Biomedical subjects

G Durrieu

Publications and source records attributed to G Durrieu.

24 records · Page 2Linked to original sources

PubMed1991

[Renal adrenergic beta receptors and experimental neurogenic hypertension].

Sinoaortic denervation SAD in dog induces a permanent rise in blood pressure and heart rate leading to an experimental model of arterial hypertension. This model is associated with a marked increase in plasma catecholamine levels during the two first months. The present study investigates the changes in some renal vasoactive systems (renin activity, aldosterone and kallikrein) and cortical renal beta adrenoceptors during the development of this experimental neurogenic hypertension in dogs. SAD dogs exhibited a biphasic change in plasma renin activity and catecholamines: 1 month after SAD, plasma noradrenaline rose and renin activity decreased. These parameters return to normal values 18 months after SAD whereas blood pressure remained elevated. In contrast, plasma aldosterone levels decreased and urinary sodium increased. Urinary kallikrein was enhanced 1 month after SAD and showed a marked decrease 18 months later when compared with pre-SAD values. Cortical renal beta adrenoceptors (evaluated by 125I-cyanopindolol) exhibited a permanent decrease (Bmax) whatever the duration of arterial hypertension. These results show that SAD-induced hypertension in dog is associated with changes in renal vasoactive system involving urinary excretion of kallikrein and cortical renal beta adrenoceptors. These alterations could be involved in the maintenance of arterial hypertension in this experimental model.

Animals↗

PubMed1990

Levodopa up-regulates platelet alpha 2-adrenoceptors.

Treatment of dogs for 21 days with oral levodopa (100 mg b.i.d.) plus benserazide (25 mg b.i.d.) induced a significant increase in the number of platelet alpha 2-adrenoceptors labelled by [3H] yohimbine with no change in Kd. The rise was maximal at the end of the treatment and remained significant during the month following the cessation of treatment. Plasma catecholamine levels did not vary. Competition experiments showed a low affinity of both dopamine and levodopa for platelet alpha 2-adrenoceptors. These results suggest that levodopa treatment regulates alpha 2-adrenoceptor number in dog platelets.

Animals↗

PubMed1990

Beta-adrenergic sensitivity in Parkinson's disease: effect of levodopa treatment.

The beta-adrenergic sensitivity in never-treated and levodopa-treated patients with Parkinson's disease (PD) was studied through the evaluation of lymphocyte beta-adrenoceptor number ([125I]cyanopindolol binding sites) and chronotropic and metabolic (plasma nonesterified fatty acids--NEFA) responses to isoproterenol. No change was found in Bmax values or affinity constant Kd between never-treated patients, levodopa-treated patients with PD, and controls. At rest, no difference was observed in heart rate, plasma catecholamine, or NEFA levels between the three groups. Isoproterenol sensitivity (chronotropic response and plasma NEFA increase) was similar in never-treated and treated PD. The results suggest that peripheral beta-adrenergic sensitivity is unaffected either by the pathophysiological process of PD or by levodopa treatment.

Aged↗

PubMed1990

Adrenergic supersensitivity in parkinsonians with orthostatic hypotension.

The adrenergic status was studied through evaluation of platelet alpha 2-adrenoceptor number [( 3H]yohimbine binding sites), plasma catecholamine levels and blood pressure response to noradrenaline infusion in three groups of subjects (1) Parkinsonians with orthostatic hypotension; (2) Parkinsonians without orthostatic hypotension; and (3) control subjects. In Parkinsonians with orthostatic hypotension, systolic and diastolic blood pressures significantly (P less than 0.05) decreased from 144 +/- 9 and 76 +/- 6 mmHg in the lying position to 95 +/- 12 and 60 +/- 7 mmHg after 5 min standing. In these patients, noradrenaline plasma levels were significantly low (62 +/- 11 pg ml-1, (P less than 0.05) when compared with controls (219 +/- 13 pg ml-1) whereas no difference was noticed in Parkinsonians without orthostatic hypotension (195 +/- 14 pg ml-1). The noradrenaline dose required for a 25 mmHg increase in systolic blood pressure was significantly (P less than 0.01) lower in Parkinsonians with orthostatic hypotension (0.19 +/- 0.03 microgram kg-1) when compared with Parkinsonians without orthostatic hypotension (0.86 +/- 0.11 microgram kg-1) or with controls (0.68 +/- 0.1 microgram kg-1). Platelet alpha 2-adrenoceptor number was higher in Parkinsonians with orthostatic hypotension (313 +/- 52 fmol mg-1 protein) than in Parkinsonians without orthostatic hypotension (168 +/- 9 fmol mg-1 protein) or in controls (175 +/- 4 fmol mg-1 protein) with no change in Kd. This study demonstrates that in patients with Parkinson's disease, orthostatic hypotension is associated with an increase in both vascular sensitivity to noradrenaline and platelet alpha 2-adrenoceptor number.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1990

Blood pressure and plasma catecholamines in never-treated parkinsonian patients: effect of a selective D1 agonist (CY 208-243).

We found blood pressure (BP), heart rate (HR), plasma norepinephrine (NE), and epinephrine (E) levels in the lying and the standing positions to be similar in never-treated parkinsonian patients (stages 1 and 2) and age-matched controls. CY 208-243, a new centrally active D1 agonist, significantly decreased BP, HR, and NE (but not E) values in the lying position; it elicited orthostatic hypotension and blunted the rise in NE elicited by standing up. These results indicate that the early stages of Parkinson's disease are not accompanied by major changes in autonomic cardiovascular function and suggest the involvement of central D1-receptors in the control of sympathetic tone.

Antiparkinson Agents↗

PubMed1987

A randomised placebo-controlled pilot dose-response study with anisoylated plasminogen streptokinase activator complex in acute coronary artery occlusions.

The aim of this study was to determine the dose-response relationship of anisoylated plasminogen streptokinase activator complex (APSAC) by means of a between group double-blind comparison of the new agent and placebo. 50 patients with symptoms of acute myocardial infarction of less than 6 hours duration and whose coronary artery occlusion had been confirmed by coronary angiography were randomly allocated to 5 treatment groups (15, 20, 25 or 30U of APSAC, or placebo) and treatment was given as an intravenous injection over 2 minutes. Angiography was performed again at 15, 30, 45, 60 and 90 minutes and the films were assessed centrally by 2 independent cardiologists. Six patients were excluded from the angiographic analysis, 4 because their angiograms revealed patent arteries before APSAC was administered, 1 patient was excluded because streptokinase had been infused just after randomisation because of cardiogenic shock and 1 because the angiogram was not available due to problems in the film development. Clinical and laboratory examinations carried out for 72 hours after treatment showed that the drug was well tolerated. The reperfusion rates were as follows: placebo, 0/9; APSAC 15U, 5/8; APSAC 20U, 5/9; APSAC 25U, 6/9; APSAC 30U, 5/9. Reperfusion was achieved in 60% of treated patients but no dose relationship was revealed.

Anistreplase↗