Effects Of Sympathetic Nerve Stimulation Research Articles

Release of nucleosides and nucleotides from the rabbit heart by sympathetic nerve stimulation.

The release of endogenous purine compounds from the isolated Langendorff perfused heart during sympathetic nerve stimulation has been studied. The contents of adenosine, inosine, hypoxanthine and AMP in heart muscle and in the perfusate was studied by HPLC. Adenosine or AMP, administered via the perfusate, was rapidly inactivated by the heart. The recovery of adenosine after a single passage was 13 per cent and that of AMP 40 per cent. The recovery of adenosine was increased by inhibitors of adenosine deaminase or nucleoside uptake; that of AMP by inhibition of ecto‐5'‐nucleotidase. The efflux of adenosine and, especially, inosine was increased by sympathetic nerve stimulation in a time‐ and frequency‐dependent manner. Simultaneously the tissue level of the two nucleosides increased. Nerve stimulation did not enhance AMP efflux in the absence of drugs and did not significantly enhance tissue AMP levels. The effect of sympathetic nerve stimulation was mimicked by noradrenaline and was blocked by adrenoceptor blocking agents. The release of adenosine induced by nerve stimulation was enhanced by uptake inhibitors and by an inhibitor of adenosine deaminase. The release of inosine was simultaneously reduced. In the presence of an inhibitor of ecto‐5'‐nucleotidase nerve stimulation induced a significant release of AMP, but no significant alteration in the release of adenosine or inosine was found. It is concluded that sympathetic nerve stimulation leads to release of both adenine nucleotides and adenosine from the perfused rabbit heart. These substances are rapidly catabolized by 5'‐nucleotidase and by uptake followed by deamination, respectively, to form mainly inosine. It is proposed that the release of adenosine may reflect the energy state of the cardiac cells, while the nucleotide release may depend on depolarization.

Effect of sympathetic nerve stimulation and cardiac denervation on MBF during LAD occlusion.

Effect of sympathetic nerve stimulation and cardiac denervation on MBF during LAD occlusion.

Effects of sympathetic nerve stimulation on intra-oral mechanoreceptor activity in the cat.

1. Micro-electrode recordings were made from intra-oral mechanoreceptor neurones in the trigeminal ganglion and mesencephalic nucleus of the fifth nerve in the cat.2. The effect of cervical sympathetic trunk stimulation on the discharge of the mechanoreceptors to a controlled force was observed.3. Almost half of the mechanoreceptor neurones studied were modulated by sympathetic stimulation. Sympathetic stimulation both decreased the impulse frequency to a controlled force application and raised the threshold in these receptors. The remainder were unaffected by sympathetic stimulation.4. In previous studies involving recordings from either the trigeminal ganglion or mesencephalic nucleus no spontaneously active slowly adapting intra-oral mechanoreceptors have been observed, yet in peripheral alveolar nerve studies many workers have reported spontaneously discharging neurones. In the present study spontaneous activity has been recorded from intra-oral mechanoreceptors both in the trigeminal ganglion and in the mesencephalic nucleus after cutting the cervical sympathetic trunk. The spontaneous activity could be abolished in all cases but one, by sympathetic stimulation. It is suggested that reported spontaneous activity from intra-oral mechanoreceptors could be due to cutting the peripheral nerve and therefore the sympathetic supply, thus removing an inhibitory influence from the sensory unit. The means by which the sympathetic supply inhibits the sensory unit has not been resolved.

Release of prostaglandins I 2 and E 2 from the perfused mesenteric arterial bed of normotensive and hypertensive rats. Effects of sympathetic nerve stimulation and norepinephrine administration

The spontaneous output of prostaglandin (PG) I 2 from the perfused mesenteric arterial bed in vitro was significantly higher in hypertensive rats than in normotensive rats. Sympathetic nerve stimulation (at 10Hz) of the mesenteric arterial bed from normotensive rats caused a rapid and short-lived (< 4 min) two-fold increase in PGI 2 output and a smaller increase in PGE 2 output. Sympathetic nerve stimulation (at 10Hz) of the mesenteric arterial bed from hypertensive rats failed to increase PGI 2 and PGE 2 output. It is not possible to conclude whether this lack of response is a cause or a result of hypertension. Surprisingly, norepinephrine administration stimulated PGI 2 and PGE 2 release from the mesenteric arterial bed of both normotensive and hypertensive rats. Obviously, differences exist in the responsiveness of rat mesenteric arteries to endogenous and exogenous norepinephrine concerning PG release between the normotensive and hypertensive states.

Effects of sympathetic nerve stimulation, right atrial pacing on myocardial metabolism and cardiac function in dog hearts with coronary constriction: R.Sato, S.Yoshida, K.Ohno, K.Nohara, N.Ishiyama and O.Iimura. 2nd Dept. of Internal Medicine, Sapporo Medical College, Sapporo, Japan

Effects of sympathetic nerve stimulation, right atrial pacing on myocardial metabolism and cardiac function in dog hearts with coronary constriction: R.Sato, S.Yoshida, K.Ohno, K.Nohara, N.Ishiyama and O.Iimura. 2nd Dept. of Internal Medicine, Sapporo Medical College, Sapporo, Japan

The effect of sympathetic nerve stimulation on responses of cutaneous pacinian corpuscles in the cat

In the cat electrical stimulation of the distal segments of transected sympathetic nerves to the forelimb produces either an increase or a decrease in the responsiveness of the Pacinian corpuscles under the glabrous skin of the forepaw when the corpuscles are stimulated with high frequency mechanical vibration. The minimum latency of the change in Pacinian response is about 1–2 sec. As these effects could be simulated by reduction in the forelimb blood supply it is probable that the changes in cutaneous corpuscle responsiveness following sympathetic stimulation are caused by local changes in blood flow.

Prostaglandins do not modulate the positive chronotropic and inotropic effects of sympathetic nerve stimulation and injected norepinephrine in the isolated blood perfused canine atrium

In isolated canine atrium, perfused with blood from a donor dog, the infusions of both prostaglandins (PG)I 2 and E 2 (0.1–1 μg/min) into the sinus node arterial cannula neither altered the sinus rate and developed tension nor the positive chronotropic and inotropic responses elicited by either electrical stimulation or by injected norepinephrine. Infusion of arachidonic acid (10–100 μg/min), a precursor of PGs, or indomethacin (15–20 μg/min), an inhibitor of PG synthesis, into the sinus node arterial cannula also failed to alter the increase in sinus rate or developed tension produced by either adrenergic stimulus in the isolated atria. When arachidonic acid, 100–300 μg/kg or PGI 2, 1 μg/kg, were injected into the jugular vein of the donor dog, they produced a fall in systemic blood pressure; this effect of arachidonic acid but not of PGI 2 was abolished by indomethacin, 1 mg/kg. During administration of either arachidonic acid or indomethacin to the donor dog, the positive chronotripic and inotropic responses to adrenergic stimuli in the isolated atria also remained unaltered. These data indicate that PGs do not modulate adrenergic transmission in the blood perfused canine atrium.

Non-uniform effects of sympathetic nerve stimulation on ventricular refractoriness in healed myocardial infarction: Comparison to acute infarction

Non-uniform effects of sympathetic nerve stimulation on ventricular refractoriness in healed myocardial infarction: Comparison to acute infarction

Sympathetic nervous control of blood flow in the gills of the Atlantic cod,Gadus morhua

The effects of sympathetic nerve stimulation, adrenaline and isoprenaline on the inflow pressure and efferent arterial and venous flow rates were studied in a cod gill preparation perfused at constant flow rate. The dominant effect of adrenaline was a reduced inflow pressure, accompanied by an increase in arterial flow and a decrease in venous flow. Isoprenaline also decreased the inflow pressure, but the changes in both outflow rates were small or absent. Sympathetic nerve stimulation gave arterial and venous flow changes comparable to the adrenaline effects, but the inflow pressure increased during nerve stimulation. Propranolol has little effect on the nerve responses, but phentolamine abolished or reversed the increase in inflow pressure, and also decreased or abolished the changes in outflow rates. The possible sites of action of the sympathetic fibres, and the distribution of adrenoceptors in the effector tissue is discussed. It is concluded that the main effect of sympathetic nerve stimulation is α-adrenoceptor mediated, involving constriction of the arterio-venous pathway. Theβ-adrenoceptor mediated control of total branchial vascular resistance may largely depend on circulating catecholamines.

Effect of exogenous and endogenous prostacyclin on the contractility of rabbit splenic capsular smooth muscle.

1. Using sensitive and specific radioimmunoassays release of prostaglandins (PGs) E2, F2α, 6-keto-F1α and thromboxane B2 (TXB2) from rabbit splenic capsular strips was determined. 2. Contraction of the strips by noradrenaline increased the release of 6-keto-PGF1α, PGE2, PGF2α and TXB2 as compared to basal conditions. Indomethacin inhibited synthesis and release of PGs and TXB2 and simultaneously increased noradrenaline-induced contractions. 3. Arachidonic acid and dihomo-γ-linolenic acid, both substrates for the enzyme fatty acid cyclooxygenase, dose-dependently antagonized noradrenaline-induced contractions. On the other hand, fatty acids, which are not substrates for the cyclooxygenase, had no effect. Pretreatment of the smooth muscle strips with indomethacin inhibited the effect of arachidonic acid and dihomo-γ-linolenic acid. 4. The PG endoperoxides PGG2 and PGH2 as well as their derivative prostacyclin (PGI2) were more effective than arachidonic acid as inhibitors of noradrenaline-induced contractions. The stable degradation product of PGI2, 6-keto-PGF1α, did not influence the contractions. The effects of the PG endoperoxides and PGI2 were not inhibited by indomethacin. 5. The 6(9)oxycyclase inhibitor 9,11-azoprosta-5,13-dienoic acid antagonized the inhibitory effects of arachidonic acid and PGG2 on the contractions, but did not modify the effect of PGI2. 6. Inhibitors of PGI2 synthesis such as 15-hydroperoxyarachidonic acid and 9,11-azoprosta-5,13-dienoic acid increased, like indomethacin, noradrenaline-induced contractions of the rabbit splenic capsular strips in the absence of exogenous PG precursors. On the other hand, a specific inhibitor of TX synthesis, 11,9-epoxyiminoprosta-5,13-dienoic acid, was without effect on the contractions. 7. The results are compatible with the view that endogenous PGI2 modulates the contractile response of rabbit splenic capsular smooth muscle to noradrenaline. The hypothetical PGI2 receptor on the smooth muscle seems to resemble in its specificity the PGI2 receptor on thrombocytes of various species as only PGE1 in higher concentrations has effects comparable to PGI2. 8. Besides the presynaptic inhibition of noradrenaline release by PGE the postsynaptic inhibition of noradrenaline-induced smooth muscle contraction by endogenous PGI2 might represent, at least in vitro, another feed-back mechanism to attenuate the effects of sympathetic nerve stimulation. Synthesis and release of antiaggregatory and contraction-inhibiting PGI2 by splenic tissue might play a role in the function of the spleen as a storage site for thrombocytes.

Effect of sympathetic nerve stimulation on hypocapnic airway constriction.

SummaryTwo series of experiments were conducted to determine the effect of sympathetic nerve stimulation on hypocapnic airway constriction in the isolated left lower lobe (LLL) of the dog anesthetized with sodium pentobarbital. In the first series, hypocapnic airway constriction was produced by lobar artery occlusion. The bronchodilator effect of sympathetic stimulation on hypocapnic airway constriction was compared to the bronchodilator effect of sympathetic stimulation on the constrictor effects of vagal nerve stimulation. In the second series, the LLL was isolated and pump perfused. Hypocapnic airway constriction was produced by reducing the inspired CO2 from 5 to 0% in O2. The increase in lobar artery pressure caused by sympathetic stimulation was used as an index of the effectiveness of sympathetic stimulation to the LLL. In neither series did sympathetic stimulation have a significant effect on hypocapnic airway constriction.

Inhibition of vasoconstrictor responses by 6-keto-PGE 1 in the feline mesenteric vascular bed

The effects of 6-keto-PGE 1 on vascular resistance and vascular responses to sympathetic nerve stimulation and vasoconstrictor hormones were investigated in the feline mesenteric vascular bed. Infusions of 6-keto-PGE 1 into the superior mesenteric artery dilated the mesenteric vascular bed and markedly inhibited vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine and angiotensin II. The effects of 6-keto-PGE 1 and PGE 1 on vascular resistance and vasoconstrictor responses were quite similar and both substances inhibited responses to nerve stimulation and pressor hormones in a reversible manner. Responses to nerve stimulation, norepinephrine and angiotensin II were inhibited to a similar extent during infusion of 6-keto-PGE 1 and PGE 1. Results of these studies suggest that 6-keto-PGE 1, a newly identified prostaglandin metabolite, and PGE 1 possess the ability to inhibit the vasconstrictor effects of sympathetic nerve stimulation and pressor hormones by a nonspecific action on vascular smooth muscle in the feline small intestine.

Effects of sympathetic nerve stimulation on lung fluid and protein exchange.

Effects of sympathetic nerve stimulation on lung fluid and protein exchange.

Vascular reactivity of the isolated tibia of the dog

Experiments were performed to assess the responsiveness of vessels subserving bone tissue to nerve stimulation and to exogenously administered catecholamines and acetylcholine. Tibias of mongrel dogs were isolated and dissected free; the periosteum was left intact. The main nutrient artery was prepared and cannulated. Ring electrodes were placed around the artery. The preparation was perfused at constant flow with aerated (95% O2 - 5% CO2) Krebs-Ringer solution (37 degrees C) by means of a roller pump. The perfusion pressure was continuously recorded. For each preparation, the flow rate was used at which the response to a standard dose of norepinephrine was the largest. Periarterial electrical stimulation caused frequency-dependent increases in perfusion pressure; because these responses were blocked by phentolamine, they must be due to activation of sympathetic nerves. Injections of norepinephrine caused dose-dependent increases in perfusion pressure that were abolished by phentolamine. Acetylcholine caused dose-dependent, atropine-sensitive decrease of the constrictions caused by norepinephrine infusions. These experiments demonstrate that the isolated perfused tibia of the dog is a satisfactory preparation to investigate the direct effects of sympathetic nerve stimulation and naturally occurring vasoactive amines on bone blood vessels.

Altered effect of sympathetic nerve stimulation on ventricular fibrillation threshold due to coronary perfusion changes

Altered effect of sympathetic nerve stimulation on ventricular fibrillation threshold due to coronary perfusion changes

The effects of intravenous anaesthetics on the cardiovascular system of the rabbit.

1 A pithed rabbit preparation is described that allows selective stimulation of the vertebral outflows. 2 The responses to stimulation of sympathetic vasopressor fibres were blocked by hexamethonium and phentolamine but potentiated by cocaine, whereas the responses to stimulation of cardioaccelerator fibres were blocked by propranolol. 3 Ketamine, althesin and pentobarbitone enhanced the effects of noradrenaline and attenuated the effects of sympathetic nerve stimulation. Thiopentone enhanced the effects of both noradrenaline and sympathetic nerve stimulation. 4 In pithed rabbits a transient, dose-related cardiovascular depression was produced by each agent irrespective of whether vasomotor tone was present whereas in decerebrate rabbits the corresponding cardiovascular depression was longer lasting. 5 It is concluded that the cardiovascular depression produced by intravenous anaesthetics in intact rabbits is due to a combination of central and peripheral effects.

Effects of sympathetic nerve stimulation in the presence of a slow parasympathetic secretion in the parotid and submaxillary glands of the rabbit.

Sympathetic secretory responses from the parotid and the submaxillary glands of the rabbit were studied; sympathetic excitation occurred either alone or during a slow parasympathetic background secretion, imitating the resting secretion normally present. The fairly rapid sympathetically evoked flow of saliva from the parotid gland was, in the background secretion, further increased and obtained at low frequencies, which at sympathetic stimulation alone were subthreshold. The effects, which could be repeated with sympathomimetic drugs in a pilocarpine induced secretion, were abolished by alpha and beta-adrenoceptor blockade in combination. The submaxillary gland gave a very scanty secretion on sympathetic excitation, the effects being mediated via beta-adrenoceptors. The responses were not increased in a background secretion but the main effect of sympathetic activation was to retard the salivary flow. The retardation was attributed to vasoconstriction accompanying sympathetic excitation. Eliminating the vasoconstrictor responses, while retaining the sympathetic secretory effects, did not reveal any increase of the sympathetic salivary responses in the submaxillary gland.

Effects of sympathetic nerve stimulation on electrical activity of Auerbach's plexus and intestinal smooth muscle tone.

Effects of sympathetic nerve stimulation on electrical activity of Auerbach's plexus and intestinal smooth muscle tone.

Effect of sympathetic nerve stimulation on cerebral blood flow and on large cerebral arteries of dogs.

HomeCirculation ResearchVol. 41, No. 3Effect of sympathetic nerve stimulation on cerebral blood flow and on large cerebral arteries of dogs. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessAbstractPDF/EPUBEffect of sympathetic nerve stimulation on cerebral blood flow and on large cerebral arteries of dogs. D D Heistad, M L Marcus, S Sandberg and F M Abboud D D HeistadD D Heistad Search for more papers by this author , M L MarcusM L Marcus Search for more papers by this author , S SandbergS Sandberg Search for more papers by this author and F M AbboudF M Abboud Search for more papers by this author Originally published1 Sep 1977https://doi.org/10.1161/01.RES.41.3.342Circulation Research. 1977;41:342–350 Previous Back to top Next FiguresReferencesRelatedDetails September 1, 1977Vol 41, Issue 3Article InformationMetrics Download: 61 Copyright © 1977 by American Heart Associationhttps://doi.org/10.1161/01.RES.41.3.342 Originally publishedSeptember 1, 1977 PDF download

The site and receptors responsible for the inhibition by sympathetic nerves of intestinal smooth muscle and its parasympathetic motor nerves.

1. The effects of three inhibitory stimuli, sympathetic nerve stimulation, noradrenaline (NA) and isoprenaline have been examined on three forms of motor activity in the rabbit colon, the response to pelvic (parasympathetic) nerve stimulation, acetylcholine (ACh) and spontaneous tone.2. The response to pelvic nerve stimulation is most effectively inhibited by sympathetic nerve stimulation, much less effectively by NA and hardly at all by isoprenaline. The sympathetic nerves can inhibit the pelvic response at frequencies of stimulation which do not affect spontaneous tone. The inhibitory effect of sympathetic stimulation, and of NA, on the pelvic response is reduced by phentolamine 5 x 10(-6)M and unaffected by propranolol 5 x 10(-6)M suggesting the effect is mediated via alpha receptors.3. The response to ACh is inhibited by all three stimuli equally. The inhibitory effect of sympathetic nerve stimulation and of isoprenaline is reduced by propranolol 5 x 10(-6)M. The inhibitory effect of NA is also reduced by propranolol but to a lesser extent. Phentolamine 5 x 10(-6)M has a small effect in reducing the inhibitory effect of sympathetic nerve stimulation or of NA. This effect of phentolamine is lost if the participation of motor nerves in the response to ACh is excluded by either tetrodotoxin 10(-7) g/ml. or cold storage for 10-14 days. These results suggest that inhibition of the ACh response takes place mainly at the muscle by activation of beta receptors but that ACh may have a small indirect stimulant action through motor nerves and this is susceptible to inhibition through alpha receptors.4. All three stimuli are equally effective in lowering smooth muscle tone. This inhibitory effect of sympathetic nerve stimulation and of isoprenaline is reduced by propranolol 5 x 10(-6)M and unaffected by phentolamine 5 x 10(-6)M. The inhibitory effect of NA is reduced by propranolol but again is less sensitive to block than the other two inhibitory stimuli. Phentolamine is without effect on the inhibitory action of NA and the combination of phentolamine with propranolol is no more effective than propranolol alone. These results suggest that NA liberated by sympathetic nerves and isoprenaline inhibit myogenic tone in the smooth muscle by an action on beta receptors but the action of NA added to the bath cannot be fully explained in this way.