Autonomic and Autacoid Pharmacology最新文献

{"title":"Pharmacological implications of cellular localization of α1-adrenoceptors in native smooth muscle cells","authors":"J. C. McGrath,&nbsp;J. F. Mackenzie,&nbsp;C. J. Daly","doi":"10.1111/j.1365-2680.1999.tb00002.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00002.x","url":null,"abstract":"<div>\u0000 \u0000 <p><b>1</b> This study examines the cellular localization of α₁-adrenoceptors and demonstrates that binding to intracellular receptive binding sites in native smooth muscle cells may influence the pharmacological profile of agonists or antagonists. The example tissue studied was rat basilar artery.</p>\u0000 <p><b>2</b> An α₁-adrenoceptor antagonist and fluorescent analogue of prazosin, BODIPY-FL prazosin (QAPB) allowed visualization, with high resolution, of both plasma membrane and cytosolic binding sites on live native cells, as previously shown in cells harbouring recombinant receptors. QAPB-associated fluorescence binding was both time- and concentration- dependent in rat basilar smooth muscle cells and affinity for α₁-adrenoceptors was calculated from specific binding curves as 1.1 nM.</p>\u0000 <p><b>3</b> Concentration-dependent binding of QAPB detected in smooth muscle cells dissociated from rat basilar arteries was composed of diffuse and clustered fluorescence. Visually the diffuse component of fluorescence was the more evident up to a concentration of 5 nM QAPB. Confocal visualization of an optical section through the cell showed that the clustered component was located mainly intracellularly. In rat basilar artery smooth muscle cells the intracellular binding sites were located in close proximity to the nuclear membrane.</p>\u0000 <p><b>4</b> 3D models of QAPB-associated fluorescence demonstrate that a high proportion of effective binding sites are intracellular, showing not only that a high proportion of receptors are located inside the cell but also that in this location they can bind ligands. This has implications for. pharmacological analysis in relation to the consequences of intracellular binding <i>per se</i> and for differential effects upon the pharmacology of particular ligands according to whether they can enter the cell.</p>\u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00002.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prejunctional effects of angiotensin II and bradykinin in the heart and blood vessels","authors":"D. Moura,&nbsp;H. Pinheiro,&nbsp;M. Q. Paiva,&nbsp;S. Guimaraes","doi":"10.1111/j.1365-2680.1999.tb00004.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00004.x","url":null,"abstract":"<div>\u0000 \u0000 <p><b>1</b> Angiotensin and bradykinin facilitate the release of noradrenaline from sympathetic nerve terminals and cause positive inotropy in rat isolated atria and ventricles. The effect of bradykinin was enhanced by the ACE inhibitor, ramiprilat.</p>\u0000 <p><b>2</b> The facilitated release of noradrenaline in rat ventricle by bradykinin was blocked by the β₂-receptor antagonist HOE-140. This response is also reduced by removing the endocardium, suggesting the release of a mediator from the endocardium.</p>\u0000 <p><b>3</b> The facilitated noradrenaline release by angiotensin II and bradykinin was blocked by the angiotensin receptor antagonist saralasin to the same extent. In contrast, losartan caused only minor blockade in a range of vascular and cardiac tissues. This suggests that angiotensin and bradykinin exert these responses by interacting with a prejunctional receptor different from the established AT₁ subtype.</p>\u0000 <p><b>4</b> These results suggest that bradykinin mediates facilitation of noradrenaline release via the local release of angiotensin onto an atypical AT₁ receptor.</p>\u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00004.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proceedings of the Catecholamine Symposium held at the Joint Meeting of the British Pharmacological Society and Societade Portuguesa de Farmacologia, 8–9 April 1999. Casa Diocesana, Seminario de Vilar, Porto, Portugal.","authors":"Daniel Moura","doi":"10.1111/j.1365-2680.1999.tb00001.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00001.x","url":null,"abstract":"","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00001.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73716069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sertraline inhibits the contractile responses to noradrenaline, KCI and electrical field stimulation of rat isolated vas deferens","authors":"N. I. Kalyoncu,&nbsp;R. Ozyavuz,&nbsp;S. Karaoglu","doi":"10.1111/j.1365-2680.1999.tb00010.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00010.x","url":null,"abstract":"<div>\u0000 \u0000 <p><b>1</b> The aim of this study was to investigate the effect of sertraline, a selective serotonin re-uptake inhibitor, on contractile responses to noradrenaline (NA), KCI, serotonin (5-HT) and electrical field stimulation of rat isolated vas deferens.</p>\u0000 <p><b>2</b> Pre-treatment with 10^-4 M sertraline showed inhibitory effects on responses to NA, KCI, 5-HT and electrical field stimulation, while pre-treatment with 10 ^-6 and 10^-5 M sertraline caused potentiation of responses to NA (10^-7 and 10^-6 M).</p>\u0000 <p><b>3</b> A voltage-dependent calcium channel activator, Bay K 8644, restored the inhibited responses when sertraline was washed out of the organ bath, although restoration could not be seen when sertraline was not removed.</p>\u0000 <p><b>4</b> The inhibition of the contractile responses by sertraline pre-treatment may be via a mechanism through calcium channels which is additional to the selective serotonin re-uptake inhibitory effect of sertraline.</p>\u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00010.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vitro and in vivo approaches to the characterization of the α2-adrenoceptor","authors":"A. L. Hudson,&nbsp;E. S. J. Robinson,&nbsp;M. D. Lalies,&nbsp;R. J. Tyacke,&nbsp;H. C. Jackson,&nbsp;D. J. Nutt","doi":"10.1111/j.1365-2680.1999.tb00003.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00003.x","url":null,"abstract":"<div>\u0000 \u0000 <p><b>1</b> In order to more fully understand the role of the α₂-adrenoceptor in brain function, a combination of <i>in vitro</i> and <i>in vivo</i> techniques were utilized including radioligand binding, autoradiography, brain microdialysis and antisense oligonucleotides.</p>\u0000 <p><b>2</b> Binding studies showed the tritiated form of the selective α₂-adrenoceptor antagonist, RX821002 (methoxy-idazoxan) labelled an apparent single population of sites in rat brain membranes with high affinity (1 nM), for which prazosin had low affinity (1107 nM). Similar studies in rabbit brain membranes found that prazosin and oxymetazoline were able to displace. [³H]-RX821002 in a biphasic manner indicating the presence of subtypes of α₂-adrenoceptors.</p>\u0000 <p><b>3</b> Receptor autoradiography revealed a distribution of [³H]-RX821002 binding in rat brain consistent with the labelling of all %aL₂-adrenoceptor subtypes, namely α_2A/D-, α_2B and α_2C.</p>\u0000 <p><b>4</b> In rat, <i>in vivo</i> brain dialysis experiments demonstrated peripherally administered RX821002 elevated basal noradrenaline in frontal cortex and also, although to a lesser extent, in ventral hippocampus. RX821002 was also able to elevate extracellular dopamine in the striatum.</p>\u0000 <p><b>5</b> A 7-day i.c.v. infusion of an antisense oligonucleotide targeting the α_2A/D-adrenoceptor, resulted in a significant reduction in the autoradiographic density of [³H]-RX821002 binding in specific brain areas, notably the lateral septal nuclei and anterior hypothalamic area.</p>\u0000 <p><b>6</b> Several years of research by our group has extended our knowledge of the pharmacology and function of the α₂-adrenoceptor and has provided evidence of the roles of this receptor in the control of monoamine turnover. The successful use of antisense technology to knockdown expression of the α_2A/D subtype provides future opportunities to explore the physiology of this receptor subtype.</p>\u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00003.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798208","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological analysis of vasoconstrictor responses to periarterial purinergic nerve stimulation","authors":"X.-P. Yang,&nbsp;S. Chiba","doi":"10.1111/j.1365-2680.1999.tb00009.x","DOIUrl":"10.1111/j.1365-2680.1999.tb00009.x","url":null,"abstract":"1. Periarterial electrical nerve stimulation at a low frequency (1 Hz) readily induced a vasoconstrictor response of the canine splenic artery in a pulse number-related manner (1-30 pulses of trains). The vasoconstrictor response to trains of up to 10 pulses at 1 Hz of stimulation appeared to be monophasic, whereas it became clearly distinguished into two phases at a longer train of 30 pulses. 2. The monophasic vasoconstrictor responses to trains of 1, 3 or 10 pulses were not modified by an alpha1-adrenoceptor blocking agent, prazosin (0.1 microM), but were completely inhibited by the P2X receptor desensitization with alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-methylene ATP; 1 microM). The 1st phase of vasoconstriction induced by a train length of 30 pulses was not influenced by the treatment with prazosin, but was abolished by alpha,beta-methylene ATP. The 2nd phase response was markedly inhibited by prazosin, and the remaining response of this phase was blocked by alpha,beta-methylene ATP. 3. Rauwolscine (0.3 microM), an alpha2-adrenoceptor antagonist, enhanced the vasoconstrictor responses to trains of 1, 3 or 10 pulses. Particularly at 10 pulses of electrical stimulation, the vasoconstrictor responses were significantly potentiated. The blockade of neuronal uptake of noradrenaline with imipramine (1 microM) did not affect the vasoconstrictor responses to trains of 1, 3 or 10 pulses. 4. It is concluded that short pulse trains of stimulation at a low frequency may selectively activate a purinergic component of sympathetic cotransmission, and the prejunctional alpha2-adrenergic feedback mechanism may tonically participate into the modulation of ATP release. Imipramine-sensitive neuronal uptake mechanism may not play an important role in regulating vascular responses to periarterial purinergic nerve stimulation.","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1365-2680.1999.tb00009.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21798135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential regulation of mesenteric and femoral blood flow in the rat as revealed by computerized data acquisition and evaluation","authors":"A. Heinemann,&nbsp;C. H. Wachter,&nbsp;P. Holzer","doi":"10.1046/j.1365-2680.1998.1810039.x","DOIUrl":"10.1046/j.1365-2680.1998.1810039.x","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ul>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>A set-up for computerized acquisition and evaluation of haemodynamic data was constructed. Blood flow (BF) in the superior mesenteric and femoral artery of urethane-anaesthetized rats was measured with the ultrasonic transit time shift technique. The signals for arteial blood pressure and BF were fed into a personal computer via an analogue-digital converter. Mean arterial blood pressure, heart rate and vascular conductance (CV) were calculated on-line. For subsequent analysis of the data, algorithms were programmed to filter the data, and to determine average and peak values for each parameter.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>Systemic hypertension induced by phenylephrine (3–300 nmol kg⁻¹), angiotensin II (0.1–3.0 nmol kg⁻¹) and arginine vasopressin (0.03–1.0 nmol kg⁻¹) was accompanied by constriction of the mesenteric artery. In contrast, the femoral artery responded to phenylephrine with constriction, to angiotensin II with dilatation and to arginine vasopressin with dilation followed by constriction. The haemodynamic effects of endothelin-1 (0.03–3.0 nmol kg⁻¹) were generally biphasic, the initial hypotension being associated with dilatation, and the delayed hypertension being accompanied by constriction of both the mesenteric and femoral arterial bed.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>Terbutaline (3–1.0 nmol kg⁻¹) and calcitonin gene-related peptide (0.03–1 nmol kg⁻¹) caused systemic hypotension along with mesenteric and femoral vasodilatation.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>Telmisartan (1 mg kg⁻¹), an angiotensin AT₁ receptor antagonist, dilated the mesenteric artery, but had no effect on femoral VC. In contrast, the α₁-adrenoceptor antagonist prazosin (0.1 mg kg⁻¹), dilated the femoral artery without altering mesenteric VC. Similarly, the β-adrenoceptor antagonist propranolol (1 mg kg⁻¹) had no effect on mesenteric VC, but constricted the femoral arterial bed.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>These data demonstrate that the haemodynamic effects of exogenously administered drugs can widely differ between the mesenteric and femoral arterial beds of urethane-anaesthetized rats. Furthermore, vascular tone of these two arterial beds in maintained by different vasoconstrictor systems. While the femoral artery is mainly under adrenergic control, the renin-angiotensin axis is predominant in the mesenteric arterial bed. In addition, this study also demonstrates that computerized analysis enables quick and accurate estima","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1046/j.1365-2680.1998.1810039.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20642027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of K+ channel blocking drugs and nitric oxide synthase inhibition on the response to hypoxia in rat pulmonary artery rings","authors":"M. R. Karamsetty,&nbsp;R. M. Wadsworth,&nbsp;K. A. Kane","doi":"10.1046/j.1365-2680.1998.1810049.x","DOIUrl":"10.1046/j.1365-2680.1998.1810049.x","url":null,"abstract":"<div>\u0000 \u0000 <p>\u0000 \u0000 </p><ul>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>The aims of this study were to investigate the effects of potassium (K⁺) channel blockers and the nitric oxide (NO) synthase inhibitor, L-nitroarginine (L-NOARG), on the response produced by acute hypoxia in rat intrapulmonary artery rings <i>in vitro</i>.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>In rat phenylephrine-precontracted pulmonary artery rings, hypoxia (pO₂= 7 mmHg) induced a response which consisted of a rapidly developing initial contraction (phase 1), a transient relaxation (phase 2) and a slowly developing sustained contraction (phase 3) over 30 min. The NOS inhibitor, L-NOARG (300 μm), attenuated phase 1 and 3, and amplified phase 2 of the response to hypoxia. The voltage-gated K⁺ channel blocker 4-aminopyridine (4-AP) (10 mM) also abolished phase 3 and magnified phase 2 of the response to hypoxia.</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>The hypoxic response was not modified by the calcium-activated K⁺ channel (K_Ca) blockers, tetraethylammonium (TEA) (20 mM) or charybdotoxin (50 or 200 nM), nor by the ATP-dependent K⁺ channel (K_ATP) blocker, glibenclamide (10 μM).</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>L-NOARG (300 μM) and 4-AP (10 mM) also abolished carbachol-induced endothelium-dependent NO-mediated relaxation. Relaxation produced by the NO releasing agent 3-morpholino sydnonimine (SIN-1) was reduced by 4-AP (10 mM) and TEA (20 mM).</p>\u0000 </li>\u0000 \u0000 <li><span> </span>\u0000 \u0000 <p>The data suggest that NO production is reduced during severe hypoxia in rat intrapulmonary artery rings and that this underlies the sustained phase of the hypoxic contraction. The data also suggests that 4-AP- sensitive K⁺ channels play an important role in the release andor action of NO, and therefore, in the response to hypoxia.</p>\u0000 </li>\u0000 </ul>\u0000 \u0000 </div>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1046/j.1365-2680.1998.1810049.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20642028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of the L-arginine/nitric oxide neural pathway in non-adrenergic, non-cholinergic relaxation of the bovine oesophageal groove","authors":"M. V. Barahona,&nbsp;S. Sánchez-Fortún,&nbsp;M. D. San Andrés,&nbsp;E. Ballesteros,&nbsp;J. Contreras,&nbsp;M. San Andrés","doi":"10.1046/j.1365-2680.1998.1820065.x","DOIUrl":"10.1046/j.1365-2680.1998.1820065.x","url":null,"abstract":"1. The distribution and localization of nitric oxide synthase (NOS) immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity in the bovine oesophageal groove were investigated by immnunohistochemical and histochemical staining techniques. Functional in vitro studies were performed to correlate the presence of NOS-immunoreactivity (IR) and NADPH-d staining with smooth muscle relaxations involving the L-arginine/nitric oxide neural pathway in the bovine oesophageal groove activity. 2. NOS-IR and NADPH-d were expressed in nerve cell bodies of the myenteric, submucosal and intramuscular ganglia, and in nerve fibres distributed around blood vessels and throughout the different muscular layers of the bovine oesophageal groove. 3. In oesophageal groove strips treated with guanethidine (10(-5) M) and atropine (10(-7) M) to block noradrenergic neurotransmission and muscarinic receptors, respectively, electrical field stimulation (EFS, 0.5-32 Hz, 1 ms duration, 20-s trains) induced relaxations which were practically abolished by tetrodotoxin (TTX, 10(-6) M). 4. Incubation with an inhibitor of nitric oxide synthesis, NG-nitro-L-arginine (L-NOARG, 3 x 10(-5) M), significantly inhibited relaxations induced by EFS. This inhibition was partially reversed by L-arginine (L-arg, 5 x 10(-3) M). D-NOARG (3 x 10(-5) M) had no effect on EFS-induced relaxations. 5. NO added as an acidified solution of NaNO2 (10(-6) - 10(-3) M) and S-nitroso-L-cysteine (10(-7) - 10(-4) M) caused concentration-dependent relaxations of the bovine oesophageal groove. These relaxations were unaffected by L-NOARG (3 x 10(-5) M). 6. The presence of NO-synthesizing enzyme in nerves and ganglia, and the pharmacological evidence for NO-mediated smooth muscle relaxation suggested that the L-arg/NO neuronal pathway is involved in the inhibitory neurotransmission of the bovine oesophageal groove.","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1046/j.1365-2680.1998.1820065.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20645107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention by a somatostatin analogue of the hypertensive and cardiovascular structural changes induced by blockade of adenosine receptors","authors":"C. Calhau,&nbsp;F. Martel,&nbsp;M.N.M.P. Alçada,&nbsp;I. Azevedo","doi":"10.1046/j.1365-2680.1997.00459.x","DOIUrl":"10.1046/j.1365-2680.1997.00459.x","url":null,"abstract":"<p> <b>1</b> Long-term administration of the adenosine receptor antagonist, 1,3-dipropyl-8-sulfophenylxanthine (DPSPX), causes arterial hypertension and cardiovascular hypertrophic and hyperplastic changes (Matias, Albino-Teixeira, Polónia &amp; Azevedo, 1991). As somatostatin is a repressor of cell growth, and adenosine is a potent inducer of the somatostatin gene, we investigated the putative involvement of somatostatin in the cardiovascular effects of DPSPX.</p><p> <b>2</b> DPSPX (90 μg kg⁻¹ h⁻¹, i.p.) or saline and the somatostatin analogue, octreotide (75 μg kg⁻¹ day⁻¹, s.c.), or saline were infused through Alzet minipumps to Wistar rats. Blood pressure was measured with the tail-cuff technique. Seven days after implantation of the minipumps the rats were killed and the tissues prepared for microscopy.</p><p> <b>3</b> DPSPX induced arterial hypertension and cardiovascular hypertrophic and hyperplastic changes as previously described (Matias <i>et al</i>., 1991). Treatment of the rats with octreotide alone had no effect either on blood pressure or in blood vessel morphology. However, octreotide prevented both the hypertensive and the cardiovascular morphologic effects of DPSPX.</p><p> <b>4</b> The results are compatible with the involvement of somatostatin in the long-term cardiovascular effects of adenosine.</p>","PeriodicalId":100151,"journal":{"name":"Autonomic and Autacoid Pharmacology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1046/j.1365-2680.1997.00459.x","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20302870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}