in salt intake, ie, from a usual intake of &ap;10 to &ap;5g of salt per day over a more prolonged period of time. We carried out a meta-analysis to assess the effect of a modest salt reduction on blood pressure. Our data sources were MEDLINE, EMBASE, Cochrane library, CINAHL, and the reference lists of original and review articles. We included randomised trials with a modest reduction in salt intake and a duration of 4 or more weeks. Meta-analysis, meta-regression, and funnel plots were performed. A total of 17 trials in hypertensives (n=734) and 11 trials in normotensives (n=2220) were included in our study. The median reduction in 24-h urinary sodium excretion was 78 mmol (equivalent to 4.6g of salt/day) in hypertensives and 74 mmol in normotensives. The pooled estimates of blood pressure fall were 4.96/2.73 ± 0.40/0.24 mmHg in hypertensives (P<0.001 for both systolic and diastolic) and 2.03/ 0.97 ± 0.27/0.21 mmHg in normotensives (P<0.001 for both systolic and diastolic). Weighted linear regression analyses showed a dose response between the change in urinary sodium and blood pressure. A reduction of 100 mmol/day (6g of salt) in salt intake predicted a fall in blood pressure of 7.11/3.88 mmHg (P<0.001 for both systolic and diastolic) in... [ABSTRACT FROM AUTHOR]

Introduction: The sodium-hydrogen exchanger (NHE) is integral to the processes that facilitate cell growth and may contribute to the development of left ventricular hypertrophy. The aim of this study was to examine the relationship between platelet sodium-hydrogen exchanger activity and left ventricular mass index (LVMI). Methods: Twenty male untreated Caucasians (mean age ± s.d.: 48 ± 13; body mass index: 29 ± 4 kg/m[SUP2]) with a wide range of blood pressures were studied (mean BP: 152 ± 22/93 ± 15 mm Hg; range: 115-190/61-117 mm Hg). Sodium-hydrogen exchanger activity was determined as the rate of sodium-dependent recovery of intracellular pH in isolated platelets loaded with BCECF and acidified to pH 6.25 using nigericin. LVMI was calculated from measurements made by M-mode echocardiography. Associations between continuous variables were examined using parametric tests. Results: The mean rate of pHi recovery was 0.15 ± 0.03 dpHi/s (range: 0.09-0.21). Mean LVMI was 120 ± 32 g/m[SUP2] (range: 56-178) and was not significantly correlated with either systolic (r = 0.39, P = 0.09) or diastolic blood pressure (r = 0.27, P = 0.3). Platelet NHE activity was not significantly correlated with LVMI (r = 0.06; P = 0.8). Platelet NHE activity was not significantly different between subjects with (n = 7 with LVMI > 131 g/m[SUP2]) and without left ventricular hypertrophy (n = 13). Conclusions: The results of this study show that platelet NHE activity is not significantly correlated with LVMI. These data contrast with previously described correlations of LVMI with exchanger activity measured in leucocytes and erythrocytes; and indicate that the relationship between LVMI and exchanger activity may be specific to the cell type in which exchanger activity is measured. [ABSTRACT FROM AUTHOR]

Polymorphisms of the epithelial sodium channel may raise blood pressure by increasing renal sodium reabsorption. This study examines frequency distributions and associations with hypertension of the T594M and of the G442V polymorphisms of the β subunit of the epithelial sodium channel in a population-based sample. We studied a stratified random sample of 459 subjects (279 women), aged 40-59 years, of black African origin from general practices' lists within a defined area of South London. All were first generation immigrants. The polymorphic variants were detected using single strand conformational polymorphism technique (SSCP). The prevalence of hypertension (BP &ges;160 and/or 95 mm Hg or on drug therapy) was 43%; of these, 76% were on drug therapy. The main analysis was carried out by three ordered blood pressure categories (I to III) according to increasing blood pressure and presence or absence of drug therapy. The frequency of the 594M variant (heterozygotes and homozygotes) was 4.6%; the frequency of the 442V variant was higher (27.0%). The frequency of the 594M variant increased with increasing blood pressure category (P = 0.05) and was more common in hypertensives than normotensives. By contrast the frequency of the 442V variant did not vary across increasing blood pressure categories (P = 0.62). No gender difference was observed. Adjustment for age, sex and body mass index did not alter these findings. These results suggest that the 594M variant may contribute to high blood pressure in black people of African origin whereas the G442V polymorphism is unlikely to influence blood pressure in this population. [ABSTRACT FROM AUTHOR]

Abnormalities in acid-base regulation have previously been reported both in hypertensive humans and animals and a link between abnormalities in renal sodium handling and acid excretion may be particularly important in black hypertensives. The objectives of this study were to compare indices of urinary acid excretion (urinary pH, ammonium and titratable acid excretion) between normotensives and hypertensive people of African origin. Measurements were carried out in 86 black individuals of African origin in a case-control design (19 normotensive; 67 hypertensive). Of these, 17 normotensive and 17 patients with essential hypertension were matched for age, sex and weight. Group comparisons were carried out by unpaired t-tests or two-way analysis of variance and group values are given as means ± s.d. Urinary pH was significantly higher in the hypertensives both in the unmatched groups and in the matched groups. In the 17 matched pairs: urinary pH in the hypertensive individuals was 6.36 ± 0.54 and 5.84 ± 0.53 in the normotensives, respectively; P = 0.007. Additionally, urinary titratable acidity was significantly lower in the hypertensives than in the normotensives (25.4 ± 13.7 vs 16.7 ± 10.7 mmol/24 h; P = 0.047) but there were no significant differences in urinary ammonium excretion. The mechanisms for the apparent reduction in acid excretion in the hypertensives is not clear but these results highlight the possibility that hypertension in blacks is associated with abnormalities of renal sodium and hydrogen exchange with compensatory increases in renal ammonium production. [ABSTRACT FROM AUTHOR]

• Use non-pharmacological measures in all hypertensive and borderline hypertensive people. • Initiate antihypertensive drug therapy in people with sustained systolic blood pressures (BP) &ges;160 mm Hg or sustained diastolic BP &ges;100 mm Hg. • Decide on treatment in people with sustained systolic BP between 140 and 159 mm Hg or sustained diastolic BP between 90 and 99 mm Hg according to the presence or absence of target organ damage, cardiovascular disease or a 10-year coronary heart disease (CHD) risk of &ges;15% according to the Joint British Societies CHD risk assessment programme/risk chart. • In people with diabetes mellitus, initiate antihypertensive drug therapy if systolic BP is sustained &ges;140 mm Hg or diastolic BP is sustained &ges;90 mm Hg. • In non-diabetic hypertensive people, optimal BP treatment targets are: systolic BP <140 mm Hg and diastolic BP <85 mm Hg. The minimum acceptable level of control (Audit Standard) recommended is <150/<90 mm Hg. Despite best practice, these levels will be difficult to achieve in some hypertensive people. • In diabetic hypertensive people, optimal BP targets are; systolic BP <140 mm Hg and diastolic BP <80 mm Hg. The minimum acceptable level of control (Audit Standard) recommended is <140/<90 mm Hg. Despite best practice, these levels will be difficult to achieve in some people with diabetes and hypertension. • In the absence of contraindications or compelling indications for other antihypertensive agents, low dose thiazide diuretics or beta-blockers are preferred as first-line therapy for the majority of hypertensive people. In the absence of compelling indications for beta-blockade, diuretics or long acting dihydropyridine calcium antagonists are preferred to beta-blockers in older subjects. Compelling indications and contra-indications for all antihypertensive drug classes are specified. • For most hypertensives, a combination of antihypertensive drugs will be... [ABSTRACT FROM AUTHOR]

The acute effects on urinary electrolyte excretion and plasma potassium were compared of the anti-hypertensive dihydrofuropyridine cicletanine with the thiazide bendrofluazide in 6 patients with uncomplicated essential hypertension. Cicletanine 50 mg or 100 mg and bendrofluazide 5 mg caused no acute decrease in blood pressure compared to placebo for 24 h after treatment. In the 24 h after a single dose of cicletanine 50 mg there was no increase in urinary sodium, potassium or volume compared to placebo. After a single dose of cicletanine 100 mg there was a significant increase in 2 h urinary sodium excretion compared to cicletanine 50 mg and in the first 6 h a significant increase in urinary potassium compared to placebo. Urine volume did not change significantly. After bendrofluazide 5 mg urinary sodium excretion increased significantly in the first 6 h as well as in the subsequent 18 h compared to placebo and both cicletanine 50 mg and 100 mg. Urinary potassium excretion was also significantly increased in the first 6 h after bendrofluazide compared to placebo, and urine volume significantly increased from 6 to 24 h after bendrofluazide 5 mg compared to placebo and cicletanine 100 mg. Plasma potassium was significantly reduced and plasma renin activity significantly increased 24 h after bendrofluazide 5 mg but these measurements were not significantly different from placebo after cicletanine 50 or 100 mg. These results suggest that cicletanine 100 mg has milder acute natriuretic effects than the thiazide bendrofluazide 5 mg. In contrast cicletanine 50 mg is associated with no major acute renal effects. In view of evidence that with long-term treatment both cicletanine 50 and 100 mg have anti-hypertensive effects, these findings suggest that cicletanine may act by a different mechanism in lowering blood pressure at low and high dose. [ABSTRACT FROM AUTHOR]

Focuses on problems associated with using Fura-2 to measure free intracellular calcium concentrations in human red blood cells. Introduction of Fura-2; Influence of high concentration of haemoglobin on the properties of Fura-2; Measurement of the excitation spectra of Fura-2 and red blood cell using Fura-2.

High blood pressure is the most important risk factor for cardiovascular disease. With the information on systolic blood pressure from the recently published meta-analysis of prospective studies, we calculated the reductions in stroke and ischaemic heart disease with control of all hypertensives to a systolic blood pressure of 140 mmHg. For adults there would be a reduction of 28-44% in stroke and 20-35% in ischaemic heart disease depending on age. In the UK, this would prevent approximately 21 400 stroke deaths and 41 400 ischaemic heart disease deaths each year. Around half of those who suffer a stroke or ischaemic heart disease survive, there would be a proportionate decrease in these people as well. These amount to approximately 42 800 strokes and 82 800 ischaemic heart diseases saved, making a total of 125 600 events saved a year in the UK. This would result in a reduction in disability and major cost savings both to individuals, their families and the Health Service. The blood pressure levels and control of blood pressure in many countries are similar to those in the UK, so the reductions in stroke and ischaemic heart disease worldwide, if the same control of high blood pressure could be obtained, would be immense. [ABSTRACT FROM AUTHOR]

Focuses on the regression of atherosclerotic renal artery stenosis with aggressive lipid lowering therapy in patients with coronary heart disease. Explanation of lipid lowering therapy; Risk factors associated with atherosclerotic renal artery stenosis.

Twelve patients with essential hypertension on no other drug treatment were entered into a randomised crossover study of 5, 10 and 20 mg capsules of nifedipine given 3 times a day and 20 mg tablets given twice a day. Each dose was given for 2 weeks in a random order. All forms of nifedipine were effective in lowering blood pressure. However, 5 mg capsules were less effective than the 10 and 20 mg capsules or 20 mg tablets. There was little to choose between the latter. All doses of nifedipine were more effective 1 and 3 h after the dose compared to subsequent times afterwards. Indeed, as time elapsed after the last dose up to 12 h, there was a gradual increase in blood pressure. However, even at 12 h the 10, 20 mg capsules and 20 mg tablets were still causing an approximate 10% reduction in blood pressure. Nifedipine tablets are as effective as capsules though they might be longer acting, particurarly around 6 h after the last dose. [ABSTRACT FROM AUTHOR]

A response by F. J. He and G. A. MacGregor to a letter to the editor about their article concerning salt and blood pressure in children that was previously published is presented.

Focuses on dihydropryidine calcium channel blockers and its side effect on peripheral oedema. Causes of peripheral oedema; Treatment of mild oedema; Incidence of oedema in younger patients and older patients.

Discusses the occurrence of gingival hyperplasia due to calcium channel blockers with reference to a case study in Great Britain. Highlights of the case of a middle-aged patient with a history of hypertension and hypercholesterolaemia; Key observations related to the occurrence of gingival overgrowth; Process of the growth of gingival hyperplasia.

Aims: Previous studies have reported tight linkage disequilibrium between the T235 and the A(-6) molecular variants of the angiotensinogen gene. This study was designed primarily to ascertain whether a similar relationship exists between the M235 and the G(-6) variants of the gene. We have investigated the degree of agreement between the genotypes of the M235T and the G(-6)A polymorphisms in two ethnic groups. Methods: Subjects were an heterogeneous group of normotensive and hypertensive subjects of Caucasian (n = 77) and Afro-Caribbean (n = 51) origin. DNA was extracted from whole blood and was genotyped for both the M235T and G(-6)A polymorphisms using PCR-based methods. Results: The distribution frequencies of the MM, MT, and TT genotypes were 0.39, 0.42, and 0.20 in white subjects, and 0.09, 0.17, and 0.74 in black subjects, respectively (chi-square, P < 0.0001). The distribution of AA, GA, and GG genotypes also differed between the two groups as follows: 0.22, 0.48, and 0.30 in white subjects, and 0.82 and 0.18 and 0 in black subjects respectively (chi-square, P < 0.0001). The agreement for TT-AA, MT-GA, and MM-GG was 93%, 91%, and 76% respectively in white and 100%, 67% and 0% respectively in black subjects. Conclusions: The results indicate ethnic differences in the distribution of both M235T and G(-6)A genotypes. The trend towards a decrease in the degree of agreement in the order of TT-AA > MT-GA > MM-GG suggests that linkage disequilibrium between the M235 and G-6 variant does not mirror that observed with the T235 and A-6 variants. These observations may have significant implications regarding the associations between the G(-6)A polymorphism and hypertension. However, this needs to be further investigated. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor on the treatment of hypertension published in the November 1999 issue of the medical journal 'Journal of Human Hypertension.' Diagnosis of hypertension with an angiotensin converting enzyme; Effects of the drug, losartan on patients with hypertension.

Focuses on the determination of aneurysmal aortoiliac disease and severe proximal renal artery stenosis in a patient with a history of acute myocardinal infarction, using digital aortography. Cause of secondary hypertension and chronic renal failure; Effect of the increase of severity of peripheral vascular disease on renal artery stenosis; Requirement of renal artery disease patients to undergo angioplasty.

Focuses on the diagnosis of secondary hypertension. Role of clinical genetics in the diagnosis; Measurement of blood pressure in a genetic clinic; Description of case study of a patient diagnosed with hypertension.

Examines the association between nitric oxide (NO) activity and essential hypertension. Reason for the use of plasma and urinary nitrate as an index of endogenous NO; Measurement of urinary and plasma nitrate; Comparison of normotensive and hypertensive people.