Drugs online research references
Eur J Pharmacol. 1986 Sep 23;129(1-2):131-8.
Is pindolol a mixed agonist-antagonist at central serotonin (5-HT) receptors?
Hjorth S, Carlsson A.
The effects of the non-selective beta-adrenergic blocking agent pindolol upon central monoaminergic neurotransmission in rats were studied by means of in vivo biochemical methods. It was found that (-)-pindolol elicited a clearcut, selective, dose-dependent and stereospecific reduction of brain 5-HT synthesis rate. The synthesis reduction was not accompanied by any change in the tissue tryptophan levels and could not be prevented by depleting the monoamine stores by means of reserpine. Furthermore, in non-pretreated animals, (-)- but not (+)-pindolol (nor the beta 1- and beta 2-selective adrenoceptor antagonists metoprolol, betaxolol and ICI 118,551) decreased the 5-HIAA level and the 5-HIAA/5-HT ratio while neither enantiomer altered the concentrations of 5-HT or NA, or DA and its metabolites. It is suggested that these effects of (-)-pindolol may be due to direct stimulation of 5-HT receptors in the CNS. The action of the compound is discussed within the context of literature data indicating its ability to act as an antagonist of certain other aspects of 5-HT receptor activation. The possibility is considered that, in addition to its beta-adrenergic properties, (-)-pindolol is a mixed agonist-antagonist at central 5-HT receptors.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2429847&dopt=Abstract
Clin Exp Hypertens. 1980;2(3-4):359-77.
Evidences supporting an increased sympathetic tone and reactivity in a subgroup of patients with essential hypertension.
de Champlain J, Cousineau D, Lapointe L.
Several experimental evidences have shown that, under standarized conditions, circulating catecholamines (CA) or norepinephrine (NE) levels can be used as a valid index of the sympatho-adrenal activity in animal and man. This approach in the study of hypertensive patients has permitted to uncover that about 50% of patients with labile hypertension and about 30% of patients with stable hypertension had elevated CA levels at rest for 20 minutes in the supine position. The increased CA levels were mainly due to a rise in NE in stable hypertension and to a rise in epinephrine (E) in labile hypertension. On the basis of circulating CA levels, the hypertensive patients were divided into hyperadrenergic (CA levels above normal range) and normoadrenergic (CA levels within the normal range) subgroups. The hyperadrenergic labile or stable hypertensive subgroups were found to be also characterized by an enhanced CA or NE increase in response to change in position from supine to standing, by a faster heart rate and by an increased myocardial contractility, while these parameters were normal in the normoadrenergic subgroups. These findings support therefore the existence of an increased sympathetic tone and reactivity in association with hyperkinetic cardiac functions in an important population of hypertensive patients. In response to two weeks treatment with beta-blockers (either propranolol or metoprolol) hyperadrenergic stable hypertensive patients were found to be more responsive to this therapy than normoadrenergic patients although both groups had the same initial blood pressure. Moreover, this treatment lowered basal NE or CA levels and restored the enhanced CA or NE response to change in position toward normal in hyperadrenergic patients while it did not modify significantly circulating supine or standing CA and NE in normoadrenergic patients. These findings strongly support a participation of the sympathetic system in the maintenance of an elevated blood pressure in hyperadrenergic patients and raise the possibility of using a more rational approach in the therapy of hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7428561&dopt=Abstract
Thromb Haemost. 1992 Dec 7;68(6):683-6.
Treatment of hypertension induces a fall in platelet basal cytoplasmic calcium concentration without influencing platelet aggregation.
Wilson J, Orchard MA, Prentice CR, Lees AD, Baig MW, Perrins EJ, Davies JA.
Academic Unit of Medicine, University of Leeds, U.K.
The relationship between blood pressure and platelet basal cytoplasmic calcium concentration ([Ca2+]i) and platelet sensitivity to aggregating agents in hypertension has been investigated in hypertensive patients and normotensive subjects. Ten severely hypertensive patients whose blood pressures were poorly controlled with metoprolol, were given calcium antagonist (either nifedipine or felodipine) as a second line agent. Venous blood samples were collected at each treatment phase for measurement, in whole blood, of platelet aggregation in response to ADP and collagen, and of basal [Ca2+]i using fura-2. Control of blood pressure by the combination of metroprolol and a calcium antagonist induced a significant decrease in median [Ca2+]i from 116 (76-181) to 73 (60-83) nM, which was similar to the median value of 70 (61-80) nM obtained in 14 normotensive subjects. Overall [Ca2+]i correlated with mean blood pressure (r = 0.51). Treatment of hypertension with calcium antagonist did not change the response of platelets to collagen or ADP. The results confirm that effective treatment of hypertension significantly reduced basal [Ca2+]i in platelets but raise doubts whether elevated basal [Ca2+]i is necessarily the sole mechanism by which the sensitivity of platelets to aggregatory agents is increased in hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1287883&dopt=Abstract
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