Search PubMed⌕ Search

Biomedical subjects

R Fraser

Publications and source records attributed to R Fraser.

At least 379 records · Page 21Linked to original sources
PubMed1976

Effect of blood pressure angiotensin II and aldosterone concentrations during treatment of severe hypertension with intravenous labetalol: comparison with propranolol.

1 The actions of labetalol 1.0-2.0 mg/kg intravenously on blood pressure, heart rate, plasma angiotensin II and aldosterone concentrations have been studied in 20 recumbent hypertensive patients. 2 In all subjects there was a reduction in systolic and diastolic blood pressures within 5 min of completion of injection. 3 Severe hypotension was not seen but three patients who had a marked fall in blood pressure experienced side-effects. Postural hypotension was common at the end of the study. 4 Labetalol caused significant reduction in heart rate. 5 Labetalol induced significant lowering of plasma angiotensin II and in plasma aldosterone concentrations, which were most obvious when these were increased initially; overall there was a close correlation between concurrent measurements of angiotensin II and aldosterone concentrations. 6 In five patients a comparison was made against propranolol 10 mg intravenously. Labetalol was more effective in lowering blood pressure but less effective in reducing pulse rate of plasma angiotensin II concentration.

Aldosterone↗
PubMed1976

Renal abnormalities and vascular complications in primary hyperaldosteronism. Evidence on tertiary hyperaldosteronism.

The frequency of underlying renal or renal artery disease, and the incidence of vascular complications were reviewed in a series of 136 cases of primary hyperaldosteronism. This was in order to investigate the possible existence of 'tertiary' hyperaldosteronism, and to examine the commonly held view that primary hyperaldosteronism is a relatively benign form of hypertension. Ten cases (7-4 per cent) had evidence of renal artery stenosis and eleven (8-1 per cent) parenchymatous renal disease. In comparison with the reported frequency in large general series of hypertensives, these data show no evidence of an excess of underlying renal disease. It is unlikely, therefore, that autonomous aldosterone secreting adenomata occur commonly as a consequence of prolonged secondary hyperaldosteronism. Four cases (2-9 per cent) had evidence of the malignant-phase of hypertension, and over a mean observation time of 5-9 years, 31 cases (22-8 per cent) developed 39 vascular complications. It appears, therefore, that vascular complications are not rare in primary hyperaldosteronism, and early and effective treatment is thus necessary.

Adenoma↗
PubMed1975

Results of adrenal surgery in patients with hypertension, aldosterone excess, and low plasma renin concentration.

Fifty patients with hypertension, aldosterone excess, and low plasma renin concentration underwent adrenal surgery. There was a highly significant fall in mean systolic and diastolic pressures after the operation. The mean postoperative diastolic pressure fell to strictly normal levels, however, in only 19 out of 38 patients from whom an adrenocortical adenoma was removed and in only two out of 10 non-tumour patients. There was a significant correlation between the fall in blood pressure during spironolactone treatment and after adrenal surgery though levels were generally slightly lower during the former therapy. It is suggested that removal of an aldosterone-producing adenoma is the treatment of choice provided a good preoperative hypotensive response to spironolactone occurs, while the treatment of choice for non-tumour patients is often long-term spironolactone.

Adenoma↗
PubMed1975

Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension.

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.

Adenocarcinoma↗
PubMed1975

Familial glucocorticoid deficiency. Studies of diagnosis and pathogenesis.

The clinical and biochemical findings are described in 2 brothers who had intermittent hypoglycaemia generally precipitated by the "stress" of infection. Both were tall and pigmented. Both boys showed a failure of adrenocortical response to ACTH which was progressive in the eldest boy. The diagnosis of familial glucocorticoid deficiency (hereditary adrenocortical unresponsiveness) was confirmed by the absence of electrolyte imbalance even on a low sodium diet, and by very high levels of ACTH in plasma. High levels of deoxycorticosterone (DOC) were found in both children with normal levels of other plasma corticosteroids. It is suggested that the high levels of DOC may be in some way related to the apparent persistence of a "fetal" type of adrenocortical steroid biosynthesis for 18 months or more in these boys. After the diagnosis, established by relatively simple methods, treatment with cortisone acetate has 0een highly effective.

17-Hydroxycorticosteroids↗
PubMed1975

Effect of prolonged low-dose angiotensin II infusion on the sensitivity of adrenal cortex in man.

The effect of incremental infusions of isoleucine-5-angiotensin II on blood pressure and plasma aldosterone concentrations was studied in normal man before and after 66 hours of intravenous infusion of angiotensin II at 2 ng kg-1 min-1, sodium and potassium balance being kept roughly constant throughout. Plasma sodium and ACTH concentrations were unaltered, but plasma potassium and magnesium levels and basal plasma cortisol fell slightly after prolonged angiotensin administration. During the prolonged angiotensin infusion plasma renin activity was suppressed, and there was a sustained elevation of arterial pressure and plasma aldosterone concentration. Aldosterone excretion, while clearly increased, showed a regular circadian rhythm, with peak values in the early morning. The angiotensin II-pressor relationship was not significantly changed after the prolonged infusion of angiotensin II, while the angiotensin II-aldosterone dose-response curve was steeper than in the basal state but not identical with that of sodium depletion. No differences were observed in the pressor or aldosterone-stimulant effects of the isoleucine-5 and valine-5 forms of angiotensin II. A trophic effect of angiotensin II on the adrenal cortex may provide a partial explanation for the enhanced response of aldosterone to angiotensin II in sodium depleted man.

Adrenal Cortex↗
PubMed1975

Estimation of aldosterone, 11-deoxycorticosterone, 18-hydroxy-11-deoxy-corticosterone, corticosterone, cortisol and 11-deoxycortisol in human plasma by gas-liquid chromatography with electron capture detection.

A method for determining the plasma concentrations of six major corticosteroids, aldosterone, 18-hydroxy-11-deoxycorticosterone (18-OH-DOC), corticosterone, deoxycorticosterone (DOC), cortisol and 11-deoxycortisol using gas-liquid chromatography with electron capture detection is described. Esterification of suitable derivatives of these compounds with heptafluorobutyric anhydride (HFB) allowed detection of quantitities of steroid, ranging from 0-3 pg for androstenetrione HFB (from cortisol) to 2-3 pg for corticosterone HFB. No detectable reagent blank was obtained for any compound when water was used instead of plasma and this was also the case when plasma from an adrenalectomized subject was analysed, with the exception of 18-OH-DOC where a reproducible but negligibly small blank occurred. Coefficients of variation for replicate determinations ranged from 8% for corticosterone to 17% for aldosterone. Concentrations in a series of normal human plasma samples were as follows: aldosterone, 4-0- 18-0 ng/100 ml; 18-OH-DOC, 20-16- ng/ml; corticosterone, 0-08 - 0.-80 mug/100 ml; DOC, 2-8 - 16-0 ng/100 ml; cortisol, 2-5 - 10-0 mug/100 ml; and 11-deoxycortisol, 40-0 - 400-0 ng/100 ml. When seven normal subjects were treated with dexamethasone concentrations of DOC, cortisol and 11-deoxycortisol fell to below the limit of the normal range, those of 18-OH-DOC and corticosterone were at the lower end of the normal range while the concentration of aldosterone was not significantly affected.

Adrenal Cortex Hormones↗
PubMed1975

The limitations of statistical correlations in pathology.

Many hypotheses as to the causes of disease, for example some of those for coronary heart disease, depend on statistical correlations. It is well known that correlations do not prove a cause-and-effect relationship, yet it is often tempting to ignore this axiom.

Arteriosclerosis↗
PubMed1975

Plasma angiotensin II, renin, renin-substrate and aldosterone concentrations in acute renal failure in man.

Plasma concentrations of angiotensin II, renin, renin-substrate and aldosterone were measured in cases of acute renal failure. Angiotensin II, and renin levels were abnormally high on at least one occasion in nearly all patients. Mean angiotensin II and renin levels were highest in the first ten days of the disease. There was a highly significant positive correlation between concurrent estimations of renin and angiotensin II. Renin-substrate was also frequently elevated, but the correlations with renin and angiotensin II were not statistically significant. Despite the frequently marked elevation of plasma angiotensin II, only 2 of 17 measurements of plasma aldosterone were abnormally high. There was no significant relationship between aldosterone and plasma concentrations of angiotensin II, renin, sodium or potassium. The data are discussed in relation to current hypotheses implicating renin and angiotensin in the pathogenesis of acute circulatory renal failure.

Acute Kidney Injury↗