Pharmacological characterization of cellular mechanisms of the renal vasodilatory effect of nicotine in rats

El‐Mas, Mahmoud M.; El‐Gowilly, Sahar M.; Gohar, Eman Y.; Ghazal, A.

doi:10.1016/j.ejphar.2008.04.048

Cited by 25 publications

(27 citation statements)

References 39 publications

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“…For example, in canine lingual arteries, nicotine-induced vasoconstriction is converted to vasodilation in the presence of adrenergic and purinergic blockade (46), and in monkey mesenteric arteries, nicotine-induced vasoconstriction was reversed to an NO-mediated vasodilation by phentolamine and guanethidine (64). Thus, in mammalian vascular beds, nicotine-induced vasoconstriction is dominant, and vasodilation is observed after blockade of vasoconstriction (18). However, in toad mesenteric arteries, the dominant effect of nicotine is NO/CGRP-mediated vasodilation, and vasoconstriction is only revealed after inhibition of the vasodilator signaling pathways.…”

Section: Discussionmentioning

confidence: 97%

“…In various mammalian blood vessels, there is evidence that endothelium-independent, NOmediated vasodilation induced by nicotine is dependent on perivascular adrenergic nerves, because the vasodilation is abolished by guanethidine and chemical sympathectomy (18,32,59,70). It is proposed that nicotine binds to receptors on adrenergic terminals, causing the release of norepinephrine (NE), which then binds to adrenergic receptors on adjacent nitrergic nerves to initiate the release of NO.…”

Section: Discussionmentioning

confidence: 99%

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Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus

Jennings

Donald

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Jennings BL, Donald JA. Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus. Am J Physiol Regul Integr Comp Physiol 298: R767-R775, 2010. First published January 13, 2010 doi:10.1152/ajpregu.00148.2009.-This study determined the role of nitric oxide (NO) in neurogenic vasodilation in mesenteric resistance arteries of the toad Bufo marinus. NO synthase (NOS) was anatomically demonstrated in perivascular nerves, but not in the endothelium. ACh and nicotine caused TTX-sensitive neurogenic vasodilation of mesenteric arteries. The ACh-induced vasodilation was endothelium-independent and was mediated by the NO/ soluble guanylyl cyclase signaling pathway, inasmuch as the vasodilation was blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and the NOS inhibitors N -nitro-L-arginine methyl ester and N -nitro-L-arginine. Furthermore, the ACh-induced vasodilation was significantly decreased by the more selective neural NOS inhibitor N 5 -(1-imino-3-butenyl)-L-ornithine. The nicotine-induced vasodilation was endothelium-independent and mediated by NO and calcitonin gene-related peptide (CGRP), inasmuch as pretreatment of mesenteric arteries with a combination of N -nitro-L-arginine and the CGRP receptor antagonist CGRP-(8 -37) blocked the vasodilation. Clotrimazole significantly decreased the ACh-induced response, providing evidence that a component of the NO vasodilation involved Ca 2ϩ -activated K ϩ or voltage-gated K ϩ channels. These data show that NO control of mesenteric resistance arteries of toad is provided by nitrergic nerves, rather than the endothelium, and implicate NO as a potentially important regulator of gut blood flow and peripheral blood pressure.amphibian; autonomic nervous system; nitric oxide synthase; endothelium IN THE MAMMALIAN MESENTERIC vasculature, it is well established that the endothelium releases numerous vasoactive molecules, such as nitric oxide (NO), prostaglandins, endothelium-derived hyperpolarizing factor (EDHF), and endothelium-derived contracting factors, which contribute to the regulation of vascular tone (26). In addition, mesenteric arteries are innervated by sympathetic vasoconstrictor and primary sensory vasodilator nerves (71). NO is clearly important in maintaining the vasodilator tone of mesenteric arteries, inasmuch as inhibition of NO synthase (NOS) causes vasoconstriction and increases blood pressure (20). Endothelial NOS (eNOS) is the predominant isoform responsible for NO generation in mesenteric arteries, but there is also evidence that neural NOS (nNOS) in perivascular nitrergic nerves generates NO to provide neurally derived vasodilation (2,31,63,66). In contrast to mammals, much less is known about the role of NO in the regulation of mesenteric vascular tone in amphibians. In the small intestine, NADPH-diaphorase histochemical staining and nNOS immunoreactivity (nNOS-IR) have been demonstrated in perivascular nerves (34,35,41,49), but isoform-specific localizati...

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus

Jennings

Donald

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Rat small renal arteries express K ir 6.1 and sulfonyl urea receptor 2B in the vascular smooth muscle layer [42]. In vivo, pharmacological activation of K ATP channels causes a rise in renal blood flow [43] and K ATP channels are part of a 2 and b-adrenoceptor-dependent signaling mechanisms in VSMCs [40,44,45]. It remains to be investigated, if sympathetic innervation chronically supports hyperpolarizing currents in renal VSMCs thereby contributing to a mature VSMC phenotype and if the regulation of K ATP channel function by sympathetic nerves is part of these mechanisms.…”

Section: Sympathetic Nerves and Vascular Functionmentioning

confidence: 99%

Sympathetic denervation facilitates L-type Ca2+ channel activation in renal but not in mesenteric resistance arteries

Heumann

Koenen²,

Zavaritskaya³

et al. 2016

Journal of Hypertension

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“…The infusion of phenylephrine into the renal vasculature produced an abrupt increase in perfusion pressure, which was stabilized within 10 minutes for the remainder of the experiment. 10,23 Protocols and Experimental Groups Effect of Pioglitazone on Cyclosporine-Isoprenaline Renovascular Interaction…”

Section: The Rat Isolated Perfused Kidneymentioning

confidence: 99%

“…10,23 Briefly, rats were anesthetized with thiopental sodium (50 mg/kg, ip); the abdomen was opened by a midline incision, and the left kidney was exposed. The left renal artery was dissected free from its surrounding tissues.…”

Section: The Rat Isolated Perfused Kidneymentioning

confidence: 99%

PPARγ Dependence of Cyclosporine–Isoprenaline Renovascular Interaction: Roles of Nitric Oxide Synthase and Heme Oxygenase

El‐Gowelli

Abd-Elrahman

Saad

et al. 2011

Journal of Cardiovascular Pharmacology

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We previously showed that cyclosporine (CSA) impairs renal vasodilations caused by β-adrenoceptor activation. This study investigated whether the peroxisome proliferator-activated receptor gamma (PPARγ) and related nitric oxide synthase (NOS)/heme oxygenase (HO) signaling mediates the CSA-β-adrenoceptor interaction. The vasodilatory response elicited by a bolus injection of isoprenaline (1 μmole) in phenylephrine-preconstricted perfused kidneys of rats was reduced after prior infusion of zinc protoporphyrin IX (ZnPP, HO inhibitor) or GW9662 (PPARγ antagonist), suggesting the involvement of PPARγ and HO-derived CO in the isoprenaline response. In contrast, the inhibition of NOS activity by N-nitro-l-arginine methyl ester had no effect on isoprenaline responses. CSA (5 μM) significantly attenuated isoprenaline vasodilations, an effect that was abolished in the presence of GW9662 and accentuated by ZnPP. Also, supplementation with the PPARγ agonist pioglitazone or with l-arginine or hemin, substrates for NOS and HO, respectively, eliminated the unfavorable effect of CSA on isoprenaline vasodilations. The protection conferred by pioglitazone against CSA-evoked attenuation of isoprenaline vasodilations was maintained in N-nitro-l-arginine methyl ester-treated kidneys and disappeared after treatment with ZnPP or GW9662. In conclusion, the activation of the HO/CO/PPARγ cascade is probably the cellular mechanism that underlies the beneficial effect of pioglitazone on the CSA-isoprenaline interaction. Further, the facilitation of the HO/CO or NOS/NO pathway seems to offset this harmful effect of CSA.

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Pharmacological characterization of cellular mechanisms of the renal vasodilatory effect of nicotine in rats

Cited by 25 publications

References 39 publications

Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus

Mechanisms of nitric oxide-mediated, neurogenic vasodilation in mesenteric resistance arteries of toad Bufo marinus

Sympathetic denervation facilitates L-type Ca2+ channel activation in renal but not in mesenteric resistance arteries

PPARγ Dependence of Cyclosporine–Isoprenaline Renovascular Interaction: Roles of Nitric Oxide Synthase and Heme Oxygenase

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