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Biomedical subjects

J J Morton

Publications and source records attributed to J J Morton.

At least 19 recordsLinked to original sources
PubMed1979

T and B lymphocytes in patients with acute anterior uveitis and ankylosing spondylitis, and in their household contacts.

During episodes of acute anterior uveitis, patients had a T-lymphopenia and a temporary increase in B-lymphocytes. The T-lymphopenia was not present in patients investigated early in their first attacks, and it persisted after the patients recovered clinically. In household contacts of patients with uveitis, there was a temporary T-lymphopenia. A similar degree of T-lymphopenia was present in patients with ankylosing spondylitis who had not had uveitis, but not in their household contacts. In patients with spondylitis, there was no greater reduction of T-cells when they had episodes of uveitis. In all groups of subjects studied, T-lymphopenia could be abolished, in vitro, with thymosin, a bovine thymic-hormone estract. The finding of T-lymphocyte depletion in the contacts of uveitis patients, as well as in the patients themselves, suggests that there may be lateral transmission of an infective agent (or agents) in the households during (or before) attacks of uveitis.

Acute Disease↗
PubMed1979

Hyponatraemic hypertensive syndrome with renal-artery occlusion corrected by captopril.

Malignant hypertension with severe hyponatraemia, hypokalaemia, depletion of sodium and potassium, and elevated blood levels of renin, angiotensin I, angiotensin II, aldosterone, and arginine vasopressin developed in a woman with renal-artery occlusion. Plasma angiotensin II was disproportionately high in relation to exchangeable sodium. Captopril, by inhibiting conversion of angiotensin I to angiotensin II, further elevated the blood levels of renin and angiotensin I but corrected all other abnormalities. Unilateral nephrectomy was subsequently curative.

Aldosterone↗
PubMed1979

Relationship between exchangeable sodium and blood pressure in different forms of hypertension in man.

1. Arterial pressure and exchangeable sodium (NaE) were measured in patients with Conn's syndrome, essential hypertension, renal artery stenosis and chronic renal failure. Comparison was made with a control group. Urine sodium excretion was measured separately from the two kidneys in patients with renal artery stenosis. 2. Compared with control, mean NaE was significantly increased in Conn's syndrome, and was normal in essential hypertension, renal artery stenosis and chronic renal failure. 3. The correlation of arterial pressure with NaE was positive and significant in Conn's syndrome, essential hypertension and chronic renal failure. 4. In contrast the correlation was significantly negative in unilateral renal artery stenosis. Patients with lowest NaE had hyponatraemia, hypokalaemia and secondary hyperaldosteronism. 5. Urinary sodium excretion from the unaffected kidney in unilateral renal artery stenosis correlated positively with arterial pressure, possibly reflecting the phenomenon of pressure-natriuresis. Patients subsequently responding least well to surgery excreted least sodium from the untouched kidney for a given arterial pressure. 6. The findings suggest important roles for arterial pressure in the regulation of sodium balance (predominant in renal artery stenosis), and for sodium balance in the regulation of arterial pressure (predominant in Conn's syndrome). The observations in essential hypertension are compatible either with an exact balance between these mechanisms or with the existence of some other mechanism raising blood pressure.

Adult↗
PubMed1979

Inhibitors of the renin-angiotensin system in experimental hypertension, with a note on the measurement of angiotensin I, II and III during infusion of converting-enzyme inhibitor.

1 Prolonged infusion (11 h) of both saralasin and angiotensin-converting enzyme inhibitor (SQ20881) gradually lowered BP in two-kidney hypertensive rats to levels similar to that in normotensive rats infused with dextrose. 2 Saralasin did not lower BP in DOCA-salt hypertensive rats. 3 These observations support the notion that in chronic renal hypertension, angiotensin II may maintain hypertension by a slowly developing action. 4 Plasma angiotensin II in rats infused with SQ20881 was suppressed relative to renin, but was not eliminated. 5 Chromatography of angiotensin II extracts from dogs infused with converting enzyme inhibitor (SQ14,225) showed that the very high levels of angiotensin I achieved after treatment with SQ14,225 can lead to falsely high estimated angiotensin II levels as a result of angiotensin I cross-reacting with the angiotensin II assay.

Angiotensin I↗
PubMed1979

Blood pressure reduction by incremental infusion of labetalol in patients with severe hypertension.

1. Labetalol was given by incremental intravenous infusion to nineteen severely hypertensive patients, of whom nine were refractory to previous oral antihypertensive therapy. 2. Smooth reduction of arterial pressure was achieved in twelve subjects; one remained resistant to labetalol up to 160 mg/h; a sudden fall in pressure occurred in the remaining six. No serious complications were encountered. Blood pressure control was accompanied by slight byt significant reduction in heart rate and in plasma angiotensin II and aldosterone concentrations. 3. The administration of labetalol in this way appears to be a useful technique in patients requiring rapid reduction of arterial pressure, although close and continuous supervision is necessary.

Adolescent↗
PubMed1979

Effect of the angiotensin II antagonist saralasin on plasma aldosterone concentration and on blood pressure before and during sodium depletion in normal subjects.

The effect of the angiotensin II antagonist saralasin on plasma aldosterone, plasma angiotensin II and blood pressure was studied in six normal supine subjects both before and during sodium depletion. Before sodium depletion, infusion of saralasin produced no consistent changes; during sodium depletion, infusion of the angiotensin antagonist caused a fall in plasma aldosterone and an increase in plasma angiotensin II in each subject. It is concluded that angiotensin II plays a major part in stimulating aldosterone secretion during sodium depletion in man.

Adult↗
PubMed1979

Potassium in the syndrome of inappropriate antidiuretic hormone secretion.

Serum potassium concentration was normal (greater than or equal to 3.6 mmol/l) in 29 of 32 patients with the syndrome of inappropriate antidiuretic hormone excess (SIADH) associated with a bronchogenic carcinoma. In 11 of the patients there was no significant change in serum potassium concentration after correction of the syndrome, by fluid restriction. Hypokalaemia is thus an uncommon finding in SIADH due to bronchogenic carcinomas.

Aged↗
PubMed1979

The vasodepressor action of prostacyclin (PGI2) and its effect on plasma angiotensin II and vasopressin in unanaesthetized normotensive and hypertensive rats.

The action of prostacyclin (PGI2) on arterial pressure, heart rate, plasma concentration of angiotensin II and vasopressin was studied in groups of normal, renal hypertensive and DOC hypertensive rats. PGI2 was given by continuous iv. infusion at successive doses of 0.25, 0.5 and 1.0 microgram/kg x min, each rate for one hour. Arterial pressure was reduced to normal or below normal in the hypertensive rats, though the fall of blood pressure was greatest in the DOC hypertensive animals. Mean arterial pressure at the end of infusion was 89 mm Hg for normal rats, 87 mm Hg for renal hypertensive rats and 69 mm Hg for DOC hypertensive rats. Diastolic pressure fell more than systolic pressure suggesting a vasodilator mechanism. Heart rate was reduced significantly at the end of the infusion in the three groups of rats. Prostacyclin was also infused for 3 hours at a constant rate of 0.5 microgram/kg x min. The arterial pressure lowering effect was maintained throughout the infusion period.

Angiotensin II↗
PubMed1978

A renal carcinoma secreting inactive renin.

1. A patient presented with mild hypertension, a raised plasma total renin concentration but a normal plasma angiotensin II concentration. The discrepancy was due to a high concentration of inactive renin in the plasma. 2. A renal carcinoma was detected and removed. The tumour contained a higher proportion of inactive renin than was found in uninvolved areas of the kidney. After unilateral nephrectomy, the plasma concentration of inactive renin fell to normal. 3. Six months later, plasma inactive renin concentration again increased and a metastasis was detected in a rib. Excision of the rib together with radiotherapy resulted in a fall in plasma inactive renin to normal. 4. The inactive renin in plasma and tumour extracts was activated to the same extent by acid treatment and by trypsin.

Aged↗