Reactivity of the isolated perfused rat tail vascular bed

Franca, Adriana S.; Rossoni, Luciana Venturini; Amaral, S.M.C.; Vassallo, Dalton Valentim

doi:10.1590/s0100-879x1997000700012

Cited by 19 publications

(18 citation statements)

References 13 publications

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“…Isolated rat tail arteries were perfused as previously reported (22). Rats were first anesthetized with sodium pentobarbital (65 mg/kg, ip), and heparin (500 IU, ip) was administered 10 min later.…”

Section: Isolated Rat Tail Vascular Bed Preparationmentioning

confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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Chronic lead exposure induces hypertension in humans and animals, affecting endothelial function. However, studies concerning acute cardiovascular effects are lacking. We investigated the effects of acute administration of a high concentration of lead acetate (100 µΜ) on the pressor response to phenylephrine (PHE) in the tail vascular bed of male Wistar rats. Animals were anesthetized with sodium pentobarbital and heparinized. The tail artery was dissected and cannulated for drug infusion and mean perfusion pressure measurements. Endothelium and vascular smooth muscle relaxation were tested with acetylcholine (5 µg/100 µL) and sodium nitroprusside (0.1 µg/100 µL), respectively, in arteries precontracted with 0.1 µM PHE. Concentrationresponse curves to PHE (0.001-300 µg/100 µL) were constructed before and after perfusion for 1 h with 100 µΜ lead acetate. In the presence of endothelium (E + ), lead acetate increased maximal response (E max ) (control: 364.4 ± 36, Pb 2+ : 480.0 ± 27 mmHg; P < 0.05) and the sensitivity (pD 2 ; control: 1.98 ± 0.07, 2.38 ± 0.14 log mM) to PHE. In the absence of endothelium (E -) lead had no effect but increased baseline perfusion pressure (E + : 79.5 ± 2.4, E -: 118 ± 2.2 mmHg; P < 0.05). To investigate the underlying mechanisms, this protocol was repeated after treatment with 100 µM L-NAME, 10 µM indomethacin and 1 µM tempol in the presence of lead. Lead actions on E max and pD 2 were abolished in the presence of indomethacin, and partially abolished with L-NAME and tempol. Results suggest that acute lead administration affects the endothelium, releasing cyclooxygenasederived vasoconstrictors and involving reactive oxygen species.

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Section: Isolated Rat Tail Vascular Bed Preparationmentioning

confidence: 99%

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Silveira

Lizardo

Souza

et al. 2010

Braz J Med Biol Res

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“…Isolated tail vascular bed preparations were obtained from rats 4 weeks after MI and anesthetized with sodium pentobarbital (60 mg/kg i.p. ), as previously described (França et al, 1997). Briefly, after anesthesia, the tail artery was cannulated, and the tail was immediately severed from the body.…”

Section: Abbreviationsmentioning

confidence: 99%

Differences in Tail Vascular Bed Reactivity in Rats with and without Heart Failure following Myocardial Infarction

Pereira¹,

Sartório²,

Vassallo³

et al. 2004

J Pharmacol Exp Ther

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Myocardial infarction (MI) was induced in rats by coronary ligation to compare changes in vascular reactivity from animals that developed heart failure (InfHF) with those that did not (Inf). Infarct size was similar in both groups. In vitro preparations of tail vascular bed were used to investigate the vascular responses to acetylcholine, sodium nitroprusside, and phenylephrine. Acetylcholine-induced relaxation was impaired in the Inf group (53 Ϯ 2%, n ϭ 6) when compared with Sham (80 Ϯ 2%, n ϭ 6, P Ͻ 0.05). The maximal response (E max ) to phenylephrine increased in the Inf group (423 Ϯ 10 mm Hg, n ϭ 9, P Ͻ 0.01) and decreased in InfHF (279 Ϯ 10 mm Hg, n ϭ 7, P Ͻ 0.05) when compared with Sham (319 Ϯ 11 mm Hg, n ϭ 8). Regardless of endothelial integrity, E max to phenylephrine increased in the Inf, nitro-L-arginine methyl ester, and indomethacin groups. An increased release of a prostanoid vasodilator was detected in the Inf group. Differently, the InfHF group presented a reduction of the E max to phenylephrine and an increment of nitric oxide release. This study demonstrates that MI without heart failure impairs endothelium-dependent relaxation and increases the reactivity to phenylephrine. This increase seems to involve a muscular component. The endothelium participates with an increased release of a vasodilator prostanoid, possibly to compensate the increased smooth muscle response. When heart failure follows MI, the reactivity to phenylephrine decreases, possibly due to an increased nitric oxide release.Coronary artery ligation in rats has been used as a model of chronic left ventricular failure that closely mimics human condition (Hodsman et al., 1988). Indeed, compromised cardiac function (De Felice et al., 1989;Solomon et al., 1999) and increased peripheral resistance (Drexler and Lu, 1992;Schrier and Abraham, 1999) are found in this model. Systemic vasoconstriction can result from many compensatory mechanisms, including activation of the renin-angiotensin system, activation of the sympathetic nervous system, and alterations in the synthesis of local vascular factors (Zelis and Flaim, 1982;Gschwend et al., 2003).Much has been reported regarding endothelial dysfunction in postinfarction myocardial failure (Teerlink et al., 1993(Teerlink et al., , 1994Didion et al., 1997;Bauersachs et al., 1999;Indik et al., 2001;Gschwend et al., 2003), but there is no consensus regarding vascular function in heart failure due to heterogeneity of alterations in vascular reactivity. These alterations may depend on the duration of the disease and the type of artery studied (Stassen et al., 1997a). Despite much research on vascular reactivity in postinfarction heart failure, little is known concerning vascular reactivity in a chronic phase of myocardial infarction (MI), when heart failure is absent.The purpose of this study was, in the first place, to show that there are two animal models with similar infarction areas produced by coronary ligation: chronic MI without heart failure and with heart failure and, secondly, ...

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“…Isolated rat tail vascular beds were used in this study as previously reported (10). Briefly, the rats were anesthetized with sodium pentobarbital (65 mg/kg, ip) and heparin (500 IU, ip) was administered after loss of the righting reflex.…”

Section: Anesthetized Animalsmentioning

confidence: 99%

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

Rossoni

Pinto

Vassallo

2001

Braz J Med Biol Res

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Ouabain increases vascular resistance and may induce hypertension by inhibiting the Na + pump. The effects of 0.18 and 18 µg/kg, and 1.8 mg/ kg ouabain pretreatment on the phenylephrine (PHE; 0.1, 0.25 and 0.5 µg, in bolus)-evoked pressor responses were investigated using anesthetized normotensive (control and uninephrectomized) and hypertensive (1K1C and DOCA-salt treated) rats. Treatment with 18 µg/kg ouabain increased systolic and diastolic blood pressure in all groups studied. However, the magnitude of this increase was larger for the hypertensive 1K1C and DOCA-salt rats than for normotensive animals, while the pressor effect of 0.18 µg/kg ouabain was greater only in DOCA-salt rats. A very large dose (1.8 mg/kg) produced toxic effects on the normotensive control but not on uninephrectomized or 1K1C rats. Rat tail vascular beds were perfused to analyze the effects of 10 nM ouabain on the pressor response to PHE. In all animals, 10 nM ouabain increased the PHE pressor response, but this increase was larger in hypertensive DOCA-salt rats than in normotensive and 1K1C rats. Results suggested that a) increases in diastolic blood pressure induced by 18 µg/kg ouabain were larger in hypertensive than normotensive rats; b) in DOCA-salt rats, smaller ouabain doses had a stronger effect than in other groups; c) hypertensive and uninephrectomized rats were less sensitive to toxic doses of ouabain, and d) after treatment with 10 nM ouabain isolated tail vascular beds from DOCA-salt rats were more sensitive to the pressor effect of PHE than those from normotensive and 1K1C hypertensive rats. These data suggest that very small doses of ouabain, which might produce nanomolar plasma concentrations, enhance pressor reactivity in DOCA-salt hypertensive rats, supporting the idea that endogenous ouabain may contribute to the increase and maintenance of vascular tone in hypertension. Correspondence

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Reactivity of the isolated perfused rat tail vascular bed

Cited by 19 publications

References 13 publications

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Acute lead-induced vasoconstriction in the vascular beds of isolated perfused rat tails is endothelium-dependent

Differences in Tail Vascular Bed Reactivity in Rats with and without Heart Failure following Myocardial Infarction

Effects of small doses of ouabain on the arterial blood pressure of anesthetized hypertensive and normotensive rats

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