Angiotensin inhibition and atrial natriuretic peptide release after acute volume expansion in rats with aortocaval shunt

Willenbrock, Roland

doi:10.1016/s0008-6363(98)00335-6

Cited by 12 publications

(13 citation statements)

References 52 publications

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“…Langenickel et al (16) showed that ANP mRNA was upregulated in the LA of shunted rats, whereas the RA ANP mRNA expression remained unchanged. Willenbrock et al (25) found unchanged ANP mRNA as well as ANP concentration in both the LA and RA in this heart failure model. These data suggest that the blunted ANP release we observed in shunt animals was neither due to impaired synthesis nor depleted storage vesicles of ANP.…”

Section: Discussionmentioning

confidence: 46%

“…In several models of experimental heart failure as well as in human heart failure, ANP release after either acute volume load or exercise is blunted (7,13,17,18,24,25). Willenbrock et al (25) suggested that the ANP system is impaired in rats with an acute aortocaval shunt and that the activation of the angiotensin system contributes to the impairment of the ANP system.…”

Section: Discussionmentioning

confidence: 99%

“…Willenbrock et al (25) suggested that the ANP system is impaired in rats with an acute aortocaval shunt and that the activation of the angiotensin system contributes to the impairment of the ANP system. Inadequate ANP secretion upon stimulation may thereby contribute to fluid retention during the progression of heart failure.…”

Section: Discussionmentioning

confidence: 99%

“…However, the ANP response to acute volume expansion is blunted in cardiac hypertrophy as well as heart failure (18,23,25). It is unclear whether the impaired ANP release in heart failure is a result of neurohormonal suppression or due to an inhibition of the release mechanism itself.…”

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confidence: 99%

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Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Langenickel¹,

Pagel²,

Buttgereit³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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Stored cardiac pro-atrial natriuretic peptide (pro-ANP) is converted to ANP and released upon stretch from the atria into the circulation. Corin is a serin protease with pro-ANP-converting properties and may be the rate-limiting enzyme in ANP release. This study was aimed to clone and sequence corin in the rat and to analyze corin mRNA expression in heart failure when ANP release upon stretch is blunted. Full-length cDNA of rat corin was obtained from atrial RNA by RT-PCR and sequenced. Tissue distribution as well as regulation of corin mRNA expression in the atria were determined by RT-PCR and RNase protection assay. Heart failure was induced by an infrarenal aortocaval shunt. Stretch was applied to the left atrium in a working heart modus, and ANP was measured in the perfusates. The sequence of rat corin cDNA was found to be 93.6% homologous to mouse corin cDNA. Corin mRNA was expressed almost exclusively in the heart with highest concentrations in both atria. The aortocaval shunt led to cardiac hypertrophy and heart failure. Stretch-induced ANP release was blunted in shunt animals (control 1,195 +/- 197 fmol.min(-1).g(-1); shunt: 639 +/- 99 fmol.min(-1).g(-1), P < 0.05). Corin mRNA expression was decreased in both atria in shunt animals [right atrium: control 0.638 +/- 0.004 arbitrary units (AU), shunt 0.566 +/- 0.014 AU, P < 0.001; left atrium: control 0.564 +/- 0.009 AU, shunt 0.464 +/- 0.009 AU, P < 0.001]. Downregulation of atrial corin mRNA expression may be a novel mechanism for the blunted ANP release in heart failure.

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Section: Discussionmentioning

confidence: 46%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Langenickel¹,

Pagel²,

Buttgereit³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…The renin-angiotensin-aldosterone system (RAAS) is activated in rats with aortocaval fistula as evidenced by an increased plasma concentration of angiotensin II (Ang II) and, in rats with a large fistula, an increased plasma renin activity (Ruzicka et al 1993;Willenbrock et al 1999). Furthermore, cardiac angiotensin-converting enzyme (ACE) 1 expression is upregulated, whereas that of ACE2 is reduced, indicating that the local cardiac RAAS is also activated (Karram et al 2005).…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II control of regional haemodynamics in rats with aortocaval fistula

Duggan

Tabrizchi

2016

Experimental Physiology

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New Findings r What is the central question of this study?Hyperdynamic circulation because of arteriovenous fistula results in reduction of blood flow to organs but is a model of low circulatory resistance with activated renin-angiotensin system. The aim was to determine contributions of different subtypes of angiotensin II receptors to regional blood flow and vascular conductance in a hyperdynamic circulatory state. r What is the main finding and its importance?The renin-angiotensin system plays a pivotal role in control of regional blood flow in animals with arteriovenous fistula and makes a major contribution to the maintenance of normal arterial blood pressure. In this hyperdynamic circulatory state model, angiotensin II type 1 receptors predominated in regulating regional haemodynamics.Regional perfusion is reduced and the renin-angiotensin system activated in rats with aortocaval fistula. The effects of captopril (angiotensin-converting enzyme inhibitor), losartan (angiotensin II type 1 receptor antagonist) and PD 123319 (angiotensin II type 2 receptor antagonist) on regional blood flow and vascular conductance were assessed in rats with aortocaval fistula and sham-operated rats. Control of blood flow and vascular conductance by angiotensin II was evaluated by serial bolus injections of captopril, losartan and PD 123319 in anaesthetized rats. In rats with fistula, PD 123319 significantly decreased, whereas captopril and losartan increased, mesenteric blood flow. The decrease in mesenteric blood flow induced by PD 123319 was significantly greater in rats with fistula compared with sham operation. Captopril and PD 123319 significantly decreased renal blood flow compared with losartan, which increased it. In sham-operated rats, captopril and losartan significantly increased, whereas PD 123319 decreased, mesenteric and renal conductance. In rats with fistula, captopril and losartan significantly increased, whereas PD 123319 decreased, mesenteric conductance. The significant increase produced by losartan on mesenteric conductance was greater in rats with fistula compared with sham operation. PD 123319 produced a significantly greater decrease in renal conductance of rats with aortocaval fistula compared with sham-operated rats. Captopril, losartan and PD 123319 did not significantly affect perfusion in the hindquarter in rats with fistula or sham-operated. The renin-angiotensin system is more active in the control of regional haemodynamics in rats with aortocaval fistula and acts as a mechanism of maintaining normal arterial blood pressure in these animals. In rats with fistula, angiotensin II type 1 receptors predominate in regulating regional haemodynamics.

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Central hypercapnic chemoreflex modulation of renal sympathetic nerve activity in experimental heart failure

et al. 2002

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Activation of the sympathetic nervous system plays an important role in the pathophysiology and progression of congestive heart failure (CHF). The precise mechanisms responsible for sympathetic activation in CHF are not yet clearly established. An altered central hypercapnic chemoreflex modulation of sympathetic nerve activity (SNA) might be an explanation. Therefore, the response of postganglionic renal SNA to elevation of CO2 concentration in the inspiratory air to 2, 4, and 6% was determined in anesthetized, artificially ventilated rats after denervation of peripheral baro- and chemoreceptors 2 weeks (group A; n=8) or 6 weeks (group B; n=11) after induction of an aorto-caval shunt, or 4 weeks after aortic banding (group C; n=7). In all CHF models, left ventricular enddiastolic pressure was increased (A 8 +/- 1, B 8 +/- 1, C 10 +/- 2 mmHg) as compared to sham operated controls (A 3 +/- 1, B 4 +/- 1, C 5 +/- 1 mmHg). Indicative of left ventricular hypertrophy and pulmonary congestion, wet weight of heart (A + 60%, B + 93%, C + 49%) and lungs (A + 15%, B + 36%, C + 12%) were also enhanced as compared to controls. Elevation of inspiratory CO2 concentration to 2,4, and 6% increased renal SNA by approximately 10, 20, and 30% from resting activity in all groups. The maximum SNA responses at 6% CO2 in the groups with CHF (A + 390 +/- 95, B + 425 +/- 133, C + 368 +/- 158 microVs) did not differ from those in the respective controls (A + 510 +/- 130, B + 570 +/- 180, C + 275 +/- 25 microVs). It is concluded that under these experimental conditions the central hypercapnic chemoreflex sensitivity is not altered in either of the employed models of CHF and therefore may not play a major role for the well-known elevation of SNA in CHF.

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Angiotensin inhibition and atrial natriuretic peptide release after acute volume expansion in rats with aortocaval shunt

Cited by 12 publications

References 52 publications

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Rat corin gene: molecular cloning and reduced expression in experimental heart failure

Angiotensin II control of regional haemodynamics in rats with aortocaval fistula

Central hypercapnic chemoreflex modulation of renal sympathetic nerve activity in experimental heart failure

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