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Biomedical subjects

J B Ferriss

Publications and source records attributed to J B Ferriss.

At least 37 records · Page 2Linked to original sources
PubMed1987

Enalapril and microalbuminuria in diabetic and non-diabetic hypertension.

Nine patients with non-insulin-dependent diabetes mellitus (NIDDM) and ten non-diabetic patients with mild hypertension were treated with enalapril 20 mg daily. None had overt nephropathy, though 4 diabetic subjects had microalbuminuria. Subjects with the highest baseline albumin excretion rates (AER) showed the greatest fall on therapy. Metabolic control of diabetes did not deteriorate. Enalapril had no significant effect on AER in NIDDM patients with AER below 20 micrograms/minute or in the non-diabetic group.

Adult↗
PubMed1987

The pressor response to exercise and stress in uncomplicated insulin-dependent diabetes.

We investigated whether or not an increased pressor response to exercise or stress is a feature of the diabetic state per se or a feature of its complications was investigated. Twelve insulin-dependent diabetic patients without clinical evidence of complications and with normal albumin excretion rates (less than 20 micrograms/min) were studied together with 12 matched control subjects. Each underwent a study protocol of isometric handgrip exercise at 30% of maximum capacity for four minutes, a cold pressor test with immersion of one hand in ice-cold water for two minutes, and bicycle ergometry at a resistance of 105 watts per minute for six minutes. The tests were undertaken in the same order in all subjects. There was, in both groups, a similar and significant rise in systolic blood pressure and pulse rate in response to each stimulus. Diastolic pressure also rose significantly in response to handgrip exercise and to cold pressor stimulation, but fell slightly during bicycle ergometry in both groups. Mean plasma noradrenaline concentration rose in response to each stimulus but the changes reached conventional significance in both groups only in response to handgrip exercise. Pressor responses to exercise and stress, as tested here, are concluded to be normal in insulin-dependent diabetic patients without complications due to their disease.

Adolescent↗
PubMed1986

Diabetic orthostatic hypotension: the role of total exchangeable sodium and nephropathy.

The purpose of this report was to examine the influence of nephropathy and sodium balance on the orthostatic blood pressure and renin (PRA) responses of diabetic patients with orthostatic hypotension (OH). Four groups of similar age were studied: non-diabetic controls (n = 7), diabetics free of OH and other diabetic complications (n = 7), diabetics with OH but no nephropathy (n = 6), and diabetics with OH and nephropathy (24-hr urine protein greater than 400 mg, n = 6). In the diabetics with OH, mean systolic BP fell 49 and 47 mmHg on standing in the groups without and with nephropathy respectively. NaE (expressed as % predicted by leanness index) differed significantly between the groups and was 100 +/- 2 in the controls, 109 +/- 3 in the diabetics free of complications, 102 +/- 2 in the diabetics with OH free of nephropathy, and 121 +/- 6 in diabetics with OH and nephropathy (p less than 0.05 compared to diabetics with OH and no nephropathy). Both supine (r = 0.68, p less than 0.02) and upright (r = 0.78, p less than 0.005) mean arterial pressure correlated with NaE in diabetics with OH but not in the other groups. Upright PRA was greatest in diabetics with OH but no nephropathy and lowest in diabetics with OH and nephropathy. These findings suggest that the presence of nephropathy markedly influences sodium balance in diabetics with OH and has a substantial influence on orthostatic BP and PRA responses.

Adult↗
PubMed1984

Increased vasopressor responsiveness to angiotensin II in type 1 (insulin-dependent) diabetic patients without complications.

The blood pressure response to infused angiotensin II (0.3 to 3 ng X kg-1 X min-1) was investigated in six normotensive patients with Type 1 (insulin-dependent) diabetes free of complications and in six healthy subjects matched for age, sex and weight. Basal blood pressures (111/68 and 114/72 mmHg) and basal plasma angiotensin II levels (18.0 +/- 5.2 and 14.1 +/- 2.4 pmol/l; mean + SD) were similar in the diabetic and control groups as were 24 h urinary excretions of sodium (157 +/- 88 and 154 +/- 84 mmol/24 h). Equal increments in plasma angiotensin II were produced during the infusions in the two groups. Increases in both diastolic and systolic blood pressure were significantly greater in the diabetic patients throughout the infusion. Mean diastolic increments were: 6.7 versus 1.3 mmHg (0.3 ng dose), 11.0 versus 6.9 mmHg (1 ng dose) and 16.7 versus 12.3 mmHg (3 ng dose) (p less than 0.001). Corresponding figures for systolic pressure were: 8.7 versus 1.3 mmHg, 10.3 versus 3.7 mmHg and 15.3 versus 8.7 mmHg (p less than 0.001). Vasopressor responsiveness to angiotensin II is thus increased in Type 1 diabetic patients without complications; it may, therefore, be a consequence of the diabetes rather than of the presence of microvascular disease or hypertension.

Adult↗
PubMed1983

Poor metabolic control, hypertension and microangiopathy independently increase the transcapillary escape rate of albumin in diabetes.

Available evidence indicates that poor metabolic control and raised blood pressure each accelerate the development of diabetic microangiopathy. Microangiopathy is associated with excess albumin deposition in capillary basement membranes and it has been suggested that increased extravasation of plasma constituents may lead to basement membrane thickening. We measured the transcapillary escape rate of albumin, an indicator of the rate of extravasation of intravascular albumin from the circulation per unit time, following intravenous injection of 125I-human serum albumin. We examined the independent effects on the transcapillary escape rate of albumin of non-ketotic poor metabolic control, hypertension and microangiopathy. We studied non-diabetic control subjects and diabetic patients, initially when in non-ketotic poor metabolic control and again when control had been improved. We also studied normotensive well-controlled diabetic patients without microangiopathy, normotensive well-controlled diabetic patients with microangiopathy, hypertensive well-controlled diabetic patients without microangiopathy and hypertensive well-controlled diabetic patients with microangiopathy. The transcapillary escape rate of albumin was similar in non-diabetic control subjects (5.5 +/- 0.7%/h) and in both Type 1 (5.3 +/- 1.2%/h) and Type 2 (5.1 +/- 0.6%/h) normotensive diabetic patients without long-term complications. During poor metabolic control the transcapillary escape rate of albumin was significantly higher than in non-diabetic subjects (8.8 +/- 0.8%/h and 5.5 +/- 0.7%/h respectively, p less than 0.01). With improved control values fell significantly to 6.3 +/- 0.9%/h (p less than 0.02), not significantly different from control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Primary hyperparathyroidism associated with primary hyperaldosteronism.

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.

Adult↗
PubMed1982

Plasma angiotensin II and aldosterone in unselected diabetic patients.

The concentrations of angiotensin II and aldosterone in plasma were measured in 101 consecutive unselected out-patient diabetic patients and in fifty-three normal controls. The concentration of angiotensin II was similar in diabetics without complications and controls, but was significantly lower in patients with hypertension or peripheral neuropathy. In contrast, plasma aldosterone was not reduced in any sub-group. The concentrations of angiotensin II and aldosterone were positively correlated in controls, in diabetes without complications and in hypertensive diabetics, but this relationship was not found in patients with peripheral neuropathy, retinopathy or nephropathy. There was no evidence of overt hypoaldosteronism in any of the diabetic patients. No individual aldosterone concentration was below the range found in controls and no plasma angiotensin II concentration is reduced in patients with specific diabetic complications such as neuropathy, plasma aldosterone may be maintained by factors other than the renin-angiotensin system. This would explain why hypoaldosteronism is rare among unselected diabetics.

Adolescent↗
PubMed1980

Plasma angiotensin II and the control of diabetes mellitus.

Plasma angiotensin II was measured in twenty patients with poorly controlled non-ketotic diabetes mellitus, and again when blood glucose control improved. Plasma angiotensin II fell significantly improved control, both when patients were supine and fasting overnight, and when studied after 4 h ambulation. The change occurred with improved short-term and longer-term control. It is concluded that the degree of blood glucose control is important when assessing the renin-angiotensin system in diabetic patients.

Adolescent↗