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

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.

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

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1992.263.1.e72 ◽

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.

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1998.274.1.h290 ◽

1998 ◽

Vol 274 (1) ◽

pp. H290-H294 ◽

Cited By ~ 21

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.

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Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1978.235.6.h803 ◽

1978 ◽

Vol 235 (6) ◽

pp. H803-H808

Author(s):

E. Y. Tong ◽

A. A. Mathe ◽

P. W. Tisher

Keyword(s):

Electrical Stimulation ◽

Pulmonary Artery ◽

Monoamine Oxidase ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Sympathetic Nerves ◽

Systemic Circulation ◽

Inhibitory Mechanism ◽

Sympathetic Nerve Stimulation ◽

Mao Inhibitor

Rabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.

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Adrenergic mechanisms in the bullfrog and turtle

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1965.209.6.1287 ◽

1965 ◽

Vol 209 (6) ◽

pp. 1287-1294 ◽

Cited By ~ 46

Author(s):

Takehiko Azuma ◽

Alberto Binia ◽

Maurice B. Visscher

Keyword(s):

Electrical Stimulation ◽

Nerve Stimulation ◽

Sympathetic Nerve ◽

Low Temperatures ◽

Environmental Temperature ◽

Contractile Activity ◽

Sympathetic Nerve Stimulation ◽

Sympathetic Transmitter ◽

Cardiac Sympathetic Denervation ◽

Large Output

Epinephrine and norepinephrine contents of tissues and perfusates have been measured by fluorimetric methods to ascertain which catecholamine is the sympathetic transmitter in bullfrogs and turtles. Except for adrenal and sympathetic chain, the predominant catecholamine in bullfrogs is epinephrine. In snapping turtles, norepinephrine predominates. During perfusion of bullfrog heart or liver without stimulation, only traces of catecholamine appear in perfusates, whereas during sympathetic nerve stimulation a large output of epinephrine occurs. In the bullfrog epinephrine rather than norepinephrine seems to be the sympathetic mediator. The situation may be the reverse in the turtle. Environmental temperature did not alter bullfrog tissue catecholamine. Cardiac sympathetic denervation did not decrease myocardial catecholamine within 6 weeks at low temperatures, but in animals maintained at 20 C survival was not achieved. Epinephrine levels in bullfrog ventricle were not lowered by 5 hr of contractions induced by electrical stimulation at 30/min compared with controls in arrest. The fact that myocardial catecholamine stores are not depleted by contractile activity may result either from absence of utilization or from equivalence between breakdown and synthesis.

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

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y89-174 ◽

1989 ◽

Vol 67 (9) ◽

pp. 1101-1105 ◽

Cited By ~ 1

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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Adrenergic responses in canine cutaneous vasculature during acute hemorrhagic hypotension

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1975.228.3.752 ◽

1975 ◽

Vol 228 (3) ◽

pp. 752-755 ◽

Cited By ~ 3

Author(s):

JC Liao ◽

BG Zimmerman ◽

FH Van Bergen

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Perfusion Pressure ◽

Plasma Renin ◽

High Dose ◽

Sodium Pentobarbital ◽

Sympathetic Stimulation ◽

Sympathetic Nerve Stimulation ◽

Acute Hemorrhage ◽

Renin Level

The purpose of this study was to determine the effect of acute hemorrhage on vascular responses to sympathetic nerve stimulation and norepinephrine. The experiments were carried out with sodium pentobarbital anesthesia. The preparation employed was the dog's hindpaw perfused at constant blood flow. Changes in vascular resistance in the paw were indicated by changes in perfusion pressure. Changes in perfusion pressure elicited by sympathetic nerve stimulation and intra-arterially administered norepinephrine were determined before and after hemorrhage of 15 ml/kg in normal and acutely nephrectomized animals. The response to sympathetic stimulation was increased by about 50% in normal but not in nephrectomized dogs, whereas the response to a low dose of norepinephrine (0.5-1 mug) was not significantly changed in either group of animals. In additional experiments in which the plasma renin level was measured, the potentiation of responses to sympathetic stimulation and a high dose of norepinephrine (2 mug) occurred at the time that the renin level was increased by hemorrhage. These results indicate that the level of circulating angiotensin attained after hemorrhage may facilitate vasoconstrictor responses to adrenergic stimuli.

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Postsynaptic adrenoceptor-mediated vasoconstriction in coronary and femoral vascular beds

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.254.5.h984 ◽

1988 ◽

Vol 254 (5) ◽

pp. H984-H992 ◽

Cited By ~ 1

Author(s):

D. G. Chen ◽

X. Z. Dai ◽

R. J. Bache

Keyword(s):

Nerve Stimulation ◽

Sympathetic Nerve ◽

Perfusion Pressure ◽

Adrenergic Blockade ◽

Sympathetic Nerve Stimulation ◽

Flow Rates ◽

Vasoconstrictor Response ◽

Vascular Beds ◽

Subsequent Addition ◽

Inferior Cardiac Nerve

This study examined the response to intra-arterial norepinephrine and sympathetic nerve stimulation on perfusion pressure of cannulated dog femoral and left circumflex coronary arteries perfused at constant flow rates. Sympathetic nerve stimulation was delivered through the decentralized inferior cardiac nerve and the lumbar sympathetic chain; beta-adrenergic blockade was maintained with propranolol. In the coronary artery, the vasoconstrictor response to norepinephrine was blunted by alpha 1-adrenergic blockade with prazosin but was abolished by alpha 2-adrenergic blockade with rauwolscine, indicating postsynaptic alpha 2-adrenoceptor-mediated vasoconstriction. In the femoral artery, prazosin decreased norepinephrine-induced vasoconstriction by 20-40%; the subsequent addition of rauwolscine completely abolished vasoconstriction, indicating that both alpha 1- and alpha 2-adrenoceptors contributed to vasoconstriction. Sympathetic nerve stimulation produced frequency-dependent increases of perfusion pressure in both coronary and femoral vascular beds. Prazosin caused approximately 50% reduction in the vasoconstrictor response of the coronary vascular bed and approximately 30% reduction in the femoral bed. The addition of rauwolscine completely blocked the response to sympathetic nerve stimulation in coronary and femoral vascular beds. These studies demonstrate that postsynaptic alpha 2-adrenoceptor-mediated mechanisms participate in vasoconstriction in response to both exogenous norepinephrine and sympathetic nerve stimulation in the canine coronary and femoral vascular beds.

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