Effects of furosemide on the resting membrane potentials and the transmitter-induced responses of the Aplysia ganglion cells.

Nakai, Keiko; Sasaki, Kazuhiko; Matsumoto, Mitsuhiko; Takashima, Koichiro

doi:10.1620/tjem.156.79

Cited by 8 publications

(8 citation statements)

References 22 publications

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“…Chloride-deficient solutions stimulate irritant receptors in the larynx of animals [17,18], but their effects on the distal airway remain unclear. Frusemide has been shown to inhibit chloride transport and a number of other processes controlling neural excitability [8][9][10][11][12][13][14]. However, there are no single-fibre studies assessing effects of frusemide on airway nerves or sensory receptors in the lung.…”

Section: Discussionmentioning

confidence: 99%

“…The actions of frusemide within the airway are probably multifactorial, but the observation that it affects responses to cough challenge in normals, and to sodium metabisulphite (MBS) in asthmatic subjects has implied an effect on airway nerves. The findings that frusemide reduces neurally-mediated airway smooth muscle contraction in vitro [7], and inhibits neural function in a variety of systems outside the lung [8][9][10][11][12][13][14], support this assertion. An effect of frusemide on airway nerves, thus, makes the drug potentially useful as a probe to detect differences between airway neural responses of normal and asthmatic subjects, which has been the purpose of the current study.…”

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confidence: 97%

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Effect of frusemide on cough responses to chloride-deficient solution in normal and mild asthmatic subjects

Stone¹,

Barnes²,

Chung³

1993

Eur Respir J

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We studied the tussive effects of a chloride-deficient solution (1.26% sodium bicarbonate). Nine normal volunteers and 10 mild asthmatic subjects were studied. In two double-blind, placebo-controlled, cross-over studies, we assessed the profile of any inhibitory effects that inhaled frusemide had over these responses. Baseline cough challenge was followed by inhalation of either frusemide (40 mg), or 0.15 M NaCl control. Cough was then induced at 0.5, 2, 4 and 6 h after treatment. Forced expiratory volume in one second (FEV1) was measured before and after each challenge. Changes from the baseline cough response due to drug or control were compared nonparametrically at each time point. There was no difference in the sensitivity of normal and asthmatic subjects to the cough challenge (median cough response 15 and 14.5 on control day, 12 and 15 on frusemide day). Frusemide caused sustained inhibition of the cough response in normal subjects (p < 0.05 at 2 h, p < 0.01 at 4 h), but had only a small, nonsignificant effect in asthmatic subjects at 30 min. Falls in FEV1 of asthmatic subjects due to the chloride-deficient solution were not significant, and did not correlate with number of coughs. We conclude that mild asthmatic subjects are less sensitive than normal subjects to the influence of frusemide against low chloride challenge. This observation is not explained by bronchoconstrictor effects of the cough challenge in asthmatic subjects.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

Effect of frusemide on cough responses to chloride-deficient solution in normal and mild asthmatic subjects

Stone¹,

Barnes²,

Chung³

1993

Eur Respir J

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“…1985;Nakai et al 1988;Nicoll 1978;Thompson et al 1989;Solis et al 1988). To examine if furosemide could influence arterial pressure, HR, or ERSNA by a direct action in the brain, we examined the effect of i.c.v.…”

Section: Effects Of Icv Administration Of Furosemide On Efferent Rmentioning

confidence: 99%

“…There is no evidence for a direct depolarizing action elicited by inhibition of the Na-K-2CI transporter by furosemide in neurons, but several investigators have demonstrated that high concentrations of furosemide can inhibit the production of cerebrospinal fluid (McCarthy et al 1974;Johanson et al 1992) and affect chloride transport in neurons and astrocytes (Ernst et al 1989;Kimmelberg et ul. 1985;Nakai et al 1988;Nicoll 1978;Thompson et al 1989;Solis et al 1988).…”

Section: Effects Of Icv Administration Of Furosemide On Efferent Rmentioning

confidence: 99%

Interactions Between Furosemide and the Renal Sympathetic Nerves

Petersen¹

1999

Pharmacology & Toxicology

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“…Furosemide has been shown to affect ionic transport in the brain a t the choroid plexus, in the inner ear, in astrocytes and in neurones (McCarthy & Reed 1974;Nicoll 1978;Nakai et al 1988;Ernst et al 1989;Johanson et al 1992;Kimelberg & Frangakis 1985;Wilson & Dixon 1989;Thompson & Gahwiler 1989;Solis et al 1988). Whether central effects of furosemide exert influences on cardiovascular functions is unknown.…”

mentioning

confidence: 99%

Furosemide Elicits Immediate Sympathoexcitation via a Renal Mechanism Independent of Angiotensin II

Petersen

DiBona

1995

Pharmacology & Toxicology

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This investigation aimed at examing the hypothesis that furosemide elicits renal sympathoexcitation through stimulation of renal renin release, which in turn produces increased plasma angiotensin II levels, causing centrally mediated sympathoexcitation. In addition, direct central nervous actions of furosemide on central control of mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity were examined. Furosemide (300 mg/kg intravenously) was administered to four groups of rats: (1) control; (2) nephrectomized; (3) with intravenous losartan blockade (10 mumol/kg); and (4) with intracerebroventricular losartan blockade (10 nmol). In a fifth group of rats, furosemide was administered intracerebroventricularly (0, 2.5, 25 or 250 micrograms). To eliminate reflex control of mean arterial pressure, heart rate and efferent renal sympathetic nerve activity, all experiments were performed in rats with sinoaortic denervation and bilateral vagotomy. Experiments were performed during Saffan anaesthesia (0.9% alphaxalone/0.3% alphadolone), and rats were paralyzed with pancuronium and artifically ventilated. Furosemide produced an immediate 40% increase in efferent renal sympathetic nerve activity while the furosemide vehicle, 2 vol.% ethanolamine, did not affect efferent renal sympathetic nerve activity. The furosemide-induced increase in efferent renal sympathetic nerve activity was abolished in rats with bilateral nephrectomy but it was not affected by intravenous or intracerebroventricular losartan blockade. Intracerebroventricular angiotensin II produced an increase in mean arterial pressure and efferent renal sympathetic nerve activity whereas intravenous angiotensin II produced a pressor response in absence of increased efferent renal sympathetic nerve activity. Losartan effectively blocked responses to intravenous or intracerebroventricular angiotensin II. Intracerebroventricular administration of furosemide produced no changes in mean arterial pressure, heart rate or efferent renal sympathetic nerve activity.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effects of furosemide on the resting membrane potentials and the transmitter-induced responses of the Aplysia ganglion cells.

Cited by 8 publications

References 22 publications

Effect of frusemide on cough responses to chloride-deficient solution in normal and mild asthmatic subjects

Effect of frusemide on cough responses to chloride-deficient solution in normal and mild asthmatic subjects

Interactions Between Furosemide and the Renal Sympathetic Nerves

Furosemide Elicits Immediate Sympathoexcitation via a Renal Mechanism Independent of Angiotensin II

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