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Biomedical subjects

D Prieto

Publications and source records attributed to D Prieto.

62 records · Page 4Linked to original sources
PubMed1991

Histamine induces endothelium-dependent relaxation of bovine retinal arteries.

The effect of histamine on bovine isolated retinal small arteries (internal diameter, approximately 240 microns) was studied. Histamine induced a concentration-dependent relaxation in 43 of 53 vessels. The histamine-induced relaxation involves primarily activation of H1-receptors, with H2-receptors also affected as evidenced by the effect of selective histamine-receptor agonists and antagonists. The histamine-induced relaxation was dependent on the endothelium and seem to involve release of both endothelium-derived relaxing factor (EDRF) and a product which was inhibited by indomethacin, probably prostaglandin I2 (prostacyclin). The development of tachyphylaxis to the action of histamine seemed to rely on desensitization of the vascular smooth muscle cells to the relaxing effect of EDRF.

Acetylcholine↗
PubMed1991

Endothelin-1-induced contraction of bovine retinal small arteries is reversible and abolished by nitrendipine.

Endothelin-1 (porcine/human) induced a prompt, reversible, potent, concentration-dependent contraction of bovine isolated retinal small arteries (internal diameter, approximately 200 microns) with a concentration of endothelin-1 required to give half-maximal contraction of 2 x 10(-10) M. The maximal contraction induced by endothelin-1 was equal to 89% of the maximal contractile capacity. The vessel response to endothelin-1 was dependent on extracellular Ca2+. Withdrawal of extracellular Ca2+ or addition of nitrendipine, 10(-6) M, reduced the response of vessels contracted with 10(-9) M endothelin-1 by 80% and 75%, respectively. These results indicate that the endothelin-1-induced contraction of retinal arteries is dependent on an influx of extracellular Ca2+ through membrane potential-operated calcium channels. Endothelin-1, 10(-13)-10(-10) M, did not induce a relaxation of endothelium-intact arteries, indicating that endothelin-1 is incapable of releasing endothelium-derived relaxing factor in the retinal circulation. These results suggest that endothelin may participate in the regulation of retinal artery tone.

Acetylcholine↗
PubMed1990

Angiotensin II does not contract bovine retinal resistance arteries in vitro.

The effect of angiotensin II was studied in vitro on ring segments of bovine retinal resistance arteries (i.d. 126-271 microns) and posterior ciliary arteries (i.d. 207-1153 microns). Although the retinal resistance arteries were responsive to 5-hydroxytryptamine, prostaglandin F2 alpha, and changes in extracellular K(+)-concentration, they did not, in contrast to the posterior ciliary arteries, contract to cumulative or single doses of angiotensin II. In the latter arteries, angiotensin II induced a small concentration dependent contraction, 5% of maximal 125 mM K(+)-induced response, with a pD2-value of 9.3. The single addition of 10(-6) M angiotensin II increased the maximal vessel response of the posterior ciliary arteries three times to angiotensin II. Tachyphylaxis was pronounced in the posterior ciliary arteries, in which the response to angiotensin II could not be repeated. Indomethacin (10(-5) M), methylene blue (3 x 10(-6) M), or removal of endothelium did not make the retinal resistance arteries responsive to angiotensin II. Retinal arteries precontracted with 30 mM potassium did not respond to angiotensin II. Angiotensin II did not potentiate the 5-hydroxytryptamine- and noradrenaline concentration-response characteristics of both retinal resistance and posterior ciliary arteries. Although angiotensin II-receptors have been detected in bovine retinal vascular smooth muscle using radioligand-binding technique, the present results suggest that these receptors are non-functional in respect to regulation of retinal resistance artery tone.

Angiotensin II↗
PubMed1990

Autonomic innervation of the equine urinary bladder.

The distribution and density of intrinsic autonomic nerve fibers and cells were studied in the equine urinary bladder by means of the peroxidase-antiperoxidase immunohistochemical method to localize tyrosine-hydroxylase (TH), and by means of a histochemical technique to detect acetylcholinesterase (AChE) activity. The results suggest that the equine urinary bladder, like that of other mammalian species, possesses a rich autonomic innervation which includes catecholaminergic and acetylcholinesterase positive nerves. At least a part of these nerve fibers have an intrinsic origin from ganglion cell bodies within the bladder wall.

Animals↗
PubMed1989

Distribution and density of neuropeptide Y-immunoreactive nerve fibres and cells in the horse urinary bladder.

The distribution and density of neuropeptide Y (NPY)-immunoreactive nerve fibres and cells were determined in the urinary bladder of the horse by using the peroxidase-antiperoxidase (PAP) immunohistochemical method. Numerous undulating NPY-immunoreactive nerve fibres were found throughout the vesical wall, sometimes forming nerve bundles which ramified repeatedly as they coursed through the connective tissue septa to give rise to smaller bundles or single fibres which projected into the muscle fascicles forming muscular nerve plexuses, mainly in the bladder base. In the submucosa of this region, NPY-immunoreactive fibres formed a rather dense subepithelial plexus. Numerous NPY-immunoreactive nerve fibres supplied blood vessels and were widely distributed on the vascular adventitia constituting rich perivascular nerve plexuses. In addition, intramural ganglia containing NPY-immunoreactive nerve cell bodies and fibres were identified at the uretero-vesical junction. These results suggest that the equine urinary bladder possesses a rich NPY-peptidergic innervation which shows regional variations in the density of the muscular and subepithelial plexuses, the bladder base being the most richly innervated region. At least some of these NPY-immunoreactive nerve fibres have an intrinsic origin in ganglion cells within the vesical wall.

Animals↗
PubMedDate not supplied

Adrenoceptor-mediated regulation of the contractility in horse penile resistance arteries.

The receptors mediating the contractions to both exogenously applied noradrenaline and electrical field stimulation (EFS) were characterized in horse isolated penile resistance arteries. The alpha 1-adrenoceptor-selective antagonist, prazosin, caused competitive rightward shifts of the contractile concentration-response curves (CRC) to phenylephrine. The alpha 2-antagonist, rauwolscine, also displaced to the right the CRC to the alpha 2-adrenoceptor-selective agonist, BHT 920. EFS (0.3 ms, 20-second trains) caused tetrodotoxin-sensitive frequency-dependent contractions which were enhanced in the presence of NG-nitro-L-arginine (L-NOARG, 3 x 10(-5) M), but not affected by mechanical endothelial cell removal. In experiments performed in the presence of L-NOARG, prazosin inhibited contractions to EFS, while rauwolscine inconsistently enhanced the contractile responses. Exogenously added noradrenaline induced contractions which were not changed in endothelium-denuded arteries, but significantly increased in the presence of L-NOARG. Prazosin inhibited the noradrenaline-induced contractions, while rauwolscine did not change the response to noradrenaline either alone or in the presence of prazosin. In the presence of phentolamine (10(-5) M), isoprenaline, adrenaline and the beta 2-adrenoceptor agonist, salbutamol, concentration-dependently relaxed penile resistance arteries, while the relaxations to noradrenaline and dobutamine, which activate beta 1-adrenoceptors, were negligible. Isoprenaline-induced relaxations were not changed in the presence of the beta 1-antagonist, atenolol (10(-7)-10(-6) M), but competitively inhibited by the beta 2-adrenoceptor antagonist, butoxamine (10(-6)-10(-5) M). The present results indicate that stimulation of adrenergic nerves in horse penile resistance arteries releases noradrenaline, which induces vasoconstriction through a predominant activation of alpha 1-adrenoceptors, while postjunctional alpha 2-adrenoceptors apparently play a minor role. Functional beta 2-adrenoceptors are also present in these arteries.

Animals↗
PubMedDate not supplied

[Comparative study of 3 heterologous expression systems for obtaining recombinant Bacillus thuringiensis delta-endotoxins].

cryIA(b) and cryIA(c) genes encoding active fragments of Bacillus thuringiensis delta-endotoxins were cloned downstream of the pR and pT7 promoters from the lambda and T7 bacteriophages, respectively. cryIA(b) gene was also fused with the gene encoding protein A from Staphylococcus aureus cloned under the control of the pR promoter. There were no remarkable differences in the expression levels of the cloned genes in E. coli, but the Western blot analysis allowed distinct protein quality for the three expression systems. We conclude that the best expression model for the production of delta-endotoxins toxic fragments in E. coli is the one based on lambda pR promoter.

Bacillus thuringiensis↗