Increased cardiac workload by adrenoceptor agonists for the estimation of potential antiischemic activity in a conscious rabbit model

Kovanecz, Istvan; Papp, Julius Gy.; Szekeres, L.

doi:10.1016/s1056-8719(97)00011-7

Cited by 3 publications

(1 citation statement)

References 14 publications

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“…This model can be induced experimentally by chronic administration of a combination of isoprenaline and caffeine (Flanagan et al 2008;Buckley and Johns 2011). Caffeine is reported to increase plasma levels of noradrenaline, whereas isoprenaline increases heart rate and work load by stimulating cardiac ␤-adrenoceptors (Graham and Spriet 1995;Kovanecz et al 1997). This results in the activation of the MEK-MAPK pathway in cardiac myocytes, with a resultant increase in intracellular Ca +2 levels (Bogoyevitch et al 1996;Akazawa and Komuro 2003).…”

Section: Introductionmentioning

confidence: 99%

Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

AhmadAshfaq

SattarMunavvar

Rathore

et al. 2014

Can. J. Physiol. Pharmacol.

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This study investigated the role of α1D-adrenoceptor in the modulation of renal haemodynamics in rats with left ventricular hypertrophy (LVH). LVH was established in Wistar-Kyoto (WKY) rats with isoprenaline (5.0 mg · (kg body mass)(-1), by subcutaneous injection every 72 h) and caffeine (62 mg · L(-1) in drinking water, daily for 14 days). Renal vasoconstrictor responses were measured for noradrenaline (NA), phenylephrine (PE), and methoxamine (ME) before and immediately after low or high dose intrarenal infusions of BMY 7378, a selective α1D-adrenoceptor blocker. The rats with LVH had higher mean arterial blood pressure and circulating NA levels, but lower renal cortical blood perfusion compared with the control group (all P < 0.05). In the LVH group, the magnitude of the renal vasoconstrictor response to ME was blunted, but not the response to NA or PE (P < 0.05), compared with the control group (LVH vs. C, 38% vs. 50%). The magnitude of the drop in the vasoconstrictor responses to NA, PE, and ME in the presence of a higher dose of BMY 7378 was significantly greater in the LVH group compared with the control group (LVH vs. C, 45% vs. 25% for NA, 52% vs. 33% for PE, 66% vs. 53% for ME, all P < 0.05). These findings indicate an impaired renal vasoconstrictor response to adrenergic agonists during LVH. In addition, the α1D-adrenoceptor subtype plays a key role in the modulation of vascular responses in this diseased state.

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Section: Introductionmentioning

confidence: 99%

Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

AhmadAshfaq

SattarMunavvar

Rathore

et al. 2014

Can. J. Physiol. Pharmacol.

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Long-Term but not Short-Term Cardioprotection can be Induced by Preconditioning in Hypercholesterolemia

Szekeres¹,

Ferdinándy²,

Nagy³

et al.

Progress in Experimental Cardiology

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Pharmacological Prevention and Reversion of Erectile Dysfunction after Radical Prostatectomy, By Modulation of Nitric Oxide/Cgmp Pathways

González‐Cadavid¹

2008

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE ABSTRACTDuring Year 1 we aimed to determine the time course of histological and functional changes affecting the penile corpora cavernosa after bilateral cavernosal nerve resection (BCNR) in the rat, as an experimental model for erectile dysfunction subsequent to radical prostatectomy for prostate cancer. This condition seriously affects the quality of life of male patients and their partners. We have now determined that this neuropraxia causes the loss of smooth muscle cells by apoptosis and then an excessive collagen deposition in the penile corpora cavernosa. This in turn is responsible for the impaired corporal compliance leading to corporal veno-occlusive dysfunction (CVOD), seen in these patients, that is in part counteracted by the spontaneous induction of inducible nitric oxide synthase (iNOS) that stimulate nitric oxide and cGMP production. Long-term continuous oral administration of PDE5 inhibitors immediately after BCNR, thus raising cGMP levels, prevents CVOD and the underlying histopathology of the corpora cavernosa. This may soon be translated into the clinic, once the appropriate dosing is established, as a treatment to prevent or counteract erectile dysfunction after radical prostatectomy. SUBJECT TERMSRadical prostatectomy, quality of life, erectile dysfunction, PDE5 inhibitors Principal Investigator: Gonzalez-Cadavid, Nestor F. IntroductionDuring Year 1 we aimed to determine the time course of histological and functional changes affecting the penile corpora cavernosa after bilateral cavernosal nerve resection (BCNR) in the rat, as an experimental model for erectile dysfunction subsequent to radical prostatectomy for prostate cancer. This condition seriously affects the quality of life of a large fraction of male patients undergoing this operation and their partners. Therefore, studying the mechanism that triggers it and trying to develop a pharmacological therapy aiming to cure this type of erectile dysfunction, have considerable public health significance.Specifically in Aim 1, experiment 1 the objective was to determine whether the loss of smooth muscle cells (SMC) in the penile co...

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Increased cardiac workload by adrenoceptor agonists for the estimation of potential antiischemic activity in a conscious rabbit model

Cited by 3 publications

References 14 publications

Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

Long-Term but not Short-Term Cardioprotection can be Induced by Preconditioning in Hypercholesterolemia

Pharmacological Prevention and Reversion of Erectile Dysfunction after Radical Prostatectomy, By Modulation of Nitric Oxide/Cgmp Pathways

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Increased cardiac workload by adrenoceptor agonists for the estimation of potential antiischemic activity in a conscious rabbit model

Cited by 3 publications

References 14 publications

Functional contribution of α1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

Functional contribution of α1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

Long-Term but not Short-Term Cardioprotection can be Induced by Preconditioning in Hypercholesterolemia

Pharmacological Prevention and Reversion of Erectile Dysfunction after Radical Prostatectomy, By Modulation of Nitric Oxide/Cgmp Pathways

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Product

Resources

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Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats

Functional contribution of α_1D-adrenoceptors in the renal vasculature of left ventricular hypertrophy induced with isoprenaline and caffeine in Wistar–Kyoto rats