Stimulation Of Cervical Sympathetic Nerve Research Articles

Cardiovascular responses in spontaneously hypertensive rats with acute renal failure.

Cardiovascular status and reactivity have been investigated in spontaneously hypertensive rats (SHR) with glycerol-induced acute renal failure. SHR with acute renal failure had significantly lower mean arterial blood pressures and heart rates. The pressor responses to noradrenaline and the chronotropic responses to right cervical sympathetic and vagal nerve stimulation were diminished in uraemic SHR compared to control SHR. The cardiovascular depression observed in SHR with acute renal failure was similar to that previously noted in normotensive rats with acute renal impairment.

Responses of muscle spindles in feline dorsal neck muscles to electrical stimulation of the cervical sympathetic nerve

Previous studies performed in jaw muscles of rabbits and rats have demonstrated that sympathetic outflow may affect the activity of muscle spindle afferents (MSAs). The resulting impairment of MSA information has been suggested to be involved in the genesis and spread of chronic muscle pain. The present study was designed to investigate sympathetic influences on muscle spindles in feline trapezius and splenius muscles (TrSp), as these muscles are commonly affected by chronic pain in humans. Experiments were carried out in cats anesthetized with alpha-chloralose. The effect of electrical stimulation (10 Hz for 90 s or 3 Hz for 5 min) of the peripheral stump of the cervical sympathetic nerve (CSN) was investigated on the discharge of TrSp MSAs (units classified as Ia-like and II-like) and on their responses to sinusoidal stretching of these muscles. In some of the experiments, the local microcirculation of the muscles was monitored by laser Doppler flowmetry. In total, 46 MSAs were recorded. Stimulation of the CSN at 10 Hz powerfully depressed the mean discharge rate of the majority of the tested MSAs (73%) and also affected the sensitivity of MSAs to sinusoidal changes of muscle length, which were evaluated in terms of amplitude and phase of the sinusoidal fitting of unitary activity. The amplitude was significantly reduced in Ia-like units and variably affected in II-like units, while in general the phase was affected little and not changed significantly in either group. The discharge of a smaller percentage of tested units was also modulated by 3-Hz CSN stimulation. Blockade of the neuromuscular junctions by pancuronium did not induce any changes in MSA responses to CSN stimulation, showing that these responses were not secondary to changes in extrafusal or fusimotor activity. Further data showed that the sympathetically induced modulation of MSA discharge was not secondary to the concomitant reduction of muscle blood flow induced by the stimulation. Hence, changes in sympathetic outflow can modulate the afferent signals from muscle spindles through an action exerted directly on the spindles, independent of changes in blood flow. It is suggested that such an action may be one of the mechanisms mediating the onset of chronic muscle pain in these muscles in humans.

Effects of sympathetic stimulation on the rhythmical jaw movements produced by electrical stimulation of the cortical masticatory areas of rabbits

The somatomotor and sympathetic nervous systems are intimately linked. One example is the influence of peripheral sympathetic fibers on the discharge characteristics of muscle spindles. Since muscle spindles play important roles in various motor behaviors, including rhythmic movements, the working hypothesis of this research was that changes in sympathetic outflow to muscle spindles can change rhythmic movement patterns. We tested this hypothesis in the masticatory system of rabbits. Rhythmic jaw movements and EMG activity induced by long-lasting electrical cortical stimulation were powerfully modulated by electrical stimulation of the peripheral stump of the cervical sympathetic nerve (CSN). This modulation manifested itself as a consistent and marked reduction in the excursion of the mandibular movements (often preceded by a transient modest enhancement), which could be attributed mainly to corresponding changes in masseter muscle activity. These changes outlasted the duration of CSN stimulation. In some of the cortically evoked rhythmic jaw movements (CRJMs) changes in masticatory frequency were also observed. When the jaw-closing muscles were subjected to repetitive ramp-and-hold force pulses, the CRMJs changed characteristics. Masseter EMG activity was strongly enhanced and digastric EMG slightly decreased. This change was considerably depressed during CSN stimulation. These effects of CSN stimulation are similar in sign and time course to the depression exerted by sympathetic activity on the jaw-closing muscle spindle discharge. It is suggested that the change in proprioceptive information induced by an increase in sympathetic outflow (a) has important implications even under normal conditions for the control of motor function in states of high sympathetic activity, and (b) is one of the mechanisms responsible for motor impairment under certain pathological conditions such as chronic musculoskeletal head-neck disorders, associated with stress conditions.

Noradrenergic constriction of cerebral arteries as detected by transcranial doppler (TCD) in the rabbit

Interpretation of transcranial Doppler (TCD) recordings requires assumptions about flow or diameter of the insonated vessel. This study aimed at assessing if activation of the sympathetic system could affect blood velocity (bv) in basal cerebral arteries. In anaesthetized rabbits, stimulation of cervical sympathetic nerve (cervSN) was used selectively to activate the sympathetic pathway to the head while monitoring bv in all major cerebral arteries. cervSN stimulation at 10 Hz produced: 1. in internal carotid artery (ICA) and ICA-supplied arteries (ICA-s), a consistent bv increase ranging between 20 and 70%, 2. in the basilar artery, a transient decrease by 15–30%. These effects were mimicked, in both territories, by injection of phenylephrine into the ICA. Because cerebral blood flow is known to be reduced by cervSN stimulation, the increase in bv in ICA and ICA-s must be ascribed to constriction of the insonated vessels. These effects should be considered when monitoring bv during sympathetic activation tests or exercise. (E-mail: silvestro.roatta@unito.it)

Functional characterization of α-adrenoceptors mediating pupillary dilation in rats

Previously, we reported that the α 1A-adrenoceptor, but not the α 1D-adrenoceptor, mediates pupillary dilation elicited by sympathetic nerve stimulation in rats. This study was undertaken to further characterize the α-adrenoceptor subtypes mediating pupillary dilation in response to both neural and agonist activation. Pupillary dilator response curves were generated by intravenous injection of norepinephrine in pentobarbital-anesthetized rats. Involvement of α 1-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective α-adrenoceptor antagonists, phentolamine (0.3–3 mg/kg) and phenoxybenzamine (0.03–0.3 mg/kg), as well as by the selective α 1-adrenoceptor antagonist, prazosin (0.3 mg/kg). The α 2-adrenoceptor antagonist, rauwolscine (0.5 mg/kg), was without antagonistic effects. α 1A-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1–1 mg/kg) and 5-methylurapidil (0.1–1 mg/kg), the α 1B-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2( S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3–1 mg/kg), as well as the α 1D-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved. Mydriatic responses to norepinephrine were significantly antagonized by intravenous administration of both WB-4101 and 5-methylurapidil, but neither by L-765314 nor by BMY-7378. L-765314 (0.3–3 mg/kg, i.v.) was also ineffective in inhibiting the mydriasis evoked by cervical sympathetic nerve stimulation. These results suggest that α 1B-adrenoceptors do not mediate sympathetic mydriasis in rats, and that the α 1A-adrenoceptor is the exclusive subtype mediating mydriatic responses in this species.

Effects of sympathetic nerve stimulation on long posterior ciliary artery blood flow in cats.

A new technique using ultrasonic flowmetry was developed in order to directly measure blood flow in the long posterior ciliary artery (LPCA) of anesthetized cats. Basal LPCA blood flow averaged about 0.6 ml/min and was stable over the experimental period. Electrical stimulation of the cervical preganglionic cervical sympathetic nerve produced frequency-dependent anterior segment ocular vasoconstrictor responses. Ipsilateral nictitating membrane contractions were simultaneously measured as a well-established index of neural sympathetic activation. LPCA frequency-response relationships were shifted to the right in comparison with those for the nictitating membrane. When elicited at two min intervals, submaximal evoked responses of both systems were stable for more than 90 min. Ocular vasoconstrictor and nictitating membrane responses were blocked in a dose-dependent fashion by intravenous treatment with the non-selective a-adrenoceptor antagonist, phentolamine (0.3-3.0 mg/kg), as well as with the selective alpha1-adrenoceptor antagonist, prazosin (3-30 microg/kg). In contrast, neither evoked response was further antagonized by subsequent administration of the alpha2-adrenoceptor antagonist, yohimbine (500 microg/kg). These results demonstrate the usefulness of ultrasonic flowmetry to study mechanisms controlling ocular anterior segment circulation and suggest that, as previously established for the nictitating membrane and anterior choroid, adrenergic neurogenic vasoconstriction in tissues perfused by the LPCA is mediated predominantly by alpha1-adrenoceptors.

Sympathetic modulation of muscle spindle afferent sensitivity to stretch in rabbit jaw closing muscles.

Previous reports showed that sympathetic stimulation affects the activity of muscle spindle afferents (MSAs). The aim of the present work is to study the characteristics of sympathetic modulation of MSA response to stretch: (i) on the dynamic and static components of the stretch response, and (ii) on group Ia and II MSAs to evaluate potentially different effects. In anaesthetised rabbits, the peripheral stump of the cervical sympathetic nerve (CSN) was stimulated at 10 impulses s(-1) for 45-90 s. The responses of single MSAs to trapezoidal displacement of the mandible were recorded from the mesencephalic trigeminal nucleus. The following characteristic parameters were determined from averaged trapezoidal responses: initial frequency (IF), peak frequency at the end of the ramp (PF), and static index (SI). From these, other parameters were derived: dynamic index (DI = PF - SI), dynamic difference (DD = PF - IF) and static difference (SD = SI - IF). The effects of CSN stimulation were also evaluated during changes in the state of intrafusal muscle fibre contraction induced by succinylcholine and curare. In a population of 124 MSAs, 106 units (85.4 %) were affected by sympathetic stimulation. In general, while changes in resting discharge varied among different units (Ia vs. II) and experimental conditions (curarised vs. non-curarised), ranging from enhancement to strong depression of firing, the amplitude of the response to muscle stretches consistently decreased. This was confirmed and detailed in a quantitative analysis performed on 49 muscle spindle afferents. In both the non-curarised (23 units) and curarised (26 units) condition, stimulation of the CSN reduced the response amplitude in terms of DD and SD, but hardly affected DI. The effects were equally present in both Ia and II units; they were shown to be independent from gamma drive and intrafusal muscle tone and not secondary to muscle hypoxia. Sympathetic action on the resting discharge (IF) was less consistent. In the non-curarised condition, IF decreased in most Ia units, while in II units decreases and increases occurred equally often. In the curarised condition, IF in group II units mostly increased. The results have important functional implications on the control of motor function in a state of 'high' sympathetic activity, like excessive stress, as well as in certain pathological conditions such as sympathetically maintained pain.

Differential neural activation of vascular α-adrenoceptors in oral tissues of cats

The aim of this study was to determine the relative contribution of α 1- and α 2-adrenoceptors involved in sympathetic-evoked vasoconstrictor responses in tissues perfused by the lingual arterial circulation in pentobarbital anesthetized cats. Blood flow in the lingual artery was measured by ultrasonic flowmetry. Laser–Doppler flowmetry was utilized to measure oral tissue vasoconstrictor responses in the maxillary gingiva and from the surface of the tongue. Electrical stimulation of the preganglionic superior cervical sympathetic nerve resulted in frequency-dependent blood flow decreases at all three sites. These responses were stable over time and were uniformly antagonized by administration of phentolamine (0.3–3.0 mg kg −1). The selective α 1-adrenoceptor antagonist, prazosin (10–300 μg kg −1), attenuated vasoconstriction in the lingual artery and gingiva, but was ineffective in blocking vasoconstriction in the tongue. Subsequent administration of rauwolscine (300 μg kg −1) antagonized remaining vasoconstrictor responses. In contrast, rauwolscine (10–300 μg kg −1), given alone, blocked evoked vasoconstriction in the tongue, and was without effect on gingival or lingual artery vasoconstrictor responses. Subsequent administration of prazosin (300 μg kg −1) largely antagonized remaining neurally elicited responses. These results suggest that neural vasoconstrictor responses in some regional vascular beds in the cat oral cavity are mediated by both α 1- and α 2-adrenoceptors. In contrast, tongue surface vasoconstrictor responses to sympathetic nerve activation appear to be mediated primarily by α 2-adrenoceptors.

α1A-Adrenoceptors Mediate Sympathetically Evoked Pupillary Dilation in Rats

Evidence suggests that in some species (cats, rabbits, and possibly humans) alpha-adrenoceptors in the iris dilator muscle are "atypical" in that they cannot be readily classified by conventional criteria. This study was undertaken in an attempt to characterize the alpha-adrenoceptor subtype(s) mediating sympathetically elicited mydriasis in rats. Frequency-response pupillary dilator curves were generated by stimulation of the preganglionic cervical sympathetic nerve (1-32 Hz) in pentobarbital-anesthetized rats. Evoked responses were inhibited by systemic administration of nonselective alpha-adrenergic antagonists, phentolamine (0.3-10 mg/kg) and phenoxybenzamine (0.03-1 mg/kg). The selective alpha(1)-adrenergic antagonist, prazosin (0.01-1 mg/kg), also was effective, although alpha(2)-adrenergic antagonism with rauwolscine (0.1-1 mg/kg) was not. alpha(1A)-Adrenoceptor-selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), as well as the alpha(1D)-adrenoceptor-selective antagonist 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1-3 mg/kg), were used to determine the subtype(s) involved. Evoked mydriasis was significantly antagonized by both WB-4101 and 5-methylurapidil but not by BMY-7378. These results suggest that, unlike some other species, adrenoceptors in the rat iris dilator mediating neurogenic mydriasis are "typical" and, in addition, can be characterized as being primarily of the alpha(1A)-adrenoceptor subtype.

Effects of a beta-adrenergic blocking agent timolol on intra ocular pressure responses induced by stimulation of cervical sympathetic nerve in the cat.

We clarified whether the intraocular pressure (IOP) response elicited by stimulation of the cervical sympathetic nerve (CSN) is influenced by changes in the baseline of IOP level and by beta-adrenergic blockade. The CSN was stimulated electrically for 30 seconds (10 V, 0.1-100 Hz, 2 milliseconds pulse duration) in urethane (100 mg/kg i.v.)-chloralose (50 mg/kg i.v.)-anesthetized, paralyzed cats. The IOP was monitored manometrically, and a controlled saline infusion was delivered into the anterior chamber to gradually increase IOP. CSN stimulation was delivered at the various baseline IOP levels so obtained. When required, a beta-adrenergic blocker timolol (2%) was delivered into the conjunctival cul-de-sac. The normal IOP in our cats was 25+/-3 mmHg. This value decreased transiently on CSN stimulation. The amplitude of this IOP response depended on stimulus frequency and the pre-stimulus baseline IOP level. Topical administration of timolol increased the IOP response to CSN stimulation at a given baseline level. These results suggest that beta-adrenergic blockade increases the alpha-adrenergic mediated-IOP reduction elicited by CSN stimulation at given baseline IOP level.

Adrenergic reactivity after inhibition of nitric oxide synthesis in the cerebral circulation of awake goats

The interaction between nitric oxide (NO) and adrenergic reactivity in the cerebral circulation was studied using in vivo and in vitro preparations. Blood flow to one brain hemisphere (cerebral blood flow) was electromagnetically measured in conscious goats, and the effects of norepinephrine, tyramine and cervical sympathetic nerve stimulation were recorded before (control) and after inhibition of NO formation with N w-nitro- l-arginine methyl ester ( l-NAME). The responses to norepinephrine, tyramine and electrical field stimulation were also recorded in segments, 4 mm in length, from the goat's middle cerebral artery under control conditions and after l-NAME. In vivo, l-NAME (10 goats, 47 mg kg −1 administered i.v.) reduced resting cerebral blood flow by 37±2%, increased mean systemic arterial pressure by 24±3%, reduced heart rate by 35±2%, and decreased cerebrovascular conductance by 52±2% (all P<0.01). Norepinephrine (0.3–9 μg), tyramine (50–500 μg), and supramaximal electrical sympathetic cervical nerve stimulation (1.5–6 Hz) decreased cerebrovascular conductance, and these decreases were significantly higher after l-NAME than under control conditions, remaining higher for about 48 h after this treatment. Norepinephrine (10 −8–10 −3 M), tyramine (10 −6–10 −3 M) and electrical field stimulation (1.5–6 Hz) contracted isolated cerebral arteries, and the maximal contraction, but not the sensitivity, was significantly higher in the arteries treated than in non-treated with l-NAME (10 −4 M). Therefore, the reactivity of cerebral vasculature to exogenous and endogenous norepinephrine may be increased after inhibition of NO synthesis. This increase might be related, at least in part, to changes at postjunctional level in the adrenergic innervation of the vessel wall, and it might contribute to the observed decreases in resting cerebral blood flow after inhibition of NO synthesis.

Sympathetic vasoconstriction in the rat anterior choroid is mediated by α 1-adrenoceptors

These experiments were undertaken in an attempt to use laser-Doppler flowmetry to measure anterior choroidal blood flow in the anesthetized rat and to study the mechanism by which sympathetic nerve stimulation might produce vasoconstriction in this vascular bed. Electrical stimulation of the preganglionic cervical sympathetic nerve produced reproducible, frequency-related ocular vasoconstrictor responses with maximal vasoconstriction seen at about 32 Hz. Ocular vasoconstrictor responses were blocked by intravenous treatment with the nonselective α-adrenoceptor antagonists, phentolamine (5 mg kg −1) and phenoxybenzamine (2 mg kg −1), as well as with the selective α 1-adrenoceptor antagonist, prazosin (0.3 mg kg −1). In contrast, the selective α 2-adrenoceptor blocker, rauwolscine (0.5 mg kg −1), only potentiated the vasoconstriction. Neither intravenous atropine (1 mg kg −1) nor propranolol (1 mg kg −1) altered the magnitude of neurally evoked vasoconstriction. These results demonstrate the usefulness of laser-Doppler flowmetry in studies of the rat anterior choroidal circulation and suggest that adrenergic neurogenic vasoconstriction in the anterior segment of the rat eye is mediated almost exclusively by α 1-adrenoceptor mechanisms.

The actions of bretylium: Adrenergic neurone blocking and other effects

The actions of bretylium: Adrenergic neurone blocking and other effects

Sympathetically-induced changes in microvascular cerebral blood flow and in the morphology of its low-frequency waves

The effect of bilateral cervical sympathetic nerve stimulation on microvascular cerebral blood flow, recorded at various depths in the parietal lobe and in ponto-mesencephalic areas, was investigated by laser-Doppler flowmetry in normotensive rabbits. These areas were chosen as representative of the vascular beds supplied by the carotid and vertebro-basilar systems, which exhibit different degrees of sympathetic innervation, the former being richer than the latter. Sympathetic stimulation at 30 imp/s affects cerebral blood flow in 77% of the parietal lobe and in 43% of the ponto-mesencephalic tested areas. In both cases the predominant effect was a reduction in flow (14.7 ± 5.1 % and 4.1 ± 2,4%, respectively). The extent of the reduction in both areas was less if the stimulation frequency was decreased. Sometimes mean cerebral blood flow showed a small and transient increase, mainly in response to low-frequency stimulation. The morphology was analysed of low-frequency spontaneous oscillations in cerebral blood flow, attributed to vasomotion. Present in 41% of the tested areas (frequency 4–12 cycles/min, peak-to-peak amplitude 10–40% of mean value), these waves decreased in amplitude and increased in frequency during sympathetic stimulation, irrespective of changes in mean flow. The possibility has been proposed that the sympathetic action on low-frequency spontaneous oscillations may contribute to the protective influence that this system is known to exert on the blood-brain barrier in hypertension.

Effects of cervical sympathetic nerve stimulation on the cerebral microcirculation: possible clinical implications.

The action of bilateral cervical sympathetic nerve (CSN) stimulation on mean cerebral blood flow (CBF) and on its rhythmical fluctuations was studied in normotensive rabbits by using laser-Doppler flowmetry (LDF). A reduction in mean CBF, mediated by alpha-adrenoceptors, was the predominant effect; it was more often present and larger in size in the vascular beds supplied by the carotid than in those supplied by the vertebro-basilar system. This suggests that the sympathetic action facilitates a redistribution of blood flow to the brain stem. The effect induced by CSN stimulation on CBF spontaneous oscillations was a consistent decrease in amplitude and an increase in frequency, irrespective of the changes produced on the mean level of CBF. The possible implications of the sympathetic action on the state of the blood-brain barrier (BBB) are discussed. Experimental and clinical data dealing with the influence of sympathetic activation on the cerebrovascular system have been compared. As a result the possibility of analysing the spontaneous oscillations of CBF for clinical purposes is suggested.

Effect of baseline vascular tone on vasomotor responses in cat lip.

1. Parasympathetic vasodilator and sympathetic vasoconstrictor responses were monitored using laser Doppler measurement of red cell flux in the lips of anaesthetized and artificially ventilated cats. 2. Three relationships were investigated: (i) that between the reflex parasympathetic vasodilator response induced by lingual nerve (LN) stimulation and baseline red cell flux (BRCF) levels adjusted by repetitive stimulation of the cervical sympathetic nerve (CSN) at various frequencies; (ii) that between the sympathetic vasoconstrictor response elicited by CSN stimulation and the adjusted BRCF levels; and (iii) that between the vasomotor response evoked by simultaneous stimulation of the LN and CSN and the adjusted BRCF levels. 3. The amplitude of the parasympathetic vasodilator response increased as BRCF decreased. In contrast, the amplitude of the sympathetic vasoconstrictor response increased in line with BRCF. 4. Simultaneous activation of the parasympathetic and sympathetic nerves induced a blood flow decrease at high BRCF levels but an increase at low levels. 5. The tendency for the skin of cold subjects to vasodilate and that of warm ones to vasoconstrict in response to various types of stimuli discussed in the light of the present findings.

Increased and decreased choroidal blood flow elicited by cervical sympathetic nerve stimulation in the cat.

The effect of electrical stimulation of the cervical sympathetic nerve on choroidal blood flow in the cat was investigated. Flow at various sites in 30 pentobarbital-anesthetized cats was continuously measured trans-sclerally using a laser Doppler flowmeter. Changes in either direction, increases and decreases, occurred in response to electrical stimulation of the peripheral cut end of the cervical sympathetic nerve. These changes in flow appeared to depend on the site of choroidal blood flow measurement, as decreases were seen at sites with a high baseline blood flow and increases at sites with a low baseline level. Both types of response were reduced when the cats were treated with the alpha-adrenoreceptor antagonist phentolamine, but not by treatment with the beta-adrenoceptor antagonist propranolol. The decrease in choroidal blood flow elicited by cervical sympathetic nerve stimulation appears to be mediated via the vasoconstrictor fibers in that nerve. A choroidal blood flow increase may occur as a secondary effect following vasoconstriction of the arterioles elicited by cervical sympathetic nerve stimulation, producing a passive net increase in choroidal blood flow.

Sympathetic and parasympathetic interaction in vascular control of the nasal mucosa in anaesthetized cats.

1. In cats anaesthetized with pentobarbitone sodium (45 mg kg-1), electrical stimulation of the parasympathetic nerve fibres to the nasal mucosa evoked frequency-dependent increases in nasal arterial blood flow whereas stimulation of the superior cervical sympathetic nerve induced marked vasoconstriction. 2. Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant (P < 0.05) and prolonged (> 30 min) attenuation of the vasodilatory response to subsequent parasympathetic stimulation. 3. Combined pretreatment with adrenergic and cholinergic blockers reduced the vasoconstrictory effect of sympathetic stimulation by 28 +/- 4% (mean +/- S.E.M.) and the parasympathetically evoked vasodilatation by 20 +/- 5%. 4. The vasodilatory effects of exogenous vasoactive intestinal polypeptide, peptide histidine isoleucine and galanin, and the vasoconstrictory effects of exogenous neuropeptide Y (NPY) and alpha,beta-methylene adenosine 5'-triphosphate were not altered by adrenoceptor antagonists and atropine whereas the effects of exogenous noradrenaline and acetylcholine were virtually abolished. 5. The atropine-resistant parasympathetic vasodilatation remained significantly attenuated for more than 30 min after the non-adrenergic sympathetically evoked vasoconstriction. 6. Exogenous NPY (25 x 10(-9) mol) mimicked the effect of sympathetic stimulation in attenuating subsequent parasympathetically evoked vasodilatation.

Modulation by neuropeptide Y of parasympathetic nerve‐evoked nasal vasodilatation via Y2 prejunctional receptor

1. In pentobarbitone anaesthetized dogs, preganglionic stimulation of the superior cervical sympathetic nerve (15V, 1 ms, 10 Hz) induced marked reduction of nasal arterial blood flow, whereas parasympathetic nerve stimulation (5 V, 1 ms, 10-30 Hz) evoked frequency-dependent vasodilatation. 2. Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant (P < 0.05) and prolonged attenuation of the vasodilator response to subsequent parasympathetic stimulation. Pretreatment with phentolamine (0.5 mg kg-1 h-1), propranolol (1 mg kg-1) and atropine (0.5 mg kg-1) reduced the vasoconstrictor effect of sympathetic stimulation by 35 +/- 4% whereas the parasympathetic nerve-evoked vasodilatation was not significantly modified. Atropine-resistant parasympathetic vasodilatation remained significantly attenuated for more than 30 min after non-adrenergic sympathetic nerve-evoked vasoconstriction. 3. Vasodilator effects of exogenous vasoactive intestinal polypeptide and peptide histidine isoleucine and vasoconstrictor effects of exogenous neuropeptide Y (NPY) and the NPY analogue [Leu31, Pro34] NPY (Y1-receptor agonist, 8 nmol kg-1), were not altered by adrenoceptor antagonists and atropine f1p4eas the effects of exogenous noradrenaline and acetylcholine were virtually abolished. Attenuation of parasympathetic-evoked vasodilatation could be mimicked by exogenous NPY (8 nmol kg-1) and the NPY analogue, N-acetyl [Leu28, Leu31] NPY 24-36 (Y2-receptor agonist, 20 nmol kg-1) but not by exogenous Y1-receptor agonist. The Y2-receptor agonist did not show significant vasoconstrictor action. 4. It is concluded that sympathetic nerve stimulation attenuates parasympathetic vasodilatation via NPY release acting on prejunctional Y2 receptors.

Effect of baseline vascular tone on vasomotor responses in cat lip

1. Parasympathetic vasodilator and sympathetic vasoconstrictor responses were monitored using laser Doppler measurement of red cell flux in the lips of anaesthetized and artificially ventilated cats. 2. Three relationships were investigated: (i) that between the reflex parasympathetic vasodilator response induced by lingual nerve (LN) stimulation and baseline red cell flux (BRCF) levels adjusted by repetitive stimulation of the cervical sympathetic nerve (CSN) at various frequencies; (ii) that between the sympathetic vasoconstrictor response elicited by CSN stimulation and the adjusted BRCF levels; and (iii) that between the vasomotor response evoked by simultaneous stimulation of the LN and CSN and the adjusted BRCF levels. 3. The amplitude of the parasympathetic vasodilator response increased as BRCF decreased. In contrast, the amplitude of the sympathetic vasoconstrictor response increased in line with BRCF. 4. Simultaneous activation of the parasympathetic and sympathetic nerves induced a blood flow decrease at high BRCF levels but an increase at low levels. 5. The tendency for the skin of cold subjects to vasodilate and that of warm ones to vasoconstrict in response to various types of stimuli discussed in the light of the present findings.