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Biomedical subjects

T Morgan

Publications and source records attributed to T Morgan.

At least 145 records · Page 8Linked to original sources
PubMed1983

Monotherapy in the treatment of hypertension.

Approximately 600 people with mild to moderate hypertension were treated with a regimen that started with monotherapy. Reduction in sodium intake achieved adequate blood pressure control in 38 percent, higher than that achieved without therapy (17 percent). Chlorothiazide and propranolol gave satisfactory blood pressure control in 43 and 56 percent of patients, respectively, as sole therapy. When initial blood pressure was greater than 110 mm Hg, satisfactory control was achieved in fewer patients (sodium restriction, 13 percent; chlorothiazide, 30 percent, propranolol 38 percent); in this group, therapy with reduction of sodium intake alone is rarely effective. All measures were about equally successful in treating isolated systolic hypertension. The group given thiazide diuretics alone had an increased number of deaths from myocardial infarcts compared with other groups. This was not seen if a beta-blocking drug or a centrally-acting drug was used in conjunction with the thiazide diuretic. Monotherapy can successfully reduce blood pressure in most patients with mild hypertension. No regimen can be stated to be unequivocally superior to another.

Benzothiadiazines↗
PubMed1983

The effect of sodium intake on the blood pressure related to age and sex.

Two hundred and one volunteers with no known hypertension and 60 patients with untreated hypertension were entered into a study that compared the effect of two levels of sodium intake on blood pressure. One hundred and fifty-four volunteers and 46 hypertensive patients reached compliance goals, with a urinary sodium excretion on the high sodium diet twice that on the reduced sodium intake. The blood pressure on the high sodium diet was 4.5 +/- 0.5 mmHg (n = 154 p less than 0.001) higher than on the reduced sodium diet in normotensive individuals and was increased by 8.4 +/- 1.5 mmHg (n = 46 p less than 0.001) in hypertensive individuals. In the volunteer group the major rise in blood pressure occurred in people over the age of 50. In the hypertensive patients the alteration in blood pressure was not age dependent. In the younger age groups some individuals had an increase in blood pressure when on the high sodium intake which was outside the spontaneous variations in blood pressure of a control group. This implied that a number of young normotensive individuals were susceptible to this alteration in sodium intake. Changes in sodium intake alter blood pressure in hypertensive people, in normotensive people over 50 and in a small number of younger normotensive people. Overall reduction of sodium intake from 200 - 70 mmol/day would reduce the blood pressure level of the population and would reduce the number of people who have a blood pressure that requires drug therapy.

Adolescent↗
PubMed1982

Changes in "active" and "inactive" renin in the juxtaglomerular apparatuses of rat nephrons and plasma induced by different salt intake.

The juxtaglomerular apparatuses (JGA) of deep and superficial nephrons were isolated by microbiopsy or by microdissection. Inactive renin content was determined by acidification of JGA or plasma to pH 3.0. In rats with low salt intake the renin content of superficial JGA was 13.4 +/- 3.0 ng AI/JGA/h before and 20.4 +/- 3.4 ng AI/JGA/h (n = 9), P less than 0.05) after acidification. The corresponding values for deep JGA were 9.1 +/- 1.2 ng AI/JGA/h and 12.7 +/- 2.7 ng AI/JGA/h (n = 9, P less than 0.01). The plasma renin concentration was 54.1 +/- 15.0 ng AI/ml/h before and 56.0 +/- 10.6 ng AI/JGA/h (n = 7, N.S.) after acidification. In rats with a normal salt intake the superficial renin JGA renin content was 11.6 +/- 2.3 ng AI/JGA/h before and 11.0 +/- 2.7 ng AI/JGA/h (n = 9, N.S.) after acidification. The renin content of deep JGA was 4.6 +/- 0.6 ng AI/JGA/h before and 8.6 +/- 3.1 ng AI/JGA/h (n = 9, P less than 0.005) after acidification. Plasma renin concentration was 34.5 +/- 4.7 ng AI/ml/h and did not change after acidification. In rats with a high salt intake superficial JGA content was 6.8 +/- 1.7 ng AI/JGA/h before and 8.4 +/- 2.1 ng AI/JGA/h (n = 9, N.S.) after acidification. The corresponding values for deep JGA were 5.7 +/- 1.6 ng AI/JGA/h and 6.9 +/- 1.6 ng AI/JGA/h (n = 9, N.S.) respectively. Plasma renin concentration was 13.1 +/- 1.1 ng AI/ml/h and this to 21.8 +/- 2.9 ng AI/ml/h (n = 8, P less than 0.01) after acidification. These results suggest that although the synthesis of active and inactive renin is linked, the secretion of the two forms may be independent.

Animals↗
PubMed1982

Formation and activation of renin in vivo.

Active and acid activated renin was measured in glomeruli of rats obtained by microbiopsy and in rat plasma. Sodium depletion increased total and active renin in the juxtaglomerular apparatus and approximately one third of the renin was in an inactive form in sodium depletion. Sodium loading decreased active and total renin and there was no inactive renin present. In plasma changes in a similar direction occurred for active and total renin but in sodium depletion there was no inactive renin present while with sodium loading approximately 40% was in the inactive form. Haemorrhage caused a release of active renin in both sodium states and did not alter the renin content of the J.G.A. Increased delivery of sodium chloride to the macula densa increased the active renin content of J.G.A. but did not alter the total renin content. These results are compatible with two different roles of the renin angiotensin system. One being concerned with intrarenal regulation of glomerular filtration and renal blood flow and the other with maintenance of vascular tone. The conversion of inactive renin to active renin being of particular importance in the regulation of G.F.R.

Animals↗
PubMed1981

The effect of prostaglandin E2 and ADH on diffusional water permeability in collecting duct of an isolated rat papilla.

The effect of prostaglandin on diffusional water permeability has been studied in collecting ducts in an isolated rat papilla. PGE2 increased water permeability. The effect was significant at a concentration of 10(-8) mol 1(-1) and was maximal with a concentration of 10(-6) mol 1(-1). The maximal increment of 0.94 +/- 0.10 (SEM) micron s-1 was approximately half that produced by maximal stimulation with antidiuretic hormone (2.18 +/- 0.12 micron s-1). A concentration of 10(-8) mol 1(-1) produced an increase in basal water permeability and 24 mu unit ml-1 ADH, which without PGE2 present gave a similar increase, had no incremental effect. ADH 100 mu unit ml-1 increased permeability to a value similar to that observed in the absence of PGE2. Thus PGE2 and ADH both increase water permeability but the increments are not additive. Indomethacin in a concentration that inhibited prostaglandin production altered the response of the collecting duct to ADH. The dose response curve was shifted to the left and the maximal increase in water permeability and the lowest dose at which a response occurred took place at concentrations less than 1/2 those required in its absence. Prostaglandins influence the action of ADH and it is likely that in life they regulate and modulate the change in water permeability induced by anti-diuretic hormone.

Animals↗
PubMed1981

Potassium maintenance. Potassium supplements or potassium sparing agents.

This paper reviews and presents data from a series of studies evaluating the extent of potassium depletion that occurs in various disease states and a comparison of the efficacy of potassium supplementation or potassium sparing diuretics in its correction. Changes in serum potassium levels are common after diuretics but are relatively minor in most people if small doses of diuretics are used. Total body potassium deficit is uncommon in people treated with a diuretic for hypertension and the fall in serum potassium results from alkalosis and a shift of potassium into the cell. Potassium sparing diuretics correct the potassium abnormality more readily than potassium supplements. Evidence is also presented that suggests that a high salt, low potassium diet may be an important cause of hypokalemia in people given diuretics.

Benzothiadiazines↗
PubMed1981

A method for the noninvasive evaluation of cardiovascular dynamics using a digital radiographic device.

The authors describe a technique for visualizing and quantitating blood flow and cardiac dynamics following the intravenous administration of contrast material (less than 1 ml/kg). This method uses a digital radiographic device while motion by the patient or test subject is stopped. Preliminary flow studies of the carotid arteries and heart of a dog are presented. This technique has the potential to quantitate physiological parameters such as relative blood flow through pairs of arteries, cardiac output, regional ejection fraction, and heart-wall movement and thickening.

Animals↗
PubMed1981

Sodium intake, blood pressure and red cell sodium efflux.

A series of studies have been undertaken correlating sodium intake, blood pressure and red cell 22Na efflux. The results for male and female patients differ. In male patients with elevated blood pressure, increased sodium intake caused a rise in blood pressure and a fall in red cell 22Na efflux rate. In female patients the results were variable and while certain females followed the above pattern, others had the converse response. Evidence is presented that the change in red cell 22Na efflux is due to a factor in plasma that inhibits the ouabain sensitive component of sodium efflux. This increases after acute and chronic sodium loading and may be similar to natriuretic factor described previously. It is postulated that increased sodium intake causes hypertension by producing a humoral factor that inhibits sodium transport out of cells and that this alters the calcium content of muscle cells and increases their contractility and thus produces hypertension.

Adolescent↗
PubMed1980

Long-term experiences with labetalol.

Labetalol has been used in 83 patients with severe hypertension resistant to a wide number of drugs. Adequate blood pressure control was achieved in 50 patients. Seven patients with a response in blood pressure had administration of the drug ceased because of side effects. Twenty-two of these resistant patients had little fall in blood pressure. Labetalol can be used safely in severe resistant hypertension and is indicated when a thiazide and beta-blocking drug has failed to reduce blood pressure.

Adult↗
PubMed1980

Comparison of piretanide and chlorothiazide in the treatment of cardiac failure.

Piretanide, a diuretic that acts on the loop of Henle, was used to treat patients with cardiac failure. Over a three-day period it caused a significant dose related diuresis and weight loss. It was as effective as chlorothiazide in the control of cardiac failure and was well tolerated by the patients. Potassium loss was less than occurred with chlorothiazide. Its role in the treatment of cardiac failure requires further study and warrants further investigation. The study also showed that many patients with cardiac failure receive diuretic drugs which are not necessary.

Adult↗