The endothelium modulates adrenergic neurotransmission to canine pulmonary arteries and veins

Greenberg, S; Diecke, F. P. J.; Peevy, Keith J.; Tanaka, T.P.

doi:10.1016/0014-2999(89)90605-5

Cited by 70 publications

(39 citation statements)

References 18 publications

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“…Various types of HVA Ca 2ϩ channels are known to be involved in neurotransmitter release, with the contribution of N channels usually ranging from 20 to 30% (for review, see Dunlap et al, 1995;Catterall, 1998;Grassi et al, 1999b). In postganglionic sympathetic fibers, N channels are primarily responsible for catecholamine release, and NO has been reported to inhibit both noradrenaline release from sympathetic nerve terminals and the vasoconstrictor response to adrenergic nerve stimulation (Tesfamariam et al, 1987;Greenberg et al, 1989). Moreover, the SNP/cGMP/PKG pathway has been considered responsible for inhibition of glutamate release in rat hippocampal nerve terminals (Sequeira et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

et al. 2002

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Although data from our laboratory and others suggest that nitric oxide (NO) exerts an overall inhibitory action on high-voltageactivated Ca 2ϩ channels, conflicting observations have been reported regarding its effects on N-type channels. We performed whole-cell and cell-attached patch-clamp recordings in IMR32 cells to clarify the functional role of NO in the modulation of N channels of human neuronal cells. During depolarizing steps to ϩ10 mV from V h ϭ Ϫ90 mV, the NO donor, sodium nitroprusside (SNP; 200 M), reduced macroscopic N currents by 34% ( p Ͻ 0.01). The magnitude of inhibition was similar at all voltages tested (range, Ϫ40 to ϩ50 mV). No significant inhibition was observed when SNP was applied together with the NO scavenger, 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide potassium salt (300 M), or after cell treatment with the guanylate cyclase inhibitor, 1H- channel open probability by 59% and increased both the mean shut time and the null sweep probability, but it had no significant effects on channel conductance, mean open time, or latency of first openings. These data suggest that NO inhibits N-channel gating through cGMP and PKG. The consequent decrease in Ca 2ϩ influx through these channels may affect different neuronal functions, including neurotransmitter release.

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Section: Discussionmentioning

confidence: 99%

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

et al. 2002

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“…Endothelium-derived relaxing factor, possibly NO, released from the dog mesenteric artery (Toda et al, 1991b) and vasodilators liberated from the endothelium of rabbit carotid arteries (Cohen and Weisbrod, 1988) also failed to influence the overflow of norepinephrine evoked by nerve stimulation. In contrast, endothelium denudation augmented the contractile response and the release of 14 C-norepinephrine in dog pulmonary arteries and veins (Greenberg et al, 1989). Since the efflux of 14 C-norepinephrine by transmural electrical stimulation in canine mesenteric arteries is blunted by NO donors, such as SIN-1, nitroglycerin, and sodium nitroprusside, and also by inhibitors of cyclic GMP phosphodiesterase, cyclic GMP is suggested to be an inhibitory modulator of norepinephrine release from adrenergic nerves (Greenberg et al, 1990).…”

Section: Interaction Of Nitrergic Cholinergic and Adrenergic Nementioning

confidence: 97%

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

2003

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“…Endogenous NO has been shown to have an inhibitory effect on the stimulated release of catecholamines from the sympathetic nerves and the adrenal medulla. For instance, blocking NO synthase facilitates the release of catecholamines into the plasma (39,51,52), facilitates the release of norepinephrine from adrenergic nerves in canine and guinea pig pulmonary blood vessels (4,21), and increases adrenal catecholamine release in pithed rats (37). It has been proposed that the inhibitory effect of NO on the action of norepinephrine is due to a postjunctional physiological antagonism (3,4).…”

mentioning

confidence: 99%

“…It has been proposed that the inhibitory effect of NO on the action of norepinephrine is due to a postjunctional physiological antagonism (3,4). An alternative explanation involves a prejunctional activation of the cGMP second messenger pathway by NO within the nerve terminal, leading to either an inhibition (21) or potentiation (56,58) of norepinephrine release. Furthermore, NO may be involved in altering the release of ATP and NPY, which are cotransmitters with norepinephrine at the sympathetic vascular neuroeffector junction.…”

mentioning

confidence: 99%

Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial bed

Kolo

Westfall

Macarthur

2004

American Journal of Physiology-Heart and Circulatory Physiology

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Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial beds. Am J Physiol Heart Circ Physiol 286: H296-H303, 2004; 10.1152/ ajpheart.00668.2003 reacts with catecholamines resulting in their deactivation. In this study, we demonstrated that coincubation of NO donors with sympathetic neurotransmitters decreased the amount of norepinephrine detected but not ATP or neuropeptide Y (NPY). Furthermore, we found that the ability of norepinephrine to increase perfusion pressure in the isolated perfused mesenteric arterial bed of the rat was attenuated by the incubation of norepinephrine with the NO donor diethylamine NONOate. Conversely, the vasoconstrictive ability of NPY and ATP was unaffected by incubation with NONOate. Periarterial nerve stimulation in the presence of the NO synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) resulted in an increase in both perfusion pressure response and norepinephrine levels. This was prevented by L-arginine, demonstrating that the effects of L-NAME were indeed specific to the inhibition of NOS. To confirm that NO was not altering the release of norepinephrine from the sympathetic nerve via presynaptic activation of guanylate cyclase, we repeated the experiments in the presence of the guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]-quinoxaloine-one (ODQ). Unlike L-NAME, ODQ infusion did not increase norepinephrine overflow, demonstrating that modulation of norepinephrine by NO at the vascular neuroeffector junction of the rat mesenteric vascular bed is not the result of presynaptic guanylate cyclase activation. These results demonstrate that, in addition to being a direct vasodilatator, NO can also alter vascular reactivity at the sympathetic neuroeffector junction in the rat mesenteric bed by deactivating the vasoconstrictor norepinephrine. sympathetic neurotransmitters; nitric oxide synthase; adenosine 5Ј-triphosphate, neuropeptide Y; vascular tone IT HAS BEEN ESTABLISHED that the neurotransmitters norepinephrine, neuropeptide Y (NPY), and ATP are colocalized in and coreleased from many sympathetic neurons (10,16,47,50). It has also been demonstrated that the application of each transmitter mimics a phase of sympathetic nerve stimulation and that each phase can be blocked with appropriate antagonists (10,16,47,50). Moreover, norepinephrine, NPY, and ATP all have presynaptic inhibitory actions on sympathetic neurotransmission and can negatively regulate their own release as well as the release of each other (49,53).Nonneuronal mediators such as the well-characterized endothelium-derived vasodilator nitric oxide (NO) can also modulate sympathetic neurotransmission. Studies have shown that on sympathetic nerve stimulation, inhibition of NO synthesis results in an increase in vasoconstriction in the rat tail artery (51), in the large coronary artery of anesthetized dogs (55), and in the vessels of the isolated adrenal medulla of the dog (1).The enhancement of vasoconstriction may be du...

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The endothelium modulates adrenergic neurotransmission to canine pulmonary arteries and veins

Cited by 70 publications

References 18 publications

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial bed

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The endothelium modulates adrenergic neurotransmission to canine pulmonary arteries and veins

Cited by 70 publications

References 18 publications

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca2+Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca2+Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

The Pharmacology of Nitric Oxide in the Peripheral Nervous System of Blood Vessels

Nitric oxide decreases the biological activity of norepinephrine resulting in altered vascular tone in the rat mesenteric arterial bed

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cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca²⁺Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells