Drugs online research references
Br J Pharmacol. 1992 Mar;105(3):653-6.
The influence of atropine and atenolol on the cardiac haemodynamic effects of NG-nitro-L-arginine methyl ester in conscious, Long Evans rats.
Widdop RE, Gardiner SM, Kemp PA, Bennett T.
Department of Physiology and Pharmacology, University of Nottingham Medical School, Queen's Medical Centre.
1. In the present study, the extent to which baroreflexes contribute to the cardiac effects of NG-nitro-L-arginine methyl ester (L-NAME) was assessed in conscious, Long Evans rats chronically instrumented with thoracic electromagnetic flow probes for the measurement of cardiac haemodynamics. 2. L-NAME (10 mg kg-1, i.v.) was administered in the absence (n = 6) and in the presence (n = 7) of atropine (1 mg kg-1) and atenolol (1 mg kg-1). 3. L-NAME caused a marked increase in mean arterial pressure and marked reductions in total peripheral conductance, cardiac output, heart rate, stroke volume, peak thoracic flow and the maximum rate of rise of aortic flow. 4. Administration of atropine, after the maximal bradycardic effect of L-NAME was established, restored the heart rate to resting levels. Concurrently, there was a reduction in stroke volume, such that cardiac output, although transiently elevated, did not show a sustained increase. No other variables were significantly affected by atropine. Additional administration of atenolol had no effect other than to cause a slight bradycardia, such that in the presence of atropine and atenolol, heart rate was not different from that in animals receiving atropine and atenolol before L-NAME. 5. In the presence of atropine and atenolol, L-NAME had similar pressor, vasoconstrictor and cardiac haemodynamic effects to those in untreated animals, although the bradycardia was significantly attenuated. However, there was still a significant reduction in heart rate following L-NAME in the presence of atropine and atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1628153&dopt=Abstract
Br J Pharmacol. 1996 Oct;119(3):505-10.
The inhibitory effects of iberiotoxin and 4-aminopyridine on the relaxation induced by beta 1- and beta 2-adrenoceptor activation in rat aortic rings.
Satake N, Shibata M, Shibata S.
Department of Pharmacology, University of Hawaii, School of Medicine, Honolulu 96822, USA.
1. In rat aortic rings contracted by phenylephrine, the relaxation induced by isoprenaline was partly inhibited by iberiotoxin, (ibTX), tetraethylammonium, 4-aminopyridine (4-AP) and 1,9-dideoxyforskolin, but not by glibenclamide. 2. In the presence of 4-AP, 1,9-dideoxyforskolin failed to inhibit further the relaxant response to isoprenaline. Cromakalim-induced relaxation was inhibited by glibenclamide. 3. In the absence of endothelium, ibTX and 4-AP still inhibited the relaxant response to isoprenaline. 4. The inhibitory effect of ibTX on the relaxant response to isoprenaline was eliminated by pretreatment with ICI-118,551, a beta 2-adrenoceptor antagonist, but not by atenolol, a beta 1-adrenoceptor antagonist. 5. The inhibitory effect of 4-AP on the relaxation induced by isoprenaline was abolished by atenolol, but not by ICI-118,551. 6. The inhibitory effect of ibTX on the isoprenaline-induced relaxation in the presence of atenolol was completely abolished by MDL 12,330A, an adenylate cyclase inhibitor. Further, the inhibitory effect of 4-AP on the isoprenaline-induced relaxation in the presence of ICI-118,551 was markedly reduced by MDL 12,330A. 7. The relaxation induced by dibutyryl cyclic AMP was partly inhibited by 4-AP but not by ibTX. However, in the presence of KT5720, an inhibitor of cyclic AMP-dependent protein kinase, ibTX failed to inhibit further the relaxation induced by isoprenaline. 8. These results suggest that, in rat aortic rings, KCa channels are involved in the relaxation induced by isoprenaline. In addition, KCa channels are mainly activated by beta 2-adrenoceptors through cyclic AMP-dependent pathways. Further, the inhibition of isoprenaline-relaxation by 4-AP may be related to the activation of beta 1-adrenoceptors and cyclic AMP formation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8894170&dopt=Abstract
Basic Res Cardiol. 1987;82 Suppl 2:161-72.
Chronic cardiac reactions. III. Factors involved in the development of structural dilatation.
Vogt M, Jacob R, Noma K, Onegi B, Rupp H.
Physiologisches Institut II, Universitat Tubingen, F.R.G.
The significance of various factors for the development of structural dilatation in the chronically pressure-loaded and failing heart were evaluated. The investigations were performed on male rats with renal (Goldblatt II) and spontaneous (Aoki-Okamoto) hypertension at different stages of haemodynamic overload. Two groups of SHR were submitted to intermittent feeding (SHR IF); one group received additionally the beta-blocking agent atenolol (50 mg/kg b.w.; SHR IF + beta Bl.). Haemodynamic measurements were carried out under open chest conditions. Myosin isoenzyme pattern, hydroxyproline concentration and circulating blood volume were determined. Transformation to slower myocardium per se, induced by IF, did not lead to significant change in ventricular configuration. After additional blockade of beta-adrenergic receptors there were indications of unfavourable development of left ventricular configuration. Inhibition of hypertrophic mass increase due to curtailed adrenergic stimulation could be an influential factor in the development of dilatation. Further investigations, however, are required to establish the relationship between the adrenergic system, on the one hand, and degree of hypertrophy as well as structural dilatation of the ventricle, on the other hand. The established marked increase in hydroxyproline concentration of the dilated ventricle of SHR in congestive failure is consistent with the assumption of a causal link between the degree of fibrosis and structural dilatation. Observations on rats with aorto-caval shunt and Goldblatt II rats with eccentric hypertrophy and corresponding increase in filling potential or circulating blood volume indicate a correlation between the latter and ventricular size. Thus, we assume that curtailed protein synthesis, fibrosis and regulatory processes related to water and electrolyte balance, but not myocardial transformation per se, play a role in the development of structural dilatation. The relative contribution of each factor, however, may depend on the experimental model that is used.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3663015&dopt=Abstract
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