Sympathetic co-transmission: the coordinated action of ATP and noradrenaline and their modulation by neuropeptide Y in human vascular neuroeffector junctions

Huidobro‐Toro, J. Pablo; Donoso, M. Verónica

doi:10.1016/j.ejphar.2004.07.008

Cited by 56 publications

(36 citation statements)

References 42 publications

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“…One interpretation of these data is that under conditions of blockade of postjunctional ␣ 1 -adrenoceptors, NPY acting at postjunctional Y 1 receptors makes an enhanced contribution to neurally mediated vasoconstriction at higher frequencies of RNS. However, the fact that NPY and norepinephrine often act synergistically at postjunctional and/or extrajunctional sites argues against this explanation (15,28). Another possibility is that blockade of prejunctional Y 1 receptors by BIBO3304TF-enhanced neural norepinephrine release under the conditions of the current experiment.…”

Section: Discussionmentioning

confidence: 97%

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion

Eppel¹,

Luff²,

Denton³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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The aim of this study was to determine the contribution of neuropeptide Y (NPY) Y1 receptors in neurally mediated reductions in renal medullary perfusion. In pentobarbital sodium-anesthetized rabbits, electrical stimulation of the renal nerves (RNS, 0.5-16 Hz) decreased renal perfusion in a frequency-dependent manner. Under control conditions, 4 Hz reduced cortical and medullary perfusion by -85 +/- 3% and -43 +/- 7%, whereas 8 Hz reduced them by -93 +/- 2% and -73 +/- 4%, respectively. After Y1 receptor antagonism with BIBO3304TF (0.1 mg/kg plus 0.2 mg x kg x (-1) x h(-1)), RNS reduced perfusion less (by -65 +/- 9% and -12 +/- 8% at 4 Hz) x alpha1-Adrenoceptor antagonism with prazosin (0.2 mg/kg plus 0.2 mg kg(-1)h(-1)) also inhibited RNS-induced reductions in renal perfusion (-80 +/- 4% and -37 +/- 10% reductions in the cortex and medulla, respectively, at 8 Hz). When given after BIBO3304TF treatment, prazosin inhibited RNS-induced reductions in cortical and medullary perfusion more profoundly (-57 +/- 12% and -25 +/- 9% reductions, respectively, at 8 Hz) x Y1 receptor- and alpha1-adrenoceptor-blockade were confirmed by testing vascular responses to renal arterial NPY and phenylephrine boluses. NPY-positive immunolabeling was observed around interlobular arteries, afferent and efferent arterioles, and in the outer medulla. In conclusion, Y1 receptors and alpha1-adrenoceptors contribute to RNS-induced vasoconstriction in the vessels that control both cortical and medullary perfusion. Consistent with this, NPY immunostaining was associated with blood vessels that control perfusion in both regions. There also seems to be an interaction between Y1 receptors and alpha1-adrenoceptor-mediated neurotransmission in the control of renal perfusion.

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Section: Discussionmentioning

confidence: 97%

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion

Eppel¹,

Luff²,

Denton³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The common feature is that ATP can be stored in large dense core vesicles together with neurotransmitters. It was found co-stored with acetylcholine in guinea pig cortex, calf superior cervical ganglion, and motor nerve terminals of rat diaphragm [76]; with noradrenaline, it was found in human blood vessels, smooth muscles, and endothelial cells [80]; it was also found in adrenal chromaffin cells together with serotonin, with neuropeptide Y and glutamate in astrocytes, and with dopamine in neuron-differentiated PC12 [81][82][83][84]. Moreover, in other cell types in the nervous tissue, particularly astrocytes, ATP was found also in small synaptic-like vesicles [85].…”

Section: Atp Storagementioning

confidence: 99%

ATP synthesis and storage

Bonora

Patergnani

Rimessi

et al. 2012

Purinergic Signalling

378

269

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Since 1929, when it was discovered that ATP is a substrate for muscle contraction, the knowledge about this purine nucleotide has been greatly expanded. Many aspects of cell metabolism revolve around ATP production and consumption. It is important to understand the concepts of glucose and oxygen consumption in aerobic and anaerobic life and to link bioenergetics with the vast amount of reactions occurring within cells. ATP is universally seen as the energy exchange factor that connects anabolism and catabolism but also fuels processes such as motile contraction, phosphorylations, and active transport. It is also a signalling molecule in the purinergic signalling mechanisms. In this review, we will discuss all the main mechanisms of ATP production linked to ADP phosphorylation as well the regulation of these mechanisms during stress conditions and in connection with calcium signalling events. Recent advances regarding ATP storage and its special significance for purinergic signalling will also be reviewed.

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“…The sympathetic neurotransmitters ATP, NE, and NPY are released from nerve terminals to result in direct postjunctional vasoconstriction, as well as prejunctional feedback inhibition of their own and each others' release (23,33). We found that NS increases perfusion pressure to a greater extent in mesenteric arterial preparations of SHR than those of WKY controls (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effects of angiotensin-(1–7) on the nerve stimulation-induced release of norepinephrine and neuropeptide Y from the mesenteric arterial bed

Byku

Macarthur

Westfall

2010

American Journal of Physiology-Heart and Circulatory Physiology

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Neuropeptide Y (NPY) is a cotransmitter with norepinephrine (NE) and ATP in sympathetic nerves. There is evidence for increased activity of the sympathetic nervous system and the renin-angiotensin system (RAS), as well as a role for NPY in the development of hypertension in experimental animal models and in humans. Angiotensin II (ANG II) is known to facilitate sympathetic neurotransmission, an effect greater in spontaneously hypertensive rats (SHR) than normotensive Wistar-Kyoto (WKY) rats. A newly discovered product of the RAS is angiotensin-(1-7) [ANG-(1-7)]. There is evidence suggesting that ANG-(1-7) opposes the actions of ANG II, resulting in hypotensive effects. The objective of this study was to investigate the role of ANG-(1-7) on the nerve-stimulated overflow of NE and NPY from the mesenteric arterial bed of SHR and the mechanisms involved in mediating any effects produced. ANG-(1-7) (0.001, 0.01, 0.1 microM) decreased nerve-stimulated NE and NPY overflow, as well as perfusion pressure in preparations obtained from SHR. This effect was greater in preparations of SHR than WKY controls. In addition, ANG-(1-7) decreased NE overflow to a greater extent than NPY overflow. Administration of the Mas receptor antagonist, D-Ala(7) ANG-(1-7), attenuated the decrease in both NE and NPY overflow due to ANG-(1-7) administration. However, the angiotensin type 2 receptor antagonist, PD-123391, attenuated the effect of ANG-(1-7) on NE overflow without affecting the decrease in NPY overflow. Moreover, in the presence of N(G)-nitro-L-arginine methyl ester, ANG-(1-7) decreased NPY overflow, but not NE overflow. ANG-(1-7) decreases the nerve-stimulated overflow of NE and NPY in preparations of SHR, whereas ANG II enhances it. Therefore, ANG-(1-7) may counteract the effects of ANG II by acting on ANG type 2 and Mas receptors.

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Sympathetic co-transmission: the coordinated action of ATP and noradrenaline and their modulation by neuropeptide Y in human vascular neuroeffector junctions

Cited by 56 publications

References 42 publications

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion

ATP synthesis and storage

Inhibitory effects of angiotensin-(1–7) on the nerve stimulation-induced release of norepinephrine and neuropeptide Y from the mesenteric arterial bed

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Sympathetic co-transmission: the coordinated action of ATP and noradrenaline and their modulation by neuropeptide Y in human vascular neuroeffector junctions

Cited by 56 publications

References 42 publications

Type 1 neuropeptide Y receptors and α1-adrenoceptors in the neural control of regional renal perfusion

Type 1 neuropeptide Y receptors and α1-adrenoceptors in the neural control of regional renal perfusion

ATP synthesis and storage

Inhibitory effects of angiotensin-(1–7) on the nerve stimulation-induced release of norepinephrine and neuropeptide Y from the mesenteric arterial bed

Contact Info

Product

Resources

About

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion

Type 1 neuropeptide Y receptors and α₁-adrenoceptors in the neural control of regional renal perfusion