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PubMed1998

Specialised sympathetic neuroeffector associations in rat iris arterioles.

Vascular sympathetic neuroeffector associations have been examined in rat iris arterioles using serial section electron microscopy and reconstruction techniques. Examination of random sections showed that, of all profiles of varicosities (199) seen to lie closer than 4 microns to vascular smooth muscle cells, only a small proportion (29/199) were found in close association with vascular smooth muscle cells, where adjacent membranes were separated by less than 100 nm. However, serial section examination, from intervaricose region to intervaricose region, of 79 varicosities similarly observed lying within 4 microns of vascular smooth muscle cells showed that 54 formed close associations with vascular smooth muscle cells. In serial sections, all these varicosities were also closely associated with melanocytes and of the 25 remaining varicosities, 22 formed close associations with melanocytes alone, whilst 3 did not come into close association with any effector cell. The increased observation of close associations with vascular smooth muscle cells in serial sections, compared with random sections, is consistent with the demonstration that the area of contact only occupies, on average, a small percentage (5%) of the total surface area of the varicosity as seen in the 3-dimensional reconstructions. In both random and serial sections, close associations were observed between varicosities and vascular smooth muscle cells or melanocytes irrespective of whether fibres were present singly or in small nerve bundles. Three-dimensional reconstruction of associations of varicosities and vascular smooth muscle cells demonstrated several common features, such as accumulations of synaptic vesicles and loss of Schwann cell covering at the region of membrane facing the effector cell. The similarity in the appearance of the neuroeffector association seen in this study and those described in previous studies provides evidence for the existence of a common sympathetic neuroeffector association, irrespective of the receptor subtype involved in neurotransmission.

Animals↗
PubMed2006

Fundamentals of neurogastroenterology: basic science.

The focus of neurogastroenterology in Rome II was the enteric nervous system (ENS). To avoid duplication with Rome II, only advances in ENS neurobiology after Rome II are reviewed together with stronger emphasis on interactions of the brain, spinal cord, and the gut in terms of relevance for abdominal pain and disordered gastrointestinal function. A committee with expertise in selective aspects of neurogastroenterology was invited to evaluate the literature and provide a consensus overview of the Fundamentals of Neurogastroenterology textbook as they relate to functional gastrointestinal disorders (FGIDs). This review is an abbreviated version of a fuller account that appears in the forthcoming book, Rome III. This report reviews current basic science understanding of visceral sensation and its modulation by inflammation and stress and advances in the neurophysiology of the ENS. Many of the concepts are derived from animal studies in which the physiologic mechanisms underlying visceral sensitivity and neural control of motility, secretion, and blood flow are examined. Impact of inflammation and stress in experimental models relative to FGIDs is reviewed as is human brain imaging, which provides a means for translating basic science to understanding FGID symptoms. Investigative evidence and emerging concepts implicate dysfunction in the nervous system as a significant factor underlying patient symptoms in FGIDs. Continued focus on neurogastroenterologic factors that underlie the development of symptoms will lead to mechanistic understanding that is expected to directly benefit the large contingent of patients and care-givers who deal with FGIDs.

Adenosine Triphosphate↗
PubMed1990

Neuropeptide Y: a missing link?

Yet another 'orphan' molecule that had to find its place in life after isolation and sequencing, neuropeptide Y appears to be an important cardiovascular neuroregulator and also links the sympathetic and renin-angiotensin systems. The peptide's physiologic and pathophysiologic roles, as well as its potential therapeutic value, are examined.

Animals↗
PubMed1986

Dynamic responses of electrically coupled systems.

An identified pair of electrically coupled neurons in the buccal ganglion of the freshwater snail Helisoma trivolvis is an experimentally accessible model of electrical synaptic transmission. In this investigation, electrical synaptic transmission is characterized using sinusoidal frequency (Bode) responses computed by Laplace transforms and responses to brief stimuli. The frequency response of the injected neuron shows a 20-dB/decade attenuation and a phase shift from 0 degree at low frequencies to -90 degrees at high frequencies. The response of a coupled cell shows a 40-dB/decade attenuation and a phase shift from 0 degrees at low frequencies to -180 degrees at high frequencies. A simple mathematical model of electrical synaptic transmission is described that displays each of these crucial features of the measured frequency responses. Methods are described to estimate the frequency responses of coupled systems based on presynaptic measurements. The responses of the coupled system to brief pulses of current were computed using the principle of superposition. The electrical properties of coupled systems impose a minimum delay in reaching a peak in all postsynaptic responses. The delays in the postsynaptic responses to brief stimuli are related to the electrical and anatomical parameters of coupled networks.

Animals↗
PubMed1994

Resistance artery structure and neuroeffector mechanisms in hypertension induced by inhibition of nitric oxide synthase.

Oral administration of NW-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase, results in blood pressure elevation. In this study we investigated resistance artery structure and neuroeffector mechanisms in rats treated with L-NAME. After 5 days of treatment the morphology of resistance arteries was unchanged, whereas after 2 or 4 weeks, when rats were hypertensive, the media was thicker and the media-to-lumen ratio was enhanced. When L-NAME administration was stopped for 2 weeks, the media-to-lumen ratio remained increased. At all time periods under L-NAME and 2 weeks after stopping treatment, the dose-response to norepinephrine was significantly more sensitive than in controls, with a concomitant slight increase in efficacy. Cocaine (3 mumol/L) or L-NAME (100 mumol/L) applied in vitro produced a leftward displacement of the dose-response of arteries from controls to norepinephrine, and abolished the difference with vessels from L-NAME-treated rats. Responses evoked by electrical field stimulation were also displaced to the left in L-NAME-treated rats and by L-NAME in vitro, and exhibited a slight increase in maximal response. Dose-response curves to methoxamine, which is not subject to neuronal reuptake, were displaced to the left by L-NAME in vivo and in vitro, similarly to those of norepinephrine, but were not displaced by cocaine in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Oxidoreductases↗
PubMed1990

Endotoxin does not directly alter norepinephrine release or vasoactivity in dog pulmonary artery and portal vein.

The direct effect of Escherichia coli endotoxin on the release of norepinephrine (NE) and the contractile response consequent to the release of NE were studied in isolated, superfused segments of dog pulmonary artery and portal vein during resting conditions and during electrical stimulation (ES). High-pressure liquid chromatography with electrochemical detection was used to quantify the endogenous NE released and that remaining in the tissue after stimulation. Endotoxin (1 micrograms/ml and 10 micrograms/ml in superfusate) had no effect on the release of NE from either pulmonary artery or portal vein. Endotoxin also had no effect on vasoactivity in response to ES. Thus, in isolated pulmonary artery and portal vein, endotoxin, in the doses employed, does not directly affect release of NE from adrenergic nerve endings, nor does it affect the sequence of events that starts with transmitter-receptor interaction and ends with contraction of smooth muscle cells.

Adrenergic Fibers↗
PubMed1984

Na+,K+-ATPase inhibitors and the adrenergic neuroeffector interaction in the blood vessel wall.

Augmentation of the constrictor response of blood vessels to sympathetic nerve stimulation caused by inhibitors of Na+,K+-ATPase can be explained by (a) inhibition of neuronal uptake, (b) displacement of stored norepinephrine, (c) facilitation of exocytotic release of the adrenergic transmitter, (d) diminution in intraneuronal deamination, (e) reduction in extraneuronal uptake, (f) facilitation of postjunctional alpha 2-adrenoceptors, (g) inhibition of poststimulation relaxation, and, possibly, (h) prevention of endothelium-dependent relaxation.

Animals↗
PubMed1984

Autonomic nerves in the precapillary vessel wall.

A wide variety of substances are utilized as neurotransmitters in perivascular autonomic nerves, including noradrenaline, acetylcholine, ATP, 5-hydroxytryptamine, and a number of peptides. A general model for the autonomic innervation of the vessel wall is outlined, and variations in the innervation patterns in different precapillary vessels are described. Evidence that noradrenaline and ATP are cotransmitters in some precapillary vessels is presented. In the rat tail artery, ATP appears to be responsible for the fast depolarizations that are recorded in response to perivascular nerve stimulation, whereas noradrenaline is responsible for the slow maintained depolarization.

Acetylcholine↗
PubMedDate not supplied

Comparative effects of nitrendipine and verapamil on neuroeffector transmission in the rabbit ear artery.

The purpose of the present study was to evaluate and compare the effects of the calcium antagonists nitrendipine and verapamil on nerve-evoked constrictions and on norepinephrine (NE) release in the isolated, perfused rabbit ear artery. The response of the ear artery to nerve stimulation consists of an early phasic constriction (P response) and a late, slow-developing tonic constriction (T response). Both calcium antagonists were much more potent in causing inhibition of the T than P responses. For nitrendipine the EC50 (6.6 +/- 2.3 X 10(-8)M) for inhibition of T response was 450 times lower than the EC50 for inhibition of P response. Verapamil exhibited less selectivity for T response: the EC50 for inhibition of T response was 17 times lower than the EC50 for inhibition of the P response. Nitrendipine (3.3 X 10(7) to 3.3 X 10(-5) M) did not alter the nerve-evoked release of [3H]NE from arteries preincubated with [3H]NE. Verapamil at 3.3 X 10(-6) and 3.3 X 10(-5)M enhanced both spontaneous and nerve-evoked [3H]NE release.

Animals↗
PubMedDate not supplied

Pre- and postsynaptic effects of indoramin on sympathetic neuroeffector transmission in rabbit aorta and pulmonary artery.

The effects of indoramin on sympathetic neuroeffector transmission in rabbit isolated blood vessels were examined. Indoramin reduced the contractions of pulmonary artery evoked by electrical-field stimulation. The IC50 was 7.4 X 10(-8) M. In the presence of cocaine + corticosterone + propranolol, the IC50 was 5 X 10(-7) M. Amphetamine did not antagonize the steady-state inhibition caused by indoramin. Indoramin caused a slight enhancement of the field-stimulation-evoked 3H-overflow from pulmonary artery preloaded with 3H-noradrenaline. In the presence of cocaine + corticosterone + propranolol, indoramin also enhanced the stimulation-evoked 3H-overflow slightly. The effect of indoramin on stimulation-evoked 3H-overflow depended only slightly on stimulation frequencies (1-30 Hz): small enhancement at 1 Hz and nonsignificant changes at 3-30 Hz. Pretreatment with indoramin did not attenuate the inhibitory effect of clonidine on the stimulation-evoked 3H-overflow seen with bretylium. Indoramin and desmethylimipramine reduced the 3H-accumulation by aorta preloaded with 3H-noradrenaline. The IC50 was 3 X 10(-5)M (indoramin) and 10(-8)M (desmethylimipramine). Indoramin inhibited the contractions of aorta evoked by noradrenaline, phenylephrine, histamine and serotonin in a competitive manner. The corresponding pA2 values were 7.54, 7.98, 7.45, and 6.61. Indoramin decreased the maximal contractions of rabbit aorta evoked by potassium. These results suggest that indoramin is a potent competitive antagonist of postsynaptic alpha 1-adrenoceptors, while it may only have a slight inhibitory effect on presynaptic alpha 2-adrenoceptors. Indoramin is devoid of bretylium-like adrenergic neurone blocking activity, while it may act as reserpine. It is a weak inhibitor of the uptake-1 mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic Fibers↗
PubMed2001

Separate modulation of neuropeptide Y1 receptor on purinergic and on adrenergic neuroeffector transmission in canine splenic artery.

Our previous study demonstrated that the vasoconstrictor responses to trains of up to 10 pulses at 1 Hz of stimulation appeared to be purinergic monophasic, whereas a longer train of 30 pulses induced a biphasic vasoconstriction consisting of an initial, transient purinergic constriction followed by a prolonged adrenergic response. Neuropeptide Y (NPY) at doses of 0.01 and 0.1 microM produced a dose-dependent inhibition on the monophasic and biphasic vasoconstrictor responses to nerve stimulation. The treatment with Leu31 Pro34 neuropeptide Y (LP-NPY) (0.03 microM) did not affect the monophasic responses to short pulse trains of stimulation. However, LP-NPY markedly potentiated the second phase response to 30 pulse trains of stimulation, although it did not modify the first one. The LP-NPY-induced potentiation was abolished by BIBP 3226 (1 microM), a selective NPY Y1 receptor antagonist. The results indicate that the activation of NPY Y1 receptors may enhance the prolonged adrenergic vasoconstriction but not the transient purinergic response in the canine splenic artery.

Animals↗
PubMed1985

Dual inhibitory action of ATP on adrenergic neuroeffector transmission in rabbit pulmonary artery.

The aim of this study was to determine whether the inhibitory action of ATP on sympathetic neuroeffector transmission in the isolated pulmonary artery is due to ATP itself or one of its dephosphorylated breakdown products, ADP, AMP or adenosine. Furthermore, the mechanism of the inhibitory action was investigated. ATP (10(-6)-3 X 10(-4) M), the degradation-resistant ATP-analogue, beta, gamma-methylene-5'-triphosphate (10(-5)-3 X 10(-4) M), ADP (10(-6)-3 X 10(-4) M), AMP (10(-5)-3 X 10(-4) M), adenosine (10(-5)-3 X 10(-4) M) and 2-chloroadenosine (10(-7)-3 X 10(-4) M) reduced the contractions evoked by field-stimulation. This was also the case for prostaglandin E2 (3 X 10(-9)-3 X 10(-7) M), while prostaglandin F2 alpha (1.4 X 10(-8) M) slightly augmented the neurogenic response. The time course of the inhibitory effect of purinergic compounds on the stimulation evoked contractions was studied. In the case of ATP and ADP the inhibition was biphasic: an initial marked block (1 min. after drug addition) which in the continued presence of either compound recovered partially 10 min. later and then remained almost constant for another 90 min. The other purinergic agents caused a monophasic reduction. In the presence of indomethacin (5 X 10(-5) M), ATP and ADP also reduced the neurogenic contractions in a monophasic manner. Indomethacin did not alter the beta, gamma-methylene-5'-triphosphate-induced inhibition. Dilazep (3 X 10(-6) M) plus deoxycoformycin (3.6 X 10(-6) M), augmented the inhibitory effect of ATP. In contrast, theophylline (5 X 10(-5) M) did not alter the effect of ATP. The inhibitory effect of ATP (10(-4) M) on stimulation-evoked contractions was inversely proportional to the extracellular Ca2+ concentration (0.3-5.2 mM) and to frequency of stimulation (3-15 Hz). These results suggest that ATP initially causes a presynaptic inhibition of noradrenaline release evoked by field-stimulation. This phase I block is probably mainly due to an ADP-mediated short-lasting release of prostaglandins of the E type. The continuous inhibition (phase II) is probably due to ATP and its metabolites, possibly mainly adenosine. The phase II inhibition may possibly involve a decreased entry of Ca2+ into adrenergic nerve terminals during depolarization.

Adenosine↗
PubMed1990

Neuropeptides in hypertension: role of neuropeptide Y and calcitonin gene related peptide.

1. The effect of neuropeptide Y (NPY) on cardiovascular function at three levels of the noradrenergic axis where the peptide is known to co-exist with noradrenaline (NA) and or adrenaline (A) was studied in normotensive Sprague-Dawley (SD), Wistar-Kyoto (WKY) or spontaneously hypertensive rats (SHR). 2. In the perfused mesenteric arterial bed, NPY and the structurally similar peptide intestinal polypeptide (PYY) decreased the periarterial nerve stimulation induced release of NA and potentiated the increase in perfusion pressure to nerve stimulation or exogenously applied agonists (e.g. angiotensin, vasopressin, phenylephrine). In contrast to NPY and PYY, C-terminal NPY fragments inhibited NA release and produced a parallel decrease in perfusion pressure thus supporting the concept of Y1 (post) and Y2 (pre) NPY receptors. 3. In the mesenteric artery of SHR the prejunctional inhibitory effect of NPY was attenuated while the postjunctional response was enhanced. 4. Following intrathecal (Int) injection of NPY, there was a decrease in blood pressure, total peripheral resistance (predominantly by a decrease in mesenteric vascular resistance) and renal nerve activity. The depressor effect of Int NPY was attenuated in the SHR. 5. Unilateral injections of NPY into the posterior hypothalamic nucleus increased blood pressure, hindquarter and renal vascular resistance and renal nerve activity. The pressor effect was enhanced in the SHR. 6. Periarterial nerve stimulation of the perfused mesenteric artery produced a frequency dependent vasodilation in beds pretreated with guanethidine and precontracted with methoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Vasodilator component in sympathetic nerve activity destined for the skin of the dorsal foot of mildly heated humans.

1. Skin sympathetic nerve activity (SSNA) was recorded in seven male subjects from the peroneal nerve by microneurography, and the temporal correspondence of spontaneously occurring SSNA bursts with vasodilatation and sweating responses on the dorsal foot was studied during a mild body heating at rest. 2. Some SSNA bursts were followed by a sweat expulsion with a latency of 2.4 +/- 0.4 s, and some bursts by a transient vasodilatation with a latency of 2.2 +/- 0.4 s (means +/- S.D.). SSNA bursts followed both by a sweat expulsion and by a vasodilatation response (Type 1), those followed only by a sweat expulsion (Type 2) and those followed only by a vasodilatation, response (Type 3) were 70%, 10% and 1% of the total bursts examined, respectively. 3. For Type 1 bursts, there was a significant, but weak linear relationship among the burst amplitude, the amplitude of the corresponding vasodilatation and the amplitude of the corresponding sweat expulsion. 4. It was concluded that SSNA contains vasodilatory activity which is synchronous with sudomotor nerve activity. The results suggest that such vasodilatory activity contributes to sustaining the sweat gland function by supplying sufficient blood.

Adult↗
PubMed1984

Met5-enkephalin-Arg6-Phe7 inhibition of noradrenaline and acetylcholine release from peripheral organs.

The effect of the opioid heptapeptide Met5-enkephalin-Arg6-Phe7 was measured on the contractions of the longitudinal muscle of the guinea-pig ileum and mouse vas deferens; on release of endogenous and newly synthesized acetylcholine from the longitudinal muscle strip preparation of the guinea-pig ileum and of 3H-noradrenaline from mouse vas deferens. Met5-enkephelin-Arg6-Phe7 depressed the contractions of the longitudinal muscle strip of guinea-pig ileum elicited by low frequency stimulation (IC50 366.5 +/- 71.5 nM). The Ke value of naltrexone against the heptapeptide was found to be 0.50 +/- 0.08 nM. Bestatin prolonged and strongly potentiated the action of the opioid peptide in this tissue while captopril proved to be only slightly effective. Met5-enkephalin-Arg6-Phe7 also inhibited neuroeffector transmission in the mouse vas deferens with an IC50 value of 9.44 +/- 2.24 nM. The Ke value of naltrexone was 6.33 +/- 1.22 nM against the heptapeptide. Met5-enkephalin-Arg6-Phe7 (10(-5) M) failed to affect the low frequency stimulated release of endogenous acetylcholine from the guinea-pig ileum preparation. Addition of either bestatin or captopril with the heptapeptide resulted in a reduction of acetylcholine output. The opioid peptide by itself decreased the release of newly synthesized acetylcholine outflow from this organ. Met5-enkephalin-Arg6-Phe7 also reduced the 3H-noradrenaline outflow from mouse vas deferens and this effect was antagonized by naltrexone. From our data we conclude that Met5-enkephalin-Arg6-Phe7 affects the neural transmission of peripheral autonomically innervated organs by depressing the release of neurotransmitter. In vitro it has enkephalin-like character with a preference for the so called delta receptor interaction.

Acetylcholine↗