Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction

1998 ◽  
Vol 274 (1) ◽  
pp. H290-H294 ◽  
Author(s):  
Songping Han ◽  
Chun-Lian Yang ◽  
Xiaoli Chen ◽  
Linda Naes ◽  
Bryan F. Cox ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Biological Action ◽  
Sympathetic Nerve Stimulation ◽  
Low Frequencies ◽  
Vascular Bed ◽  
Potentiation Effect ◽  
Mesenteric Vascular Bed

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that ∼30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

Analysis of adrenergic responses in the mesenteric vascular bed of the cat; evidence that vascular beta2-adrenoceptors are innervated

1984 ◽  
Vol 62 (12) ◽  
pp. 1470-1478 ◽  
Author(s):  
William M. Armstead ◽  
Howard L. Lippton ◽  
Albert L. Hyman ◽  
Philip J. Kadowitz
Keyword(s):  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Beta Adrenergic ◽  
Vascular Bed ◽  
Alpha Receptors ◽  
Mesenteric Vascular Bed ◽  
Dose Dependent ◽  
Mesenteric Vascular Resistance

Responses to sympathetic nerve stimulation and pressor hormones were investigated in the feline mesenteric vascular bed under conditions of controlled blood flow. Sympathetic nerve stimulation and norepinephrine produced frequency- and dose-dependent increases in mesenteric vascular resistance. However, when alpha-receptors were blocked with the non-equilibrium alpha-receptor antagonist, phenoxybenzamine, nerve stimulation and norepinephrine produced frequency- and dose-dependent decreases in mesenteric vascular resistance. These reductions in mesenteric vascular resistance were unchanged after indomethacin or atropine, whereas propranolol converted the mesenteric vasodilator responses to small vasoconstrictor responses. In these studies, responses to a variety of vasoconstrictor agents were enhanced after administration of propranolol. Sotalol, a nonselective beta blocker with little membrane stabilizing activity, also enhanced vasoconstrictor responses. The present data suggest that both alpha- and beta-adrenergic receptors are innervated in the feline mesenteric vascular bed, and that vasodilator responses to norepinephrine and sympathetic nerve stimulation are independent of activation of muscarinic receptors or formation of products in the cyclooxygenase pathway. These data also demonstrate that there is a nonspecific potentiation of intestinal vasoconstrictor responses after beta-adrenergic receptor blockade that is independent of a membrane-stabilizing or receptor-mediated mechanism.

Influence of sympathetic discharge pattern on norepinephrine and neuropeptide Y release

1989 ◽  
Vol 257 (3) ◽  
pp. H866-H872 ◽  
Author(s):  
J. Pernow ◽  
J. Schwieler ◽  
T. Kahan ◽  
P. Hjemdahl ◽  
J. Oberle ◽  
...  
Keyword(s):  
Neuropeptide Y ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Impulse Activity ◽  
Sympathetic Nerve Stimulation ◽  
Vasoconstrictor Response ◽  
Neuropeptide Y Release ◽  
Sympathetic Discharge ◽  
Stimulation Pattern

The effects of sympathetic nerve stimulation on vasoconstrictor responses and overflow of norepinephrine (NE) and neuropeptide Y-like immunoreactivity (NPY-LI) were studied in the dog gracilis muscle and pig spleen in vivo. A continuous regular impulse activity was compared with irregular human sympathetic and regular bursting patterns. During control conditions, stimulation with the irregular activity induced larger peak vasoconstriction than the regular activity at 0.59 Hz, but not at higher frequencies in the muscle, at 0.59 and 2.0 Hz in the spleen. The nerve stimulation-evoked overflow of NE and NPY-LI from the muscle were not influenced by the pattern of stimulation. The overflow of NPY-LI, but not that of NE, from the spleen was enhanced by the irregular activity at 0.59 and 2.0 Hz, and both NPY-LI and NE overflows were enhanced by regular burst activity at 2.0 Hz. After blockade of alpha- and beta-adrenoceptors by phenoxybenzamine and propranolol, respectively, which enhanced nerve stimulation-evoked overflow of both NE and NPY-LI, the NE overflow from the muscle evoked by the irregular activity was slightly larger at 0.59 Hz but smaller at higher frequencies compared with that evoked by regular activity, whereas the detectable overflow of NPY-LI was not largely influenced by the stimulation pattern. In conclusion, both the vasoconstrictor response and the overflow of NPY-LI and NE seem to be influenced by the pattern and frequency of sympathetic nerve stimulation.

Adrenergic and nonadrenergic cotransmitters inhibit insulin secretion during sympathetic stimulation in dogs

1992 ◽  
Vol 263 (1) ◽  
pp. E72-E78
Author(s):  
J. Lorrain ◽  
I. Angel ◽  
N. Duval ◽  
M. T. Eon ◽  
A. Oblin ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Blocking Agent ◽  
Norepinephrine Release ◽  
Sympathetic Nerve Stimulation ◽  
K Channels ◽  
Adrenoceptor Antagonist

Vascular and biochemical responses to pancreatic sympathetic nerve stimulation were investigated in the blood-perfused pancreas of anesthetized dogs. During sympathetic nerve stimulation, pancreatic perfusion pressure and norepinephrine release increased, whereas insulin secretion decreased. The latter effect did not occur after pretreatment with the alpha 2-adrenoceptor antagonist idazoxan. However, after beta-adrenoceptor blockade with propranolol, neither single administration of idazoxan nor the alpha 1-adrenoceptor antagonist prazosin or glibenclamide, a blocker of ATP-modulated K+ channels, affected the decrease in insulin secretion induced by sympathetic nerve stimulation. In contrast, the combination of glibenclamide with idazoxan markedly antagonised the decrease in insulin release evoked by the latter procedure. After depletion of catecholamines with syrosingopine, the stimulation-induced inhibition of insulin secretion remained unchanged even though no increases in pancreas perfusion pressure or norepinephrine release were observed. In this preparation, glibenclamide inhibited the decrease in insulin release by 50%. In animals pretreated with the neuronal blocking agent bretylium, all of the responses to sympathetic nerve stimulation were abolished. These results indicate that the inhibitory effects exerted by the sympathetic nervous system on insulin secretion are mediated not only by the classical neurotransmitter norepinephrine acting on alpha 2-adrenoceptors but also by a nonadrenergic cotransmitter that can maintain transmission under conditions of catecholamine deficiency. The postulated nonadrenergic cotransmitter(s) acts, at least partly, via the opening of ATP-modulated K+ channels blockable by glibenclamide, and its release can be prevented by the neuronal blocking agent bretylium.

Analysis of responses to sympathetic nerve stimulation in the feline pulmonary vascular bed

1989 ◽  
Vol 67 (1) ◽  
pp. 371-376 ◽  
Author(s):  
A. L. Hyman ◽  
P. J. Kadowitz
Keyword(s):  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Receptor Subtypes ◽  
Sympathetic Nerve Stimulation ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Vascular Bed ◽  
Beta 2 ◽  
Pulmonary Vascular Bed

The adrenergic receptor subtypes mediating the response to sympathetic nerve stimulation in the pulmonary vascular bed of the cat were investigated under conditions of controlled blood flow and constant left atrial pressure. The increase in lobar vascular resistance in response to sympathetic nerve stimulation was reduced by prazosin and to a lesser extent by yohimbine, the respective alpha 1- and alpha 2-adrenoceptor antagonists. Moreover, in animals pretreated with a beta-adrenoceptor antagonist to prevent an interaction between alpha- and beta 2-adrenoceptors, responses to nerve stimulation were reduced by prazosin, but yohimbine had no significant effect. On the other hand, in animals pretreated with a beta-adrenoceptor antagonist, yohimbine had an inhibitory effect on responses to tyramine and to norepinephrine. Propranolol had no significant effect on the response to nerve stimulation, whereas ICI 118551, a selective beta 2-adrenoceptor antagonist, enhanced responses to nerve stimulation and injected norepinephrine. The present data suggest that neuronally released norepinephrine increases pulmonary vascular resistance in the cat by acting mainly on alpha 1-adrenoceptors and to a lesser extent on postjunctional alpha 2-adrenoceptors but that this effect is counteracted by an action on presynaptic alpha 2-receptors. The present studies also suggest that neuronally released norepinephrine acts on beta 2-adrenoceptors and that the response to sympathetic nerve stimulation represents the net effect of the adrenergic transmitter on alpha 1-, alpha 2-, and beta 2-adrenoceptors in the pulmonary vascular bed.

Effects of cadmium and lead on adrenergic neuromuscular transmission in the rabbit

1977 ◽  
Vol 232 (3) ◽  
pp. C128-C131 ◽  
Author(s):  
G. P. Cooper ◽  
D. Steinberg
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Perfusion Pressure ◽  
Pressor Response ◽  
Ringer Solution ◽  
Bathing Solution ◽  
Sympathetic Nerve Stimulation ◽  
Fourfold Increase ◽  
Lead And Cadmium

The effects of inorganic lead (PbCl2) and cadmium (DdCl2) on the pressor response of rabbit saphenous arteries produced by sympathetic nerve stimulation were examined. A 1- to 3-cm length of artery was removed, placed in a bath containing mammalian Ringer solution, and perfused with the same solution at a constant rate sufficient to maintain a 40-60 mmHg perfusion pressure. Increases in perfusion pressure resulting from electrical stimulation -f periarterial nerve endings were reduced or completely blocked by the addition of 5-20 muM lead or cadmium to the bathing solution for a period of 15-30 min. Responses to norepinephrine or to direct electrical stimulation of the muscle remained relatively unaffected. During lead or cadmium blockade, the response to nerve stimulation could be restored by a fourfold increase in calcium concentration. It is concluded that lead and cadmium reduce the response to sympathetic nerve stimulation primarily through an effect on presynaptic nerve terminals.

Atrial natriuretic factor attenuates sympathetic neuroeffector responses in hindlimb vasculature of rabbits

1989 ◽  
Vol 67 (9) ◽  
pp. 1101-1105 ◽  
Author(s):  
K. P. Patel
Keyword(s):  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Sympathetic Nerve Stimulation ◽  
Arterial Infusion ◽  
Natriuretic Factor ◽  
Before And After ◽  
Atrial Natriuretic

To determine whether atrial natriuretic factor (ANF) affects vasoconstrictor responses to electrical stimulation of sympathetic nerves or intra-arterial norepinephrine (NE), changes in perfusion pressure were measured during lumbar sympathetic nerve stimulation (LSNS, 1–8 Hz), or administration of NE (50–200 ng), in an isolated constant flow-perfused hindlimb of chloralose-anesthetized rabbit before and after intra-arterial infusion of ANF (0.5 ng∙mL−1∙min−1). ANF significantly attenuated responses to LSNS (relative potency, RP = 0.65) and to NE (RP = 0.47). We conclude that ANF attenuates vasoconstrictor responses to both LSNS and NE. Thus ANF alters sympathetic nervous system mediated changes in vascular resistance possibly at the neuroeffector site.Key words: atrial natriuretic factor, sympathetic nerve stimulation, vasculature.

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