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Biomedical subjects

R Fraser

Publications and source records attributed to R Fraser.

At least 361 records · Page 20Linked to original sources
PubMed1977

Amiloride in the treatment of primary hyperaldosteronism and essential hypertension.

Amiloride (40 mg/day) was given to nineteen patients with primary hyperaldosteronism. There were significant falls in systolic and diastolic blood pressure, in total exchangeable sodium, and in serum sodium sodium and bicarbonate; while total exchangeable potassium, total body potassium, serum potassium, chloride and urea, and plasma renin, angiotensin II and aldosterone all increased significantly. Amiloride was effective in reducing blood pressure in patients with and without adrenocortical adenoma. No carry-over effect was seen on withdrawing amiloride. Similar changes were associated with amiloride treatment in five patients with essential hypertension; hyperkalaemia was not observed. Only negligible side-effects were encountered in the entire series of twenty-four patients.

Adult↗
PubMed1976

Effects of intravenous labetalol on blood pressure, angiotensin II and aldosterone in hypertension: comparison with propranolol.

1. Labetalol, a compound with both alpha- and beta-adrenoreceptor-blocking actions, was given intravenously (1-5-2-0 mg/kg) in twenty recumbent hypertensive patients. 2. There was a rapid reduction in systolic and diastolic pressures in all, maintained up to 24 h in some subjects. 3. Severe hypotension was not seen in recumbent subjects, but postural hypotension was common. 4. Labetalol caused significant lowering of heart rate. 5. Labetalol induced significant and related lowering of plasma angiotensin II and aldosterone concentrations, most obviously when these were initially high. 6. In a cross-over comparison in five patients against 10 mg of propranolol intravenously, labetalol was more effective in lowering blood pressure, but less effective in lowering pulse rate or plasma angiotensin II.

Aldosterone↗
PubMed1976

The effects of saralasin, an angiotensin II antagonist, on blood pressure and the renin-angiotensin-aldosterone system in normal and hypertensive subjects.

Blood pressure reduction with saralasin infusion was seen only in hypertensive patients with abnormally elevated basal plasma renin and angiotensin II levels, and after sodium depletion the reduction in blood pressure was more marked. In normal subjects, and in hypertensives with plasma renin and angiotensin II levels within the normal range, there was no marked fall in blood pressure across saralasin infusion regardless of the sodium status of the individual. Plasma aldosterone concentration fell during saralasin infusion in those subjects with high baseline renin and angiotensin II levels. This fall occurred in the sodium replete and deplete states. In the normal subjects, and those hypertensives with normal plasma renin levels, there was no fall in aldosterone in the sodium replete state. However, after sodium depletion the expected rise in aldosterone was abolished during saralasin infusion, the plasma aldosterone falling to within the normal sodium replete range, rising again after the saralasin infusion was stopped. This study supports the concept of a direct role for renin and angiotensin II in the maintenance of hypertension in those subjects with elevated basal plasma renin. Plasma aldosterone would appear to be controlled, at least in part, by the prevailing plasma angiotensin II level in those subjects with elevated basal levels of angiotensin II; that is in high renin hypertensives, and in normal subjects and normal renin hypertensives who are sodium deplete.

Adult↗
PubMed1976

Labetalol (AH5158), a competitive alpha- and beta-receptor blocking drug, in the management of hypertension.

The effects of intravenous labetalol, a drug with both alpha- and beta-adrenergic receptor blocking actions, have been studied in 20 severely hypertensive patients. There was a prompt and sustained fall in arterial pressure; severe hypotension did not occur in recumbent patients but postural hypotension was common. Pulse rate was consistently reduced, but bradycardia was not a problem. Significant and correlated falls in plasma angiotensin II and aldosterone were seen. In a direct comparison with intravenous propranolol, labetalol was less effective in lowering plasma angiotensin II, but more effective in reducing blood pressure. Oral labetalol provided good control of blood pressure and other features in two patients with phaeochromocytoma. Intravenous labetalol was similarly effective in controlling a hypertensive crisis following clonidine withdrawal.

Adrenergic alpha-Antagonists↗
PubMed1976

Measurement of plasma renin concentration and angiotensin II in peripheral and renal venous plasma in the management of renovascular hypertension.

Athough in general, measurement of renal vein renin appears to give a good prediction as to the subsequent response to surgery, its main value lies in its ability to reflect changes in renal plasma flow; true changes in renin secretion rate being much more difficult to detect. Although it is a little early to say how much information can be derived from saralasin infusions, caution must be exercised in necessarily assuming that the test accurately reflects subsequent surgical response.

Adult↗
PubMed1976

Response of aldosterone and blood pressure to angiotensin II infusion in anephric man. Effect of sodium deprivation.

Angiotensin II, infused intravenously, increased plasma aldosterone concentration in two of six anephric subjects taking their usual dietary quantities of sodium. After 3 days of dietary sodium restriction and weight-reducing hemodialysis, the aldosterone response to infused angiotensin II in the two previously reactive subjects was enhanced, while the four previously unreactive subjects also showed a rise in plasma aldosterone. Before and after sodium depletion the anephric subjects were less responsive than normal subjects. Even when sodium-depleted, the anephrics showed no further rise in plasma aldosterone when arterial plasma angiotensin II was increased by infusion to concentrations greater than 50-199pg/ml, in contrast to sodium-depleted normals who show progressive aldosterone responses with plasma angiotensin II concentrations up to at least 370pg/ml. Before the infusion of angiotensin II, arterial plasma renin, angiotensin II, and aldosterone were detectable in the anephrics, but were unchanged by dietary sodium restriction or weight-reducting hemodialysis. Sodium depletion caused significant falls in weight, plasma sodium, and blood pressure, but no changes in plasma potassium or cortisol. Increases in blood pressure in relation to increments of arterial plasma angiotensin II were unaffected by sodium depletion, as might be expected in the absence of a rise in endogenous angiotensin II.

Adult↗
PubMed1976

Free cortisol in obesity; effect of fasting.

Plasma and urinary corticosteroids were measured in 13 obese subjects before and after high and low protein diets, and after fasting. During isocaloric high and low protein diets, urinary 17-oxogenic steroids and to a lesser extent urinary free cortisol excretion rose and fell in parallel with protein intake. Plasma unbound cortisol levels were not much changed by high or low protein intake. However, during 7 to 11 days total fasting, there was a highly significant rise in plasma unbound cortisol at 24.00. A smaller rise occurred at 09.00. The overall effect was a considerable diminution of the day-night variation of plasma unbound coritsol levels during fasting, and a rise in prevailing unbound cortisol levels and urinary free cortisol excretion. In 3 subjects tested these changes were reversed immediately by glucose re-feeding.

17-Ketosteroids↗
PubMed1976

New interpretations of lipoproteins and arterial lesions of cholesterol-fed rabbits.

The serum of cholesterol-fed rabbits contains lipoproteins rich in cholesterol, in contrast to those in thoracic duct lymph, which are rich in triglyceride. This study suggests that the serum lipoproteins may be "remnant" chylomicrons which have been stripped of their triglyceride, but which have not been removed from circulation by the liver, as usually occurs rapidly in other animal species. Electrophoresis of rabbit serum showed a broad beta band corresponding to the very low density lipoprotein fraction separated by ultracentritrifugation. This broad beta band may represent the "remnant particles". This proposed "remnant particle" hyperlipidaemia in rabbits may have its parallel in Type III human hyperlipidaemia, which also has a broad beta band on electrophoresis and may be a "remnant particle" disease. It was also found that early arterial lesions in rabbits are similar to some human fatty streaks, which if allowed to age for a further two years while the rabbits eat normal food, do not regress but mature to resemble calcified fibrous plaques.

Animals↗
PubMed1976

Studies of the renin-angiotension-aldosterone system, cortisol, DOC, and ADH in normal and hypertensive pregnancy.

Compared with a group of normal pregnant women, matched for age, parity, posture, and length of gestation, women with hypertension and proteinuria in the last trimester had significantly lower plasma concentrations of renin, renin substrate and angiotensin II. Plasma aldosterone and DOC concentrations were also lower in the hypertensive group. The plasma levels of cortisol, corticosterone, and ADH showed no significant difference. Plasma renin concentration was raised throughout normal pregnancy, and part of this increase appeared to be due to the presence of an inactive form of renin. Plasma concentrations of renin substrate, angiotensin II, and aldosterone were also raised in normal pregnant women, but concurrent measurement of these substances showed no significant relationship between them, renin, and plasma electrolytes in mid- or late gestation. A study of five women in the weeks immediately after conception showed increases in plasma angiotensin II and aldosterone concentrations, which were significantly related at this very early stage of pregnancy. Total 24-hour urinary sodium increased gradually from about two weeks after gestation to the end of the study five weeks later. This increase was due mainly to a rise in overnight sodium excretion, with a fall in the day/night ratio. No relationship was found between plasma angiotension II or aldosterone concentrations and day, night, or total 24 hour sodium excretion.

Adrenal Cortex Hormones↗
PubMed1976

The effects of the angiotensin II antagonist saralasin on blood pressure and plasma aldosterone in man in relation to the prevailing plasma angiotensin II concentration.

The effect of saralasin in lowering blood pressure and plasma aldosterone concentration in normal subjects, both sodium-replete and sodium-deplete, and in patients with various forms of hypertension, is closely related to the basal plasma angiotensin II concentration. These findings confirm and extend earlier studies of angiotensin II/arterial pressure and angiotensin II/aldosterone dose-response curves. They also emphasize the importance of the renin-angiotensin system in the control of aldosterone in sodium depletion and in renal hypertension.

Aldosterone↗