Characterization of the contractile 5-hydroxytryptamine receptor in the autoperfused kidney of L-NAME hypertensive rats

Morán, Asunción; Urbina, Ana-Vega Ortiz de; Martín, Manuel Ángel Franco; Rodríguez-Barbero, Alicia; Román, Luís San

doi:10.1016/j.ejphar.2009.08.026

Cited by 13 publications

(22 citation statements)

References 51 publications

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“…5-HT showed a slight inhibition the electrically-induced PP increases, while α-methyl-5-HT did not modify them. These results are in agreement with those obtained previously by us [20][21][22]24], where 5-HT 2 receptor activation was involved in vasoconstrictor actions of renal vasculature. 5-HT 2 receptors are generally considered as "sympathoexcitatory" [14,27,28]; however, our research team has demonstrated that the vasoconstrictor effect by 5-HT 2 in renal territory is mediated by the renin- angiotensin system [20].…”

Section: Hemodynamic Effects Produced By the Different Treatmentssupporting

confidence: 95%

“…In this line, the COX pathway modulates autonomic transmission in the peripheral circulation [42]; nitrergic nerves inhibit sympathetic neurotransmission [43] and EDHF contributes to the endotheliumdependent relaxation, which is crucial for the regulation of organ blood flow, peripheral vascular resistance and blood pressure [44]. Consequently, we decided to investigate the effects of glibenclamide (a blocker of ATP-sensitive K + channels), indomethacin (a COX 1/2 inhibitor) and L-NAME (a NO synthase inhibitor) [23,24,26,[45][46][47][48].…”

Section: Possible Involvement Of Other (Indirect) Mechanisms Resultinmentioning

confidence: 99%

“…pretreatment significantly increased SBP and PP in all cases (see Table 1); i.a. injection of 5-HT or α-methyl-5-HT (0.0125 μg/kg each) increased PP (11.2 ± 1.7 and 16.5 ± 1.4, respectively) that immediately returned to baseline levels [20][21][22]24]. .…”

Section: Data Presentation and Statistical Evaluationmentioning

confidence: 94%

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5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

García-Pedraza

García

Martín

et al. 2015

Vascular Pharmacology

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Section: Hemodynamic Effects Produced By the Different Treatmentssupporting

confidence: 95%

Section: Possible Involvement Of Other (Indirect) Mechanisms Resultinmentioning

confidence: 99%

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5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

García-Pedraza

García

Martín

et al. 2015

Vascular Pharmacology

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“…The dose of 30 mg/kg/day of L-NAME was sufficient to induce arterial hypertension,29 and the dose of 20 mg/kg/day of rosuvastatin used in our study is known to have beneficial effects on endothelial dysfunction and systemic and regional hemodynamics 23. At 2 mg/kg/day, rosuvastatin has been shown to significantly increase eNOS mRNA and protein expression and decrease iNOS mRNA and protein expression and nitrite production after ischemia reperfusion 30…”

Section: Discussionmentioning

confidence: 65%

Rosuvastatin prevents proteinuria and renal inflammation in nitric oxide–deficient rats

Girardi

Farias

Ferreira

et al. 2011

Clinics

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OBJECTIVE:The aim of the present study was to assess the effects of rosuvastatin on renal injury and inflammation in a model of nitric oxide deficiency.METHODS:Male Wistar rats were randomly divided into four groups (n = 10/group) and treated for 28 days with saline (CTRL); 30 mg/kg/day L-NAME (L-name); L-NAME and 20 mg/kg/day rosuvastatin (L-name+ROS-20); or L-NAME and 2 mg/kg/day rosuvastatin (L-name+ROS-2). Systolic blood pressure was measured by plethysmography in the central artery of the tail. The serum total cholesterol, triglycerides, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, creatinine, nitric oxide, interleukin-6, and tumor necrosis factor alpha levels were analyzed. Urine samples were taken to measure the albumin∶urinary creatinine ratio. Kidneys were sectioned and stained with hematoxylin/eosin and Masson's trichrome. Immunohistochemical analysis of the renal tissue was performed to detect macrophage infiltration of the glomeruli.RESULTS:The systolic blood pressure was elevated in the L-name but not the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups. The L-name group had a significantly reduced nitric oxide level and an increased interleukin-6 and tumor necrosis factor alpha level, albumin∶urinary creatinine ratio and number of macrophages in the renal glomeruli. Rosuvastatin increased the nitric oxide level in the L-name+rosuvastatin-2 group and reduced the interleukin-6 and tumor necrosis factor alpha levels, glomerular macrophage number and albumin∶urinary creatinine ratio in the L-name+rosuvastatin-20 and L-name+rosuvastatin-2 groups.CONCLUSION:Rosuvastatin treatment reduced glomerular damage due to improvement in the inflammatory pattern independent of the systolic blood pressure and serum lipid level. These effects may lead to improvements in the treatment of kidney disease.

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“…Since serotonin was discovered, there has been substantial interest in serotonergic regulation of cardiovascular system, but effects of this biogenic amine on different vascular beds remain unclear. Serotonin is known to influence on renal function; nonetheless, serotonergic action on renal vasculature is controversial regarding both the effect (vasoconstriction/vasodilation) as well as the magnitude . Renal vascular bed is highlighted in the organism, because renovascular resistance not only regulates renal blood flow, but also controls vascular homeostasis.…”

Section: Introductionmentioning

confidence: 99%

Pharmacological evidence that 5‐HT_1D activation induces renal vasodilation by NO pathway in rats

García-Pedraza

García

Martín

et al. 2015

Clin Exp Pharma Physio

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5-HT is a powerful vasoconstrictor substance in renal vasculature (mainly by 5-HT₂ activation). Nevertheless, 5-HT is notable for its dual cardiovascular effects, producing both vasodilator and vasoconstrictor actions. This study aimed to investigate whether, behind the predominant serotonergic vasoconstrictor action, THE 5-HT system may exert renal vasodilator actions, and, if so, characterize the 5-HT receptors and possible indirect pathways. Renal perfusion pressure (PP), systemic blood pressure (SBP) and heart rate (HR) measurement in in situ autoperfused rat kidney was determined in phenylephrine infused rats. Intra arterial (i.a.) bolus administration of 5-HT (0.00000125-0.1 μg/kg) decreased renal PP in the presence of a phenylephrine continuous infusion (phenylephrine-infusion group), without modifying SBP or HR. These vasodilator responses were potentiated by 5-HT₂ antagonism (ritanserin, 1 mg/kg i.v.), whereas the responses were abolished by 5-HT₁ /₇ antagonist (methiothepin, 100 μg/kg i.v.) or 5-HT1D antagonist (LY310762, 1 mg/kg i.v.). The i.a. administration (0.00000125 to 0.1 μg/kg) of 5-CT or L-694,247 (5-HT1D agonist) mimicked 5-HT vasodilator effect, while other agonists (1-PBG, α-methyl-5-HT, AS-19 (5-HT₇), 8-OH-DPAT (5-HT1A) or CGS-12066B (5-HT1B)) did not alter baseline haemodynamic variables. L-694,247 vasodilation was abolished by i.v. bolus of antagonists LY310762 (5-HT1D, 1 mg/kg) or L-NAME (nitric oxide, 10 mg/kg), but not by i.v. bolus of indomethacin (cyclooxygenase, 2 mg/kg) or glibenclamide (ATP-dependent K(+) channel, 20 mg/kg). These outcomes suggest that 5-HT1D activation produces a vasodilator effect in the in situ autoperfused kidney of phenylephrine-infusion rats mediated by the NO pathway.

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Characterization of the contractile 5-hydroxytryptamine receptor in the autoperfused kidney of L-NAME hypertensive rats

Cited by 13 publications

References 51 publications

5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

Rosuvastatin prevents proteinuria and renal inflammation in nitric oxide–deficient rats

Pharmacological evidence that 5‐HT_1D activation induces renal vasodilation by NO pathway in rats

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Characterization of the contractile 5-hydroxytryptamine receptor in the autoperfused kidney of L-NAME hypertensive rats

Cited by 13 publications

References 51 publications

5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

5-HT1D receptor inhibits renal sympathetic neurotransmission by nitric oxide pathway in anesthetized rats

Rosuvastatin prevents proteinuria and renal inflammation in nitric oxide–deficient rats

Pharmacological evidence that 5‐HT1D activation induces renal vasodilation by NO pathway in rats

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Pharmacological evidence that 5‐HT_1D activation induces renal vasodilation by NO pathway in rats