Inhibition of Sympathetic Constriction of the Ex Vivo Tail Artery Perfused with Blood from Rats Given Frusemide

Gerkens, John F.; Armsworth, Stuart J.; Smith, Anthony J.

doi:10.3109/10641968709160030

Cited by 8 publications

(4 citation statements)

References 18 publications

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“…This effect is also inhibited by blockade of prostanoid synthesis and requires the kidneys and an intact vascular endothelium (Gerkens 1987;Gerkens et al 1987a, b). The effect of frusemide on the response to sympathetic nerve stimulation is also abolished by the angiotensin I1 receptor blocker saralasin (Gerkens et al 1987b). Frusemide, by stimulating the renal production of prostanoids (Scherer and Weber 1979), activates the renin-angiotensin system.…”

Section: Discussionmentioning

confidence: 99%

“…Frusemide, by stimulating the renal production of prostanoids (Scherer and Weber 1979), activates the renin-angiotensin system. Angiotensin I1 probably acts on the kidneys to release a yet unknown substance that interacts with endothelium to cause vasodilatation (Gerkens et al 1987b). Chemical renal medullectomy has demonstrated that this unknown vasodilator is produced in the renal medulla and may be a lipid (Gerkens et al 1987a).…”

Section: Discussionmentioning

confidence: 99%

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Flunixin meglumine blocks frusemide‐induced bronchodilatation in horses with chronic obstructive pulmonary disease

Rubie¹,

Robinson²,

Stoll³

et al. 1993

Equine Veterinary Journal

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Summary Six horses that developed acute airway obstruction (heaves) when housed in a barn and fed poor‐quality hay were studied. Airway obstruction was verified by a maximal change in pleural pressure during tidal breathing (ΔPplmax) of at least 15 cmH2O. Frusemide (1.0 mg/kg bwt) or an equivalent volume of vehicle was then administered intravenously (iv) and lung function was measured 15, 30, 60, 120, 180, 240 and 300 mins after drug administration. The effect of frusemide on lung function was also studied after treatment of horses with the cyclooxygenase inhibitor flunixin meglumine (1.1 mg/kg every 8 h for 2 days before the experiment). Frusemide significantly reduced the ΔPplmax beginning 15 mins after drug administration. This effect persisted for 5 h. The reduction in ΔPplmax was due partly to an increase in dynamic compliance and partly to a decrease in pulmonary resistance. Tidal volume and respiratory frequency were unaffected by frusemide. Vehicle had no effect on lung function. Flunixin meglumine abolished the effect of frusemide on airway calibre but did not prevent diuresis. These results indicate that the effect of frusemide on airways of horses with heaves persists for at least 5 h, is mediated through prostanoids, and is not a result of diuresis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Flunixin meglumine blocks frusemide‐induced bronchodilatation in horses with chronic obstructive pulmonary disease

Rubie¹,

Robinson²,

Stoll³

et al. 1993

Equine Veterinary Journal

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“…This technique has been described previously (Gerkens et al 1987). Rats were anaesthetized and the trachea, carotid artery, both jugular veins and the urinary bladder cannulated.…”

Section: Rat Ex Vivo Blood Perfused Tail Arterymentioning

confidence: 99%

Inhibitory Effect of Frusemide on Sympathetic Vasoconstrictor Responses: Dependence on a Renal Hormone and the Vascular Endothelium

Gerkens

1987

Clin Exp Pharma Physio

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1. Mesenteric perfusion pressure was measured in the in situ mesentery perfused at a constant rate with blood drawn from the carotid artery of the same anaesthetized rat. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation. These responses were measured before and 30 min after the administration of frusemide (5 mg/kg i.v.) to the rat. Loss of volume due to the frusemide-induced diuresis was prevented by a urinary bladder-venous extracorporeal circuit. 2. Responses to stimulation were reduced after frusemide and were not increased by the subsequent administration of indomethacin (2 mg/kg i.v.). This indomethacin treatment rapidly and completely prevented the fall in blood pressure produced by i.v. arachidonic acid. 3. In rats where the renal papilla had been ablated by treatment with bromoethylamine (200 mg/kg i.p.) 5 weeks previously, frusemide administration did not reduce sympathetic responses in the in situ blood-perfused mesentery. 4. A segment of rat tail artery, cannulated at both ends was mounted in an organ bath and perfused with blood withdrawn from, and returned to, an anaesthetized rat. Increases in perfusion pressure produced by periarterial electrical stimulation of this ex vivo blood perfused tail artery segment were reduced by frusemide administration to the anaesthetized rat. 5. When the endothelium was removed from the tail artery segment, frusemide administration did not lead to any reduction of vasoconstrictor responses. 6. Frusemide may lead to the release of a non-prostanoid hormone from the renal medulla which results in inhibition of peripheral sympathetic vasoconstrictor responses. The release of the hormone may involve intra-renal prostaglandins. The final antivasoconstrictor effect requires an intact vascular endothelium.

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“…It has been reported that furosemide was able to reduce blood pressure prior to inducing a significant diuretic effect ( Dikshit et al ., 1973 ). From experiments performed in vivo and ex vivo in rats, it has been proposed that the final antivasoconstrictor effect of furosemide requires an intact vascular endothelium ( Gerkens et al ., 1987 ; 1988 ). More recently, furosemide has been shown to increase the release of prostacyclin, together with endothelial kinins and NO, from primary cultured bovine aortic endothelial cells ( Wiemer et al ., 1994 ).…”

Section: Introductionmentioning

confidence: 99%

Role of EDHF in the vasodilatory effect of loop diuretics in guinea‐pig mesenteric resistance arteries

Pourageaud

Bappel-Gozalbes

Marthan

et al. 2000

British J Pharmacology

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1 Relaxing e ect of loop diuretics, piretanide and furosemide in comparison with acetylcholine (ACh) was investigated in guinea-pig isolated mesenteric resistance arteries. 2 Concentration-response curves to ACh (0.001 ± 10 mM) and diuretics (0.0001 ± 1 mM) were constructed in noradrenaline (10 ± 30 mM)-precontracted arteries incubated either in normal physiological salt solution (PSS) or in 30 mM KCl PSS (K-PSS). 3 In PSS, maximal relaxations (R max ) and pD 2 to ACh were 87+2% and 7.1+0.1 (n=10). L-N Gnitro-arginine methyl ester (L-NAME, 100 mM) reduced R max by 20% (P50.01, n=7) and pD 2 by 10% (P50.01). In contrast, indomethacin (10 mM) increased R max by 19% (P50.01, n=8) and pD 2 by 10% (P50.05). Combination of L-NAME+indomethacin reversed the e ect observed with either of these inhibitors used alone. In K-PSS, R max was attenuated by 40% (P50.001, n=6) compared to PSS. L-NAME reduced R max by 65% (P50.01, n=5) and increased pD 2 by 15 fold. LNAME+indomethacin suppressed the resistant relaxation. 4 In PSS+L-NAME+indomethacin, inhibitors of small (SK Ca ; apamin, 0.1 mM) and large (BK Ca ; iberiotoxin and charybdotoxin, 0.1 mM) conductance Ca 2+ -sensitive K 7 -channels used alone had little e ect on the ACh-response. Combination of apamin+iberiotoxin reduced R max by 40% (P50.05, n=7) while apamin+charybdotoxin fully abolished the resistant relaxation. 5 In PSS, piretanide and furosemide induced relaxation with R max : 89+3% vs 84+5% and pD 2 : 8.5+0.1 vs 7.7+0.2 (P50.01) for piretanide (n=11) and furosemide (n=10), respectively. Endothelial abrasion suppressed relaxation to diuretics. L-NAME and indomethacin used alone or in combination did not signi®cantly modify the response to diuretics. 6 In K-PSS, piretanide-induced relaxation was abolished whereas that to furosemide was reduced by 70% (P50.001, n=9) compared to PSS and was suppressed by L-NAME+indomethacin. In PSS+L-NAME+indomethacin, apamin slightly reduced relaxation to diuretics whereas charybdotoxin or iberiotoxin abolished the response. 7 These results indicate that ACh-evoked relaxation is mediated by both NO/PGl 2 -dependent and -independent mechanisms. The EDHF-dependent component relies on activation of Ca 2+ -activated K + channels, is sensitive to a combination of apamin+charybdotoxin and to a smaller degree to a combination of apamin+iberiotoxin. Loop diuretic-induced relaxation is endothelium-dependent, appears to be mediated by NO, PGl 2 and EDHF for furosemide and EDHF only for piretanide. For the two diuretics, opening of BK Ca channels may be involved in the relaxation.

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Inhibition of Sympathetic Constriction of the Ex Vivo Tail Artery Perfused with Blood from Rats Given Frusemide

Cited by 8 publications

References 18 publications

Flunixin meglumine blocks frusemide‐induced bronchodilatation in horses with chronic obstructive pulmonary disease

Flunixin meglumine blocks frusemide‐induced bronchodilatation in horses with chronic obstructive pulmonary disease

Inhibitory Effect of Frusemide on Sympathetic Vasoconstrictor Responses: Dependence on a Renal Hormone and the Vascular Endothelium

Role of EDHF in the vasodilatory effect of loop diuretics in guinea‐pig mesenteric resistance arteries

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