Cardiovascular responses in rats with glycerol‐induced acute renal failure

Bowmer, C J; Warren, Maxine; Yates, M S

doi:10.1111/j.1476-5381.1983.tb11020.x

Cited by 14 publications

(13 citation statements)

References 18 publications

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“…The decreased vascular reactivity to noradrenaline supports our previous findings of reduced pressor responses to noradrenaline in uraemic rats (Bowmer et al, 1983). Similarly diminished vascular responses to noradrenaline have been observed both in humans and rats with chronic renal failure (Campese et al, 1981;Rascher etal., 1982) and in rats with ARF produced by bilateral ureter ligation (Ueda etal., 1981).…”

Section: Discussionsupporting

confidence: 79%

“…They concluded that the decreased response to noradrenaline in renal failure was due to downregulation of a-receptors in response to elevated circulating noradrenaline levels. Whilst we too have found increased plasma noradrenaline concentrations in glycerol-induced ARF (Bowmer et al, 1983) the decreased vascular responses to noradrenaline, angiotensin and potassium chloride observed in the present study suggest that, at least in this acute model of renal failure, the depression of vascular responses is less specific and not restricted to noradrenaline. The decreased contractions of the isolated blood vessels from uraemic animals to angiotensin (Figure 2) is paralleled by the reduced pressor responses to the peptide in vivo (Figure 4) which supports similar findings observed in the investigation of ARF produced by ureter ligation (Ueda etal., 1981).…”

Section: Discussionmentioning

confidence: 37%

“…In a recent study of rats with glycerol-induced acute renal failure (ARF) (Bowmer et al, 1983) we found decreased pressor responses to noradrenaline and elevated plasma noradrenaline concentrations. In addition the chronotropic responses to right cervical sympathetic and vagal stimulation were decreased.…”

Section: Introductionmentioning

confidence: 99%

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Vascular reactivity in rats with glycerol‐induced acute renal failure

Bowmer¹,

Clarke²,

Comer³

et al. 1984

British J Pharmacology

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 37%

See 1 more Smart Citation

Vascular reactivity in rats with glycerol‐induced acute renal failure

Bowmer¹,

Clarke²,

Comer³

et al. 1984

British J Pharmacology

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“…[15] performed in the model of glycerol induced AKI. These authors considered high uremia (plasma urea was signifi cantly elevated in the AKI group in our study as well) and its infl uence on the autonomic nervous system (diminished α 1 adrenoreceptors sensitivity) as a cause of MAP reduction after AKI.…”

Section: Discussionmentioning

confidence: 99%

Combined Angiotensin II Type-1 Receptor Blockade and Superoxide Anion Scavenging Affect the Post-Ischemic Kidney in Hypertensive Rats

Ivanov

Mihailović-Stanojević

Marković-Lipkovski

et al. 2016

Acta Veterinaria

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Ischemic acute kidney injury is characterized by renal vasoconstriction, fi ltration failure, tubular obstruction, tubular backleak and overproduction of angiotensin II and reactive oxygen species. Considering this complexity, the aim of our study was to investigate the effects of angiotensin II type-1 receptor blocker -Losartan and superoxide anion scavenger -Tempol, in a combined treatment on acute kidney injury in postischemic hypertensive rats.The experiment was performed in anesthetized, adult male spontaneously hypertensive rats. The right kidney was removed and the left renal artery was occluded for 40 minutes. Experimental groups received combined treatment (Losartan + Tempol) or saline in the femoral vein 5 minutes before, during and 175 minutes after clamp removal.Hemodynamics and biochemical parameters were measured and kidney specimens were collected 24h after reperfusion. Histological examination was performed by optical microscopy.Combined treatment improves renal haemodynamics parameters which were exacerbated due to acute kidney injury. Acute kidney injury signifi cantly decreased creatinine and urea clearance and increased lipid peroxidation in the plasma. Treatment with Losartan and Tempol induced a signifi cant increase of creatinine and urea clearance. Lipid peroxidation in the plasma decreased and glutathione peroxidase enzyme activity in the erythrocytes increased after Losartan + Tempol treatment. This combined treatment reduced cortico-medullary necrosis and tubular dilatation in the kidney.Our results indicate that synergism of Losartan and Tempol treatment could have benefi cial effects on blood pressure and kidney function, during postischemic acute kidney injury development in experimental hypertension.

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“…Investigations of rats with acute renal failure (ARF) have demonstrated abnormalities in the sympathetic influence on cardiac function. For example, depressed chronotropic responses in-vivo to cervical sympathetic stimulation and isoprenaline have been noted (Bowmer et al 1983;Yates et a1 1985Yates et a1 , 1986Mann et al 1986) and isolated right atria from rats with A R F exhibit reduced chronotropic responses to isoprenaline (Yates et al 1985). In addition to an impairment in cardiac chronotropic responses, we have observed that right ventricular strips removed from rats with A R F display reduced inotropic responses to a variety of cardiac stimulants, including isoprenaline, 3-isobutyl-I-methylxanthine and Ca2+.…”

mentioning

confidence: 99%

Cardiac Function in Rats with Acute Renal Failure

Robinson

Bowmer

Yates

1992

Journal of Pharmacy and Pharmacology

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Inotropic responses of isolated cardiac preparations from rats with glycerol-induced acute renal failure (ARF) were recorded, following a range of cardiac stimulants. Left atria of rats with ARF showed diminished inotropic responses only to the calcium agonist Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethyl-phenyl)-pyridine-5 -carboxylate) whilst right ventricular strips exhibited reduced responses to isoprenaline, 3-isobutyl-1-methylxanthine, Ca2+ and Bay K 8644. Investigations of cardiac mitochondrial respiration indicated that there is a site-unspecific 'pseudo' uncoupling of oxidative phosphorylation in ARF but that electron transport is unaffected. This uncoupling of oxidative phosphorylation did not have any detectable effect on either levels of total adenine nucleotides and creatine phosphate or cellular energy charge. Measurements were also made of the activity of pyruvate dehydrogenase which provides an index of mitochondrial Ca2+ levels. The proportion of pyruvate dehydrogenase in its active form was threefold higher following isoprenaline injection in hearts of rats with ARF compared with controls. The results suggest that in hearts of rats with ARF there is a change in the number, affinity, efficacy or coupling of the dihydropyridine receptor on the L-type calcium channel. Moreover, in the ventricle, a defect in cellular Ca2+ control, resulting in an increase in mitochondrial Ca2+ uptake, may contribute to the depression of inotropic response to the range of cardiac stimulants tested.

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Cardiovascular responses in rats with glycerol‐induced acute renal failure

Abstract: The present findings show that in the rat, changes in cardiovascular responsiveness occur after a brief period of uraemia which are similar to those observed in patients and rats with chronic renal failure.

Cited by 14 publications

References 18 publications

Vascular reactivity in rats with glycerol‐induced acute renal failure

Vascular reactivity in rats with glycerol‐induced acute renal failure

Combined Angiotensin II Type-1 Receptor Blockade and Superoxide Anion Scavenging Affect the Post-Ischemic Kidney in Hypertensive Rats

Cardiac Function in Rats with Acute Renal Failure

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