Effect of epinephrine on norepinephrine release from rat kidney during sympathetic nerve stimulation

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.

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Increased Norepinephrine Release During Sympathetic Nerve Stimulation and its Inhibition by Adenosine in the Isolated Perfused Kidney of Spontaneously Hypertensive Rats

Clinical and Experimental Hypertension Part A Theory and Practice ◽

10.3109/10641968309048809 ◽

1983 ◽

Vol 5 (1) ◽

pp. 41-48 ◽

Cited By ~ 8

Author(s):

Robert D. Ekas ◽

Marie L. Steenberg ◽

Mustafa F. Lokhandwala

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Spontaneously Hypertensive Rats ◽

Norepinephrine Release ◽

Hypertensive Rats ◽

Sympathetic Nerve Stimulation ◽

Isolated Perfused Kidney ◽

Spontaneously Hypertensive ◽

Perfused Kidney

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Lack of modulation by dietary unsaturated fats on sympathetic neurotransmission in rat hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1993.265.3.h886 ◽

1993 ◽

Vol 265 (3) ◽

pp. H886-H892

Author(s):

X. J. Du ◽

A. M. Dart ◽

R. A. Riemersma

Keyword(s):

Fatty Acids ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Corn Oil ◽

Saturated Fatty Acids ◽

Beta Agonist ◽

Norepinephrine Release ◽

Sympathetic Nerve Stimulation ◽

Dietary Pufa ◽

Sympathetic Neurotransmission

We examined the effect of dietary polyunsaturated fatty acids (PUFA) on cardiac sympathetic neurotransmission. Rats were fed semisynthetic diets (18.5% fat wt/wt) high in saturated fatty acids (control diet), high in n-6 PUFA (corn oil), or enriched with n-3 PUFA (Maxepa). A perfused innervated heart model was used to examine different aspects of sympathetic neurotransmission 10 wk after the feeding. Dietary PUFA increased the content of n-6 or n-3 PUFA in myocardial phospholipids compared with animals fed control diets. Myocardial norepinephrine content, sympathetic nerve stimulation-induced norepinephrine release, neural reuptake, presynaptic alpha-adrenergic inhibition of norepinephrine release, and postsynaptic inotropic response (+/- dP/dt) to sympathetic nerve stimulation or to a beta-agonist were essentially not influenced by dietary PUFA. Neural norepinephrine release during prolonged ischemia (60 min) was also similar in hearts from rats fed n-6 PUFA and control diets. Thus a modification of sympathetic neurotransmission was not achieved by feeding PUFA-enriched diets for 10 wk.

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Atrial natriuretic factor inhibits norepinephrine release evoked by sympathetic nerve stimulation in isolated perfused rat mesenteric arteries

European Journal of Pharmacology ◽

10.1016/0014-2999(86)90724-7 ◽

1986 ◽

Vol 123 (3) ◽

pp. 459-461 ◽

Cited By ~ 74

Author(s):

Mitsuaki Nakamura ◽

Tadashi Inagami

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Atrial Natriuretic Factor ◽

Mesenteric Arteries ◽

Norepinephrine Release ◽

Sympathetic Nerve Stimulation ◽

Natriuretic Factor ◽

Atrial Natriuretic

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Modulation of adrenergic transmission by angiotensins in the perfused rat mesentery

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1979.236.2.h211 ◽

1979 ◽

Vol 236 (2) ◽

pp. H211-H217 ◽

Cited By ~ 6

Author(s):

W. B. Campbell ◽

E. K. Jackson

Keyword(s):

Angiotensin Ii ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Mesenteric Arteries ◽

Norepinephrine Release ◽

Sympathetic Nerve Stimulation ◽

Rat Mesentery ◽

Angiotensin Iii ◽

Adrenergic Transmission ◽

Norepinephrine Reuptake

Isolated rat mesenteric arteries perfused with a modified Krebs solution were utilized to study the effects of angiotensin II (AII), angiotensin III (AIII), and [des-Asp1-Arg2]AII on adrenergic transmission. Angiotensin II potentiated vasoconstrictor responses to both sympathetic nerve stimulation and to exogenous norepinephrine, whereas AIII and [des-Asp1-Arg2]AII potentiated vasoconstrictor responses to exogenous norepinephrine only. When the responses to exogenous norepinephrine were compared, the order of agonist potency was AIII greater than AII greater than [des-Asp1-Arg2]AII. The potentiation of sympathetic nerve stimulation by AII was inhibited by simultaneous administration of AIII (25%), [des-Asp1-Arg2]AII (51%), [Sar1-Ile8]AII (83%), and (Ile7)AIII (80%). The potentiation of exogenous norepinephrine by AII, AIII, and [des-Asp1-Arg2]AII was inhibited by [Sar1-Ile8]AII (110%, 113%, and 108%, respectively) and by [Ile7]AIII (50%, 64%, 91%, respectively). We conclude that AII possesses the capacity both to increase norpinephrine release during sympathetic nerve stimulation and to decrease norepinephrine reuptake, whereas AIII and [des-Asp1-Arg2]AII decrease norepinephrine release and reuptake. Also, under conditions of increased N-terminal degradation of AII, blockade of norepinephrine reuptake would be increased while the release of norepinephrine by nerve stimulation would be reduced.

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