A longitudinal study of the hypertensive process in man.
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Biomedical subjects
Publications and source records attributed to T L Kho.
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The effect of propranolol on diurnal variability of BP and plasma noradrenaline levels was assessed in 15 patients with uncomplicated essential hypertension. While total variability and average noradrenaline level remained unaltered, the pressor range (difference between basal and maximum BP readings) was reduced in most patients. An inverse relationship was observed between changes in pressor range and noradrenaline.
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1. Twenty-three subjects with essential hypertension were followed for a period of up to 7 years. They were untreated during the investigations. 2. Plasma renin concentration was found to decrease temporarily in some subjects. The ultimate change was a gradual rise. In those subjects who suffered myocardial infarction renin tended to rise more sharply. 3. A relationship was established with the rise in renal vascular resistance, which almost invariably occurred over the years.
1. The cardio-renal haemodynamic and endocrine effects of the anti-hypertensive agents 2-(2,6-dichlorophenylamine)-2-imidazoline hydrochloride (clonidine, St 155) and 2-(5-fluor-o-toluidine)-2-imidazoline hydrochloride (St 600) were investigated in twelve patients with essential hypertension. 2. The anti-hypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no alteration in renal blood flow and glomerular filtration rate, and renal vascular resistance showed a significant decrease. Blood volume and plasma renin concentration did not change significantly. An inverse relation changes in plasma volume and plasma aldosterone concentration was observed. In the face of similar reductions in blood pressure, no differences were observed between systemic and renal haemodynamic and endocrine responses after clonidine and St 600.
In a prospective study of patients with essential hypertension, plasma renin levels showed a progressive increase with longer follow-up. This was associated with a parallel increase in renal vascular resistance. Arterial blood pressure and plasma volume did not change significantly during follow-up. In patients where the hypertension was complicated by myocardial infarction there was a comparatively greater increase in renin levels and renal vascular resistance which may be attributable to chronic reduction of cardiac output.
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The effects of the antihypertensive imidazoline compounds 2-(5 fluor-0-toluidine)-2-imidazoline hydrochloride (ST 600) and 2-(2, 6 dichlorophenylamine)-2-imidazoline hydrochloride (ST 155, catapres) on intra-arterial pressure, cardiac output, stroke volume, heart rate, total peripheral resistance, renal blood flow, glomerular filtration rate, renal vascular resistance, plasma volume, plasma renin and aldosterone concentration were studied in five patients with essential hypertension. The antihypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no significant decrease in renal blood flow and glomerular filtration rate. Plasma volume and plasma concentrations of renin and aldosterone also did not change significantly. In the face of similar reductions in blood pressure, no differences were observed between cardio-renal haemodynamic responses after ST 600 and catapres. However ST 600 had a longer lasting effect (8-12 hours).
The effects of the antihypertensive imidazoline compounds 2-(5 fluor-0-toluidine)-2-imidazoline hydrochloride (ST 600) and 2-(2, 6 dichlorophenylamine)-2-imidazoline hydrochloride (ST 155, clonidine, Catapres) on intra-arterial pressure, cardiac output, stroke volume, heart rate, total peripheral resistance, renal blood flow, glomerular filtration rate, renal vascular resistance, plasma volume, plasma renin and aldosterone concentration were studied in five patients with essential hypertension. The antihypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no significant decrease in renal blood flow and glomerular filtration rate. Plasma volume and plasma concentrations of renin and aldosterone also did not change significantly. In the face of similar reductions in blood pressure, no differences were observed between cardio-renal haemodynamic responses after ST 600 and clonidine. However ST 600 had a longer lasting effect (8-12 hours).