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Biomedical subjects

F O Simpson

Publications and source records attributed to F O Simpson.

At least 19 recordsLinked to original sources
PubMed2001

Different associations of blood pressure with 24-hour urinary sodium excretion among pre- and post-menopausal women. WHO Cardiovascular Diseases and Alimentary Comparison (WHO-CARDIAC) Study.

OBJECTIVE: Having found no definite relationship between blood pressure (BP) and 24h sodium excretion in women aged 48-56 years (in contrast to the results in men of the same age) in the WHO Cardiovascular Diseases and Alimentary Comparison (WHO-CARDIAC) Study, we analyzed the data to investigate whether the sodium-BP association differed between pre- and post-menopausal women. DESIGN AND METHODS: The WHO-CARDIAC is a multicenter cross-sectional study, involving, as of July 2000, 60 collaborating centers in 25 countries. In each center, 100 men and 100 women aged 48-56 years were selected randomly from the general population of the area. In this report, 2,212 women in 21 centers located in 17 countries worldwide, who had data on menopausal status, were studied. RESULTS: After adjustment for age, body mass index (BMI) and 24h urinary potassium excretion, 24h sodium excretion was positively and significantly associated with systolic blood pressure (SBP) [pooled regression coefficient: 0.037 (SE 0.01), P < 0.01] and with diastolic blood pressure (DBP) [0.023 (0.006), P< 0.01] in post-menopausal women. Pooled regression coefficients of sodium-BP association were not significant in pre-menopausal women (P< 0.05). Cross-center correlation analyses of the 21 centers showed that 24h sodium excretion was positively associated with SBP and DBP in both pre- and post-menopausal women, and this positive association between sodium excretion and SBP was significant in post-menopausal women (R2 = 0.23, P = 0.029). CONCLUSION: Different associations between sodium and BP were observed in women with pre- and post-menopausal status. There may be a tendency for salt sensitivity to increase at the menopause.

Blood Pressure↗
PubMed1996

Guidelines for antihypertensive therapy: problems with a strategy based on absolute cardiovascular risk.

It has been suggested that selection for antihypertensive therapy should be based on absolute risk of a cardiovascular disease (CVD) event and that treatment should be offered only if the 10-year risk exceeds 20%. Although interesting and challenging, this strategy would have the effect of greatly emphasizing treatment of the elderly and downplaying treatment of the middle-aged. It is argued in this paper that the use of one and the same time-frame for all age groups is illogical; some inverse age-related adjustment is needed. In addition, it is suggested that selection for active treatment would be better based not on the total absolute risk of CVD but rather on the marginal hypertensive risk (i.e. that part of the total risk which can be attributed to raised blood pressure). Problems in the use of antihypertensive drugs in people with 'high normal' blood pressure in order to compensate for risk factors such as obesity, hyperlipidaemia and smoking are discussed. The effect of antihypertensive treatment administered in large-scale trials to the most hypertensive control subjects has been (and continues to be) largely ignored; it should be taken into account in all calculations in this field. A policy based on absolute risk is certainly worth examining but it should not be considered self-evidently correct and needs testing in all its aspects before it is adopted on a large scale.

Aging↗
PubMed1995

Effect of felodipine on blood pressure, body sodium, plasma renin activity and plasma aldosterone in hypertensive and normotensive rats.

1. To explore its effect on blood pressure (BP) in relation to body sodium (Na), felodipine was given to New Zealand genetically hypertensive (GH) and normotensive (N) rats and to Japanese SHR and WKY rats, prepared for repeated measurements of body sodium (Na) by a whole body counting technique (22Na) using an Na-free pelleted diet and 22Na-NaCl fluid as the sole source of Na, with water also available. The drug was added to the food before pelleting pellets, 0.5 mg/g food. 2. Felodipine reduced BP in each strain; this effect was as great on normal Na intake as when on a zero Na intake. Felodipine caused an increase in plasma renin activity in each strain but the increase reached significant levels only in GH, SHR and WKY. Plasma aldosterone was decreased by treatment in GH and N and increased in SHR and WKY. 3. In rats on a zero Na intake (water sole drinking fluid), felodipine caused no fall in body Na (i.e. no natriuretic effect was detectable) except in WKY. When saline was freely available, felodipine tended to stimulate saline intake and was associated with an increase in body Na in all strains except SHR; body Na was high in SHR even in the absence of felodipine and did not increase further with felodipine treatment. Felodipine slightly speeded up the excretion of an Na load in rats on an ample NaCl intake (choice of 0.5% 22Na-NaCl and water) but this may have been due, in part, to the treated rats having taken, by choice, a greater intake of saline in the pre-load period. 4. In this study, felodipine reduced BP and stimulated PRA and salt appetite. Its effects on Na handling varied to some extent between the strains; there was no consistent natriuretic effect, but rather some evidence of Na retention.

Aldosterone↗
PubMed1992

Effect of enalapril on body sodium and handling of a sodium chloride load in hypertensive and normotensive rats.

1. The effect of enalapril on handling of an Na load and on body Na during 96 h of zero Na intake was measured in hypertensive rats (GH and SHR) and their normotensive controls (N and WKY) by a whole body counting method. 2. Enalapril treatment led to a greater fall in body Na in the first 24 h after the Na load (as expected from the known effect of ACE inhibition on aldosterone production) and thus to a slightly faster excretion of an amount equivalent to the load. 3. Enalapril-treated rats were unable to maintain body Na on a zero Na intake. This was also expected from the known effect on aldosterone production, though other mechanisms are not excluded. The effect was more marked in the SHR and WKY than in GH and N but there was no significant difference in this effect between the hypertensives and their respective control strains.

Animals↗
PubMed1992

Salt and hypertension: revisited.

1. There is only one known environmental factor that possibly could hold the key to much of the problem of 'essential' hypertension and this is salt. Without a high or moderately high salt intake, other environmental factors may be largely inoperative. The evidence, which still falls somewhat short of certainty, is briefly reviewed.

Humans↗
PubMed1990

A questionnaire survey of symptoms in a hypertension clinic.

OBJECTIVE: to assess symptoms of patients on antihypertensive therapy. SETTING: hospital hypertension clinic. DESIGN: self administered questionnaire (sent and returned by mail) listing 23 symptoms; four grades of response (none, mild or seldom, moderate or sometimes, severe or frequent); special scale for nocturia and appetite. PATIENTS: 302 patients completed the questionnaire (87% of those to whom it was sent); 109 of these patients completed it a second time, after an interval of four months, so that repeatability could be assessed. REPEATABILITY: scores were high, ranging from 0.92 to 0.99, for all symptoms except flushing (all grades 0.91), nausea (all grades 0.90) and sleepiness (severe, 0.82) (method of Bulpitt et al). RESULTS: overall prevalence of symptoms was high, but most were mild or infrequent. Women had significantly greater prevalence of oedema, flushing and insomnia than men and tended to assess their symptoms more often as severe or frequent. Nocturia was the only symptom more common in those above median age (62 yr) than in those below. Lack of energy was the only symptom more prevalent in the treated than in the untreated. No difference in prevalence of symptoms was detected between those taking or not taking a specific type of drug (beta blocker, diuretic, ACE inhibitor, calcium antagonist). CONCLUSION: in patients whose antihypertensive therapy has been carefully adjusted to try to avoid symptomatic side effects, the burden of such side effects appears to be very small.

Female↗
PubMed1990

Managing hypertension: drugs, life-style manipulation or benign neglect? Medical, ethical and economic considerations.

Antihypertensive drugs have been of major benefit to people with moderate or severe hypertension and have contributed enormously to fundamental physiological knowledge. Antihypertensive therapy in milder hypertension reduces the incidence of stroke by 40% or more, may reduce myocardial infarction and prevents progression to more severe hypertension or heart failure but is being criticised as not cost-effective. Much of this criticism is based on deductions from inappropriate data. Nevertheless, it is likely that money is in some cases being wasted on the treatment of people who were not truly hypertensive in the first place. It is also likely that drug dosage is often unnecessarily high. Clearly it is vital that treatment is delivered as economically as possible. A reduction in the prevalence of hypertension would be the best way to reduce costs. Obesity and a high alcohol intake are associated with a higher blood pressure at any age. A high salt intake throughout life appears to be associated with a rise in blood pressure in the second half of life and may well be the main factor in hypertension. A radical rethinking of the method of pricing of medical care should be considered, so as to provide incentives to people to adopt life-style measures that lead to avoidance of hypertension (and other cardiovascular risk factors) or, in established hypertension, to a reduction in the need for medication.

Antihypertensive Agents↗
PubMed1990

Surfeit and deficit of sodium: evidence from studies of body sodium in rats.

The concept of a basal level of body sodium (Strauss' state 'between surfeit and deficit') was studied by means of body sodium measurements in rats on different sodium intakes, in some cases after diuretic pretreatment. At a certain level of body sodium, when sodium intake was just enough to allow for body growth, a sodium chloride load (followed by a zero sodium intake) was excreted more or less quantitatively in 24-48 h. In rats pretreated with an ample sodium intake, the load was excreted more quickly and some additional sodium was also excreted. In rats pretreated with diuretic and a zero sodium diet, body sodium was very low and a sodium chloride load was retained to an extent that was more or less appropriate to the deficit. In a subsidiary part of the study, rats pretreated with a low sodium intake and frusemide and continuing on frusemide during and after the load, excreted a sodium chloride load at much the same rate as rats given a load following pretreatment with a very low sodium diet alone (i.e. not given a diuretic); after excreting the load they were able to maintain a stable (though reduced) level of body sodium in spite of cessation of sodium intake. Rats pretreated with hydrochlorothiazide, and continuing on this drug during and after the load, had a continued loss of sodium after cessation of sodium intake. The results are discussed in the light of the Strauss concept and appear to confirm it. Basal body sodium is, by inference, identified as the level at which delivery of sodium to the distal tubule exactly equals distal sodium reabsorption.

Animals↗
PubMed1990

Changes in clinical characteristics and drug treatment of hypertension over 40 years at the Dunedin Hypertension Clinic.

The clinical characteristics of the 4,170 hypertensive patients referred to the Dunedin Clinic from 1950 to 1989 have been compared for eight successive 5-year periods. A gradual decrease in the severity of referred hypertension and an increase in the proportion of patients already on treatment at the time of referral (currently 50%) were noted. For male patients, mean +/- SD initial lying blood pressure was 179 +/- 27/116 +/- 19 mm Hg in 1950-1954 and 158 +/- 25/91 +/- 14 mm Hg in 1985-1989. Corresponding prevalence data for target organ damage among male patients were retinal grade 3 or 4, 49% and 3%; cardiomegaly on chest radiograph, 60% and 26%; electrocardiogram left ventricle strain pattern, 28% and 3%; and serum urea levels greater than 10 mmol/L, 16% and 5%, respectively. For women there was a similar trend. The number of patients on drugs in each of nine categories and the percent use of each drug category for each year during 1950-1989 was recovered from computerized data files. The percentage peak usage of ganglion blockers was in 1950-1958, adrenergic neuron blockers in 1963-1970, centrally acting drugs in 1965-1968, diuretics in 1960-1982, beta-blockers in 1974-1987, alpha-blockers in 1980-1987, and angiotensin converting enzyme inhibitors and calcium antagonists in 1989. The diuretics have been the most enduring drugs, followed by the beta-blockers.

Ambulatory Care Facilities↗
PubMed1990

The control of body sodium in relation to hypertension: exploring the Strauss concept.

The overall control of body sodium relies on mechanisms that have close links to blood pressure control and hypertension. The Strauss concept of a basal level of body sodium, below which any available sodium is retained and above which any extra sodium is excreted (at a rate exponentially related to the amount present in the body), has been confirmed in rat studies. Total body sodium, on an average sodium intake, thus consists of basal plus extra: the proportions of these can vary and this makes interpretation of total body sodium difficult. Basal body sodium is, in theory, the level at which delivery of sodium to the distal nephron equals distal reabsorption of sodium. The latter is largely determined by aldosterone and, indeed, basal body sodium is high in primary aldosteronism and low in Addison's disease. The half-life of extra sodium is short in primary aldosteronism and long in Addison's disease: it is also short in some hypertensive subjects but in general lengthens with age. The exact mechanisms involved are still uncertain. Most of this work is based on step reductions in sodium intake. Step increases in sodium intake appear to lead to more complicated adjustment processes, with a delay in commencing excretion followed by some under-damping of the system before a new higher level of body sodium and a new equilibrium of intake and excretion is reached.

Animals↗
PubMed1990

Salt appetite, body sodium, handling of a NaCl load, renin, and aldosterone in genetically and spontaneously hypertensive rats.

Salt appetite, body sodium, handling of a NaCl load, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were compared in New Zealand genetically hypertensive (GH) and Japanese spontaneously hypertensive rats (SHRs) and their respective normotensive controls [normal Wistar (N) and Wistar-Kyoto (WKY) rats]. Salt appetite was increased in SHRs compared with GH, N, and WKY rats when rats were on salt-free chow and given a choice of distilled water and NaCl solution. Body sodium, measured by whole body counting, was higher in SHRs than in the other strains but did not differ among GH, N, and WKY rats. The rate of excretion of a NaCl load was not increased in GH rats and was slightly increased in SHRs only when on a very low NaCl intake. PRA and PAC (radioimmunoassay) were lower in SHRs than in GH, N, and WKY rats. PAC had a significant negative correlation with body sodium across the four strains. There is no evidence of any abnormality in sodium regulation in GH rats. However, the SHRs have an increased salt appetite and an increased body sodium even when sodium intake is limited; PRA and PAC appear to have responded appropriately to the increased body sodium.

Aldosterone↗
PubMed1990

Risk predictors in treated hypertension.

The data for patients referred to the Dunedin Hypertension Clinic (975 men, 1,348 women) between 1953 and 1977 have been examined by the Cox proportional hazards method for significant age-corrected predictors of 8-year cardiovascular and total mortality. For men, some significant predictors were systolic and diastolic blood pressure (BP), indices of target organ damage (heart and eyes) and smoking at presentation, and achieved BP and serum cholesterol at follow-up. For women, serum cholesterol, diabetes, target organ damage (heart and eyes) and smoking at presentation, and achieved BP level at follow-up were predictors. Relative risk for total or cardiovascular mortality was increased in both sexes most by smoking and by increased levels of achieved BP.

Blood Pressure↗