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R A Bobadilla

Publications and source records attributed to R A Bobadilla.

At least 19 recordsLinked to original sources
PubMed2001

Changes in vascular reactivity following subrenal aortic constriction in pregnant and nonpregnant rats.

OBJECTIVE: The present study was designed to determine whether or not subrenal aortic coarctation (SAC) is able to modify aorta reactivity in pregnant rats. METHODS: Wistar female rats were subjected to SAC, and the responses to phenylephrine and acetylcholine of aortic segments above (thoracic) and below (abdominal) the coarctation from pregnant and non-pregnant rats were explored. RESULTS: Contractile responses to phenylephrine and relaxant responses to acetylcholine were similar in the thoracic segment from pregnant and non-pregnant SAC rats, whereas both kinds of response were higher in the abdominal segment from pregnant rats (p < 0.05). L-NAME (a nitric oxide synthase inhibitor) increased the effect of phenylephrine only in the aortic rings from pregnant animals (p < 0.05) and in general abolished the response to acetylcholine, with the exception of the abdominal segment from pregnant rats, in which only a partial inhibition was observed (p < 0.05). Indomethacin inhibited the contractile response to phenylephrine and increased the relaxant activity to acetylcholine in both aortic segments from the two groups of animals (p < 0.05). CONCLUSION: The lower contractile response to adrenergic agonists and higher relaxant response to acetylcholine that are associated with normal pregnancy are lost as a consequence of the coarctation procedure. Changes in the production of endothelial nitric oxide and contractile prostanoids appear to be associated with the vascular disturbances observed in SAC rats.

Animals↗
PubMed2001

Lead induces endothelium- and Ca2+-independent contraction in rat aortic rings.

The contractile effect of lead on rat aortic rings was examined. Lead (0.1-3.1 mM) elicited concentration-dependent but endothelium-independent contractions, which were unaffected by prazosin (1 microM). The contractile effects of lead were similar when the aortic rings were bathed either in the absence or presence of external Ca2+. Lanthanum (1 mM) but not verapamil (I pM) inhibited the lead contractions; hence non-L-calcium channels are involved in such effect. In addition, lead induced contractions on aortic rings incubated in Ca2+-free EGTA-containing solution for 70 min., an experimental condition in which intracellular Ca2+-stores are depleted. Finally, the contractile effect of lead was not modified by calphostin C (an inhibitor of protein kinase C). In conclusion, the present results suggest that in rat aorta, the lead-induced contraction is independent of extra- and intracellular calcium stores. In addition, the effect of lead is independent of either catecholamines or protein kinase C. It is likely that in rat aorta, lead enters into the smooth muscle cells through non-L-calcium channels, and when acting like calcium on the contractile machinery it produces contraction. The differences observed between our results and those obtained by other authors may indicate that the mechanism of the contractile effect of lead varies among the different blood vessels.

Animals↗
PubMed1998

alpha 1D-adrenoceptors contribute to the neurogenic vasopressor response in pithed rats.

The aim of the present study was to assess the role of vascular alpha 1D-adrenoceptors in the sympathetic vasopressor response in vivo. Specifically, we evaluated the effect of a selective alpha 1D-adrenoceptor antagonist, BMY 7378 (8-(2-(4-(2-methoxyphenyl)-1-piperazinyl)ethyl)-8-azaspiro(4,5)dec ane-7,9- dione 2HCl), on the vasopressor response induced by preganglionic (T7-T9) sympathetic stimulation in the pithed rat. The vasopressor response was dose-dependently sensitive to inhibition by intravenous BMY 7378 (0.1, 0.31, 1 and 3.1 mg/kg), doses of 1 and 3.1 mg/kg being equally effective. Like BMY 7378, 5-methylurapidil (0.1, 0.31, 1 and 3.1 mg/kg) antagonized the vasopressor response to spinal stimulation; doses of 1 and 3.1 mg/kg were also equally effective. In combination experiments, BMY 7378 (1 mg/kg, i.v.) and the alpha 1A-adrenoceptor antagonist, 5-methylurapidil (1 mg/kg, i.v.), showed an additive effect. The present results demonstrate that the alpha 1D-adrenoceptor subtype plays an important role in the pressor response to sympathetic nerve stimulation in the pithed rat, and confirm the participation of the alpha 1A-adrenoceptor subtype in the same response.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1997

Possible involvement of endothelium-derived hyperpolarizing factor in vascular responses of abdominal aorta from pregnant rats.

Increased relaxant response to acetylcholine during pregnancy is proposed to be due to an estrogen-mediated increase in nitric oxide release. We studied acetylcholine-induced pathways of relaxation in the thoracic and abdominal aortic rings from pregnant and nonpregnant Wistar-Kyoto rats and measured basal and stimulated release of nitrites in these vessels. Endothelium-dependent relaxation was significantly greater in pregnant than in nonpregnant rats. Acetylcholine provoked a concentration-dependent relaxation on thoracic and abdominal aortic rings from nonpregnant and pregnant rats. After N118-nitro-L-arginine methyl ester pretreatment, the relaxation was significantly inhibited in the two preparations of nonpregnant and pregnant rodents. The relaxation was not inhibited by indomethacin in any of the aortic segments from pregnant and nonpregnant rats. After cytochrome P450 arachidonic acid metabolism inhibitor clotrimazole, a nonsignificant decrease in the Emax to acetylcholine-induced relaxation was observed in the thoracic segments of pregnant and nonpregnant rats. On the other hand, in abdominal aorta, clotrimazole decreased maximal relaxation in rings from pregnant rats (P<.05) but did not change the acetylcholine-induced relaxation from nonpregnant rats. Our results show an increase in the acetylcholine-stimulated release of nitrites in thoracic aortic rings from pregnant rats compared with rings from nonpregnant rats, which cannot be evidenced in abdominal aortic rings. These results suggest that acetylcholine-induced vasodilation in the abdominal segment from pregnant rats is mediated only in part by nitric oxide, the remainder apparently due to an endothelium-derived vasodilator, cytochrome P450-dependent, which may be endothelium-derived hyperpolarizing factor/epoxyeicosatrienoic acid.

Acetylcholine↗