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Biomedical subjects

I B Davies

Publications and source records attributed to I B Davies.

13 recordsLinked to original sources
PubMed1990

Betaxolol and glucose-insulin relationships: studies in normal subjects taking glibenclamide or metformin.

1. The potential interaction between selective beta 1-adrenoceptor blockers and sulphonylureas or biguanides was studied by comparing the beta 1-adrenoceptor antagonist betaxolol with placebo in 12 normal subjects taking glibenclamide or metformin in a single-blind crossover group study. 2. After a 4 day run-in period on no treatment, six subjects took glibenclamide 2.5 mg twice daily, and six subjects took metformin 850 mg twice daily from day 5 to day 19. All subjects took betaxolol 20 mg daily from day 10 to day 13, and placebo from day 5 to day 10 and from day 13 to day 19. 3. Plasma glucose and insulin concentrations were measured fasting and 60 min after a standard breakfast for 3 successive days during each study treatment; plasma potassium, sodium and betaxolol concentrations were also measured. 4. Fasting glucose, insulin and potassium concentrations did not differ significantly between betaxolol and placebo treatment periods in either glibenclamide- or metformin-treated groups. Post-prandial glucose and insulin concentrations were lower and higher, respectively, relative to fasting concentrations but there was no significant difference between any of the treatment periods. Glibenclamide produced significant increases in insulin concentrations compared with drug-free periods (P less than 0.01). Plasma potassium and sodium concentrations were not affected by any of the treatments. 5. Plasma betaxolol concentrations were adequate for beta 1-adrenoceptor blockade. 6. This study suggests that selective beta 1-adrenoceptor blockade with betaxolol does not change fasting or post-prandial glucose-insulin relationships during simultaneous treatment with either the sulphonylurea glibenclamide or the biguanide metformin.

Adult↗
PubMed1989

Alfuzosin and the venous reflex response: studies in normal subjects.

1. Alfuzosin is a post-synaptic alpha-adrenoceptor antagonist with antihypertensive and peripheral vasodilator properties. 2. We measured the effect of alfuzosin, 5 mg, on sympathetically-mediated venoconstriction by changes in the venous reflex response (VRR) in a randomised, double-blind, placebo-controlled, crossover study in a group of 10 healthy volunteers. 3. There was a significant inhibition of the VRR after alfuzosin compared with placebo (P less than 0.001) which was present 1 h after the dose and still evident at 6 h. 4. Supine blood pressure was significantly lower (P less than 0.01) and supine heart rate was significantly higher (P less than 0.001) after alfuzosin compared with placebo. 5. Inhibition of the VRR by alfuzosin was observed to precede the development of reflex tachycardia.

Adult↗
PubMed1981

Endogenous agonist regulation of alpha-adrenoceptors in man.

1. Plasma noradrenaline concentrations and platelet alpha-receptor properties were measured in 14 normal subjects, five phaeochromocytoma patients and nine patients with multiple system atrophy and sympathetic nervous system degeneration (MSA). 2. Plasma noradrenaline concentrations in phaeochromocytoma were 10- to 20-times greater than those of normal subjects and one-fifth to one-half of normal in MSA patients. 3. Platelet alpha-receptor numbers were increased in MSA and decreased in phaeochromocytoma compared with normal subjects. There was no change in platelet alpha-receptor affinity in either group. 4. The inverse relationship between alpha-receptor numbers and plasma noradrenaline concentrations may reflect regulation of alpha-receptor number by endogenous adrenergic agonist concentrations in man.

Adrenal Gland Neoplasms↗
PubMed1981

beta-Receptor numbers and thermodynamics in denervation supersensitivity.

1. Denervation supersensitivity to adrenergic agonists occurs after degeneration of the sympathetic nervous system in the disease called multiple system atrophy (MSA) or the Shy Drager Syndrome.2. Supersensitivity to the chronotropic effect of i.v. isoprenaline on the heart was demonstrated in eight subjects with sympathetic nervous system degeneration and MSA.3. There was an increased number of beta-receptors present in MSA as measured by [H(3)]dihydroalprenolol ([H(3)]DHA) binding to beta-receptors on lymphocytes isolated from venous blood taken from the MSA subjects compared with [H(3)]DHA binding to lymphocytes from seven normal subjects. There was no difference in the affinity of lymphocyte beta-receptors for [H(3)]DHA in MSA.4. [H(3)]DHA binding to lymphocytes from MSA subjects was decreased at lower temperatures but was unaffected by lower temperatures in lymphocytes from normal subjects.5. Equilibrium constants for [H(3)]DHA binding to normal and MSA lymphocytes were similar, indicating that the affinity of the beta-receptors was similar in both groups. The equilibrium constants were little affected by cooling from 37 to 4 degrees C suggesting that the heat of reaction (enthalpy) for [H(3)]DHA binding was low. The Gibbs free energy change on binding was negative and similar in quantity for both normal and MSA lymphocytes. There was a similar, large, increase in entropy on binding of [H(3)]DHA to both normal and MSA lymphocytes, showing that the binding reaction was entropy driven.6. If lymphocyte beta-receptors reflect the status of cardiac beta-receptors, increased numbers of cardiac beta-receptors may contribute to the denervation supersensitivity to isoprenaline in MSA with sympathetic degeneration.

Adult↗
PubMed1979

Sympathetic reflex responses during treatment of essential hypertension with hydrallazine and oxprenolol.

1. The short term effects of hydrallazine, oxprenolol and oxprenolol plus hydrallazine were studied in five patients with essential hypertension. 2. The increase in pulse rate caused by hydrallazine was prevented by combined treatment with oxprenolol, which also lowered the high plasma noradrenaline levels, associated with the use of hydrallazine. 3. Plasma renin activity was higher in the supine and standing positions with hydrallazine than with oxprenolol alone and with the patients standing this high renin level was prevented by simultaneous treatment with oxprenolol. With the patients supine, combination of oxprenolol with hydrallazine resulted in a mean plasma renin activity which was less than half that with hydrallazine alone, although this difference was not statistically significant. 4. The combination of oxprenolol with hydrallazine did not lower the blood pressure further, but reduced the increased sympathetic activity which occurred with hydrallazine alone.

Blood Pressure↗
PubMed1979

Ethnic differences in blood pressure with observations on noradrenaline and renin. 1. A working population.

115 factory workers (62 white, 53 black) were studied with measurements of blood pressure, plasma noradrenaline concentration, and plasma renin activity. Blood pressure was higher in blacks than in whites. There were no ethnic differences in plasma noradrenaline, which increased with age, but was not related to blood pressure. Mean plasma renin activity was 55% lower in blacks than whites and this difference was not related to differences in sodium intake. There were no associations between renin and noradrenaline, or between renin and blood pressure.

Adult↗
PubMed1979

Ethnic differences in blood pressure with observations on noradrenaline and renin. A hospital hypertensive population.

100 patients with essential hypertension (77 whites, 23 black) were studied with measurements of plasma noradrenaline concentration and plasma renin activity. Black patients had higher blood pressure than whites. There were no ethnic differences in mean plasma noradrenaline, but plasma renin activity was lower in blacks than whites, and this difference was not related to differences in sodium intake. Plasma noradrenaline increased with age in blacks, and in a white control group. Young white hypertensive patients (< 45 years) had higher plasma noradrenaline than controls, and in white hypertensives plasma noradrenaline was positively correlated with plasma renin.

Adolescent↗
PubMed1978

Are racial differences in essential hypertension due to different pathogenetic mechanisms?

1. Plasma noradrenaline concentration and plasma renin activity were measured in a control, British, urban population (n = 115) in which blacks were matched for age and sex with whites. 2. Similar measurements were made in subjects with essential hypertension (77 white and 23 black), and 48 healthy normotensive white civil servants. 3. In controls blood pressure was significantly higher in blacks; it correlated with age in both races and with pulse rate in blacks. There were no significant racial differences in plasma noradrenaline which was positively correlated with age in both blacks and whites. Mean plasma renin activity was 55% lower in blacks, and this difference was not related to urinary sodium excretion. 4. In hypertensive subjects plasma noradrenaline positively correlated with age in blacks. This relationship was not found in whites in whom 20% of young hypertensive subjects (less than 45 years) had significantly raised plasma noradrenaline. Plasma renin activity was again significantly lower in blacks. In white hypertensives plasma noradrenaline and renin activity were significantly correlated. 5. There may be racial differences in the pathogenesis of essential hypertension.

Black People↗