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22 results on '"Ortiz I"'

21. Vascular alpha-1D-adrenoceptors are overexpressed in aorta of the aryl hydrocarbon receptor null mouse: role of increased angiotensin II.

Author

Villalobos-Molina R, Vázquez-Cuevas FG, López-Guerrero JJ, Figueroa-García MC, Gallardo-Ortiz IA, Ibarra M, Rodríguez-Sosa M, Gonzalez FJ, and Elizondo G

Subjects
Adrenergic alpha-1 Receptor Antagonists, Adrenergic alpha-Antagonists pharmacology, Angiotensin II antagonists & inhibitors, Animals, Aorta, Thoracic drug effects, Aorta, Thoracic physiology, Blood Pressure drug effects, Blotting, Western, Captopril pharmacology, Gene Expression drug effects, In Vitro Techniques, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Norepinephrine pharmacology, Phenylephrine pharmacology, Piperazines pharmacology, Receptors, Adrenergic, alpha-1 genetics, Reverse Transcriptase Polymerase Chain Reaction, Vasoconstriction drug effects, Angiotensin II metabolism, Aorta, Thoracic metabolism, Receptors, Adrenergic, alpha-1 metabolism, Receptors, Aryl Hydrocarbon genetics
Abstract

1 The hypothesis that alpha(1D)-adrenoceptors may mediate the pro-hypertensive actions of angiotensin II (Ang II) was tested in isolated aorta (alpha(1D)-adrenoceptor bearing tissue) of the aryl hydrocarbon receptor null mouse (AhR(-/-)), which shows increased levels of Ang II, cardiac hypertrophy and hypertension. 2 The effect of captopril (an angiotensin converting enzyme inhibitor) on both blood pressure and aortic alpha(1D)-adrenoceptor expression and function in mice were determined. 3 Basal blood pressure was higher in AhR(-/-) mice, while captopril therapy decreased it to wild-type (WT) values. 4 Aortas of adult WT and AhR(-/-) mice were stimulated by phenylephrine or noradrenaline to induce contraction; the maximal effect was higher in AhR(-/-) mice, without a significant change in pEC(50). 5 PA(2) values for the selective alpha(1D)-adrenoceptor antagonist BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazynil]ethyl]-8-azaspiro [4.5]decane-7,9-dione) were 9.19 and 8.94 for WT and AhR(-/-), respectively; while Schild slopes were not different from 1. 6 PCR experiments showed c. 77% increase in AhR(-/-)alpha(1D)-adrenoceptors cDNA compared with WT mice; while western blot analysis demonstrated c. 88% increase in alpha(1D)-adrenoceptor protein in AhR(-/-) mice. 7 Captopril therapy decreased alpha(1D)-adrenoceptor-induced contraction and protein in AhR(-/-) mice to WT levels. 8 These data support the hypothesis that under conditions where Ang II is elevated, vascular alpha(1D)-adrenoceptors are increased, and further suggest that both Ang II and vascular alpha(1D)-adrenoceptors could be related in the onset of hypertension.

Published
2008
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22. Selective agonists reveal alpha(1A)- and alpha(1B)-adrenoceptor subtypes in caudal artery of the young rat.

Author

Parés-Hipólito J, Gómez-Zamudio JH, Gallardo-Ortiz IA, López-Guerrero JJ, Santamaría-Ortiz J, Ibarra M, and Villalobos-Molina R

Subjects
Adrenergic alpha-1 Receptor Antagonists, Adrenergic alpha-Antagonists pharmacology, Animals, Arteries physiology, Carbachol pharmacology, Dose-Response Relationship, Drug, Imidazoles pharmacology, In Vitro Techniques, Indoles pharmacology, Male, Phenylephrine pharmacology, Piperazines pharmacology, Prazosin pharmacology, Rats, Rats, Wistar, Receptors, Adrenergic, alpha-1 physiology, Tetrahydronaphthalenes pharmacology, Thymine pharmacology, Adrenergic alpha-1 Receptor Agonists, Adrenergic alpha-Agonists pharmacology, Arteries drug effects, Tail blood supply
Abstract

Multiple alpha(1)-adrenoceptors were evaluated in caudal artery of the young Wistar rat using selective agonists and antagonists. Arteries were exposed to the selective alpha(1A)-adrenoceptor agonist, A-61603 (N-[5-(4,5-dihydro-1H-imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) or to phenylephrine and to prazosin (alpha(1)-adrenoceptor antagonist), or the selective alpha(1A)-adrenoceptor antagonists 5-methylurapidil, RS 100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy)phenyl]-1-piperazinyl]propyl]-2,4-(1H)-pyrimidinedione), RS 17053 (N-[2(2-cyclopropylmethoxy) ethyl]-5-chloro-alpha, alpha-dimethyl-1H-indole-3-ethanamide), and the selective alpha(1D)-adrenoceptor antagonist BMY 7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione). Results showed a 100-fold higher potency of A-61603 for the alpha(1)-adrenoceptor present in the artery, compared with phenylephrine. Prazosin displaced both agonists with high affinity, whereas 5-methylurapidil, RS 100329 and RS 17053 displaced A-61603 with high affinity, indicating the presence of alpha(1A)-adrenoceptors. The selective alpha(1A)-adrenoceptor antagonists blocked phenylephrine responses with low affinity, suggesting that phenylephrine activated a second receptor population in caudal artery. BMY 7378 antagonized with low affinity both A-61603 and phenylephrine-induced contractions, indicating absence of alpha(1D)-adrenoceptors in the vessel. The results suggest that functional alpha(1B)-adrenoceptors are present in caudal arteries of the young Wistar rat.

Published
2006
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