Drugs online research references
Br J Pharmacol. 1996 Oct;119(3):551-4.
alpha-Adrenoceptor and opioid receptor modulation of clonidine-induced antinociception.
Sierralta F, Naquira D, Pinardi G, Miranda HF.
Department of Pharmacology, Faculty of Medicine, University of Chile, Santiago, Chile.
1. The antinociceptive action of clonidine (Clon) and the interactions with alpha 1, alpha 2 adrenoceptor and opioid receptor antagonists was evaluated in mice by use of chemical algesiometric test (acetic acid writhing test). 2. Clon produced a dose-dependent antinociceptive action and the ED50 for intracerebroventricular (i.c.v.) was lower than for intraperitoneal (i.p.) administration (1 ng kg-1 vs 300 ng kg-1). The parallelism of the dose-response curves indicates activation of a common receptor subtype. 3. Systemic administration of prazosin and terazosin displayed antinociceptive activity. Pretreatment with prazosin produced a dual action: i.c.v. Clon effect did not change, and i.p. Clon effect was enhanced. Yohimbine i.c.v. or i.p. did not induce antinonciception, but antagonized Clon-induced activity. These results suggest that alpha 1- and alpha 2-adrenoceptors, either located at the pre- and/or post-synaptic level, are involved in the control of spinal antinociception. 4. Naloxone (NX) and naltrexone (NTX) induced antinociceptive effects at low doses (microgram kg-1 range) and a lower antinociceptive effect at higher doses (mg kg-1 range). Low doses of NX or NTX antagonized Clon antinociception, possibly in relation to a preferential mu opioid receptor antagonism. In contrast, high doses of NX or NTX increased the antinociceptive activity of Clon, which could be due to an enhanced inhibition of the release of substance P. 5. The results obtained in the present work suggest the involvement of alpha 1-, alpha 2-adrenoceptor and opioid receptors in the modulation of the antinociceptive activity of clonidine, which seems to be exerted either at spinal and/or supraspinal level.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8894177&dopt=Abstract
Br J Clin Pharmacol. 1996 Oct;42(4):507-9.
Alpha-adrenoceptor blocking drugs and female urinary incontinence: prevalence and reversibility.
Marshall HJ, Beevers DG.
University Department of Medicine, City Hospital, Birmingham, UK.
There have been occasional reports of female stress incontinence related to prazosin therapy for hypertension. This drug is now rarely used but recently longer acting alpha-adrenoceptor blocking drugs have been introduced. We have, therefore, investigated the prevalence of urinary incontinence in all our female patients who were receiving alpha-adrenoceptor blockers in comparison with women, matched for age and parity who were receiving other drugs. We identified a total of 49 women taking alpha-adrenoceptor blocking drugs (prazosin 4, terazosin 5, doxazosin 40) among current patients who were attending our hypertension clinic. Twenty of these (40.8%) reported some urinary incontinence whereas in the control patients, only 8 (16.3%) had this symptom (P = < 0.02, relative risk 2.5, 95% CI 1.22-5.13). alpha-Adrenoceptor blockers were withdrawn in 18 of the 20 patients with incontinence and in 13, their symptoms abated. Our results suggest that there is a significantly higher prevalence of urinary incontinence in women taking alpha-adrenoceptor antagonists with reversibility on withdrawal of these drugs. As both female urinary incontinence, hypertension and the use of alpha-adrenoceptor blocking drugs are common, this distressing side effect should be borne in mind so that gynaecological or urological treatment may be avoided in some women.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8904625&dopt=Abstract
J Pharmacol Exp Ther. 1996 Nov;279(2):967-74.
Blockade of alpha-2 adrenergic receptors in the rostral ventrolateral medulla attenuates the sympathoinhibitory response to cocaine.
Abrahams TP, Liu W, Varner KJ.
Department of Pharmacology and Experimental Therapeutics, Louisiana State University Medical Center, New Orleans, USA.
The purpose of this study was to determine whether neurons in the rostral ventrolateral medulla play a role in the sympathoinhibitory response elicited by i.v. administration of cocaine and, if so, to identify the type(s) of receptors involved. Adrenergic antagonists were microinjected bilaterally into the rostral ventrolateral medulla in pentobarbital-anesthetized rats in an attempt to block the decrease in sympathetic nerve discharge (SND) elicited by cocaine (1 mg/kg i.v.). After the bilateral microinjection of saline, cocaine elicited a -56 +/- 5% (mean +/- S.E.) decrease in SND lasting 36 +/- 3 min. Cocaine also increased arterial pressure (21 +/- 3 mm Hg). Prior microinjection of the alpha-2 adrenergic antagonist idazoxan (0.3, 3 or 10 nmol) did not alter the magnitude of the sympathoinhibitory response to cocaine; however, the duration of the response was significantly reduced by all 3 doses (range 21 +/- 3 to 11 +/- 2 min). Similarly, microinjection of the alpha-2 adrenergic antagonist piperoxan (10 nmol) decreased the duration (from 45 +/- 8 to 23 +/- 4 min), but not the magnitude of the sympathoinhibitory response. Microinjection of either the alpha-1 adrenergic antagonist terazosin (0.24 nmol) or the beta adrenergic receptor antagonist propranolol (2 nmol) did not attenuate the decrease in SND elicited by cocaine. The cocaine-mediated pressor response was not affected by any of the antagonist treatments. These data show that the decrease in SND elicited by cocaine is mediated centrally and involves, at least in part, the activation of alpha-2 adrenergic receptors in the rostral ventrolateral medulla.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8930206&dopt=Abstract
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