The complex circumstellar environment of supernova 2023ixf.

The early evolution of a supernova (SN) can reveal information about the environment and the progenitor star. When a star explodes in vacuum, the first photons to escape from its surface appear as a brief, hours-long shock-breakout flare1,2, followed by a cooling phase of emission. However, for stars exploding within a distribution of dense, optically thick circumstellar material (CSM), the first photons escape from the material beyond the stellar edge and the duration of the initial flare can extend to several days, during which the escaping emission indicates photospheric heating3. Early serendipitous observations2,4 that lacked ultraviolet (UV) data were unable to determine whether the early emission is heating or cooling and hence the nature of the early explosion event. Here we report UV spectra of the nearby SN 2023ixf in the galaxy Messier 101 (M101). Using the UV data as well as a comprehensive set of further multiwavelength observations, we temporally resolve the emergence of the explosion shock from a thick medium heated by the SN emission. We derive a reliable bolometric light curve that indicates that the shock breaks out from a dense layer with a radius substantially larger than typical supergiants.

Organization of the sympathetic innervation of the forelimb resistance vessels in the cat.

UNLABELLED: Detailed information on the outflow pathway of sympathetic vasoconstrictor fibers to the upper extremity is lacking. We studied the organization of the sympathetic innervation of the forelimb resistance vessels and of the sinoatrial (SA) node in the decerebrated, artificially respirated cat. The distal portion of sectioned individual rami T1-8 and the sympathetic chain immediately caudal to T8 on the right side were electrically stimulated while the right forelimb perfusion pressure (forelimb perfused at constant flow) and heart rate were recorded. Increases in perfusion pressure were evoked by stimulation of T2-8 (maximal response T7: 55 +/- 2.3 mm Hg). Responses were still evoked by stimulation of the sympathetic chain immediately caudal to T8 (44 +/- 15 mm Hg). Increases in heart rate were evoked by the stimulation of more rostral rami (T1-5; maximal response T3: 55.2 +/- 8 bpm). These vasoconstrictor and cardioacceleratory responses were blocked by the cholinergic antagonists hexamethonium and scopolamine. Sectioning of the vertebral nerve and the T1 ramus abolished the vasoconstrictor response. Stimulation of the vertebral nerve and of the proximal portion of the sectioned T1 ramus increased perfusion pressure (69 +/- 9 and 34 +/- 14 mm Hg, respectively), which was unaffected by ganglionic cholinergic block. These data suggest that forelimb resistance vessel control is subserved by sympathetic preganglionic neurons located mainly in the middle to caudal thoracic spinal segments. Some of the postganglionic axons subserving vasomotor function course through the T1 ramus, in addition to the vertebral nerve. IMPLICATIONS: Forelimb vasculature is controlled by sympathetic preganglionic neurons located in middle to caudal thoracic spinal segments and by postganglionic axons carried in the T1 ramus and vertebral nerve. This helps to provide the anatomical substrate of interruption of sympathetic outflow to the upper extremity produced by major conduction anesthesia of the stellate ganglion or spinal cord.

Synaptic inhibitory effects of edrophonium on sympathetic ganglionic transmission.

PURPOSE: To evaluate the effect of edrophonium on synaptic transmission in the superior cervical ganglion. METHODS: In anaesthetized rats the effect of edrophonium on synaptic transmission was studied in vitro by testing whether it blocks the compound action potential recorded from postganglionic fibres evoked by stimulation of preganglionic axons. The superior cervical ganglion was excised and the cervical sympathetic trunk and internal carotid nerve were used for stimulating and recording, respectively. Drugs superfused included edrophonium (0.1-500 microM), neostigmine (0.1-10 microM), and muscarinic M1 and M2 antagonists pirenzepine and AFDX-116 (200 nM-10 microM), respectively. To evaluate a presynaptic action, the effect of edrophonium on basal and high-K+ (35 mM) evoked release of [3H]ACh from the superior cervical ganglion was studied in vitro. To evaluate a postsynaptic action, edrophonium's effect on postganglionic nerve discharge in response to arterial injection of ACh (100 micrograms) into the superior cervical ganglion was determined in vivo. RESULTS: Edrophonium (10-500 microM) decreased the compound action potential amplitude (ED50 163.5 microM). A decrease was not produced by neostigmine, nor was it reversed by pirenzepine or AFDX-116. Edrophonium blocked postganglionic cell firing in response to exogenously administered ACh. Although edrophonium did not affect basal or high-K+ evoked ACh release, when the evoked increase was calculated as a multiple of the basal release, it caused approximately a 30% (P < 0.005) reduction. CONCLUSIONS: Edrophonium blocks ganglionic cholinergic transmission postsynaptically and, possibly, presynaptically. The mechanism(s) by which this occurs does not appear to involve inhibition of cholinesterase, or activation of M1 or M2 receptor subtypes.

Heart rate changes in cardiac transplant patients and in the denervated cat heart after edrophonium.

PURPOSE: The effect of edrophonium on heart rate in cardiac transplant patients and in an animal model of acute cardiac denervation were studied, to evaluate the functional state of the peripheral parasympathetic pathway following cardiac denervation. METHODS: Edrophonium was studied in patients with normally innervated hearts (controls) and in cardiac transplants. Edrophonium was also studied in vagotomized, beta-blocked cats. In Group I animals, the vagus nerve was not stimulated. In Groups 2 & 3 the right vagus nerve was electrically stimulated to produce approximately 20% and 40% reductions in baseline heart rate, respectively. RESULTS: Maximum heart rate reduction in transplants (7.3 +/- 0.8 beats.min-1 with 0.6 +/- 0.08 mg.kg-1) was less than in controls (13.3 +/- 1.6 beats.min-1 with 0.4 + 0.05 mg.kg-1, P < 0.01). In Group I animals heart rate decreased maximally by 20.9 +/- 2.5 beats.min-1 with 9.0 +/- 1.9 mg.kg-1. In Groups 2 and 3, with doses < 1.5 mg.kg-1, reductions in heart rate were greater than in Group I and maximum reductions were obtained with lower doses (Group 2: maximum reduction by 20.3 +/- 2.8 beats.min-1 with 1.3 +/- 0.1 mg.kg-1; Group 3:22.6 +/- 4.0 beats.min-1 with 0.8 +/- 0.2 mg.kg-1, P < 0.001). Doses > 1.5 mg.kg-1 in Groups 2 and 3 produced increases in heart rate. CONCLUSION: Edrophonium produced bradycardia in cardiac transplants suggesting spontaneous release of acetylcholine from parasympathetic postganglionic neurons in the transplanted heart. The magnitude of the bradycardia was less in transplant than in control patients. Findings from animal studies suggest that the reduction in transplants can be attributed to diminution or absence of tonic cardiac parasympathetic drive. At high doses, edrophonium may interfere with parasympathetic neuron activation.

Bradycardia produced by pyridostigmine and physostigmine.

PURPOSE: The bradycardia produced by pyridostigmine and physostigmine in an animal model of acute cardiac denervation was examined according to its relation to cholinesterase inhibition and sensitivity to block by cholinergic receptor antagonists. METHODS: Cats were anaesthetised, vagotomised and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. Nicotinic and muscarinic M1 receptors were blocked with hexamethonium and pirenzepine, respectively. M2 receptors were blocked with gallamine, pancuronium and AFDX-116. RESULTS: With pyridostigmine and physostigmine the dose-response relationship for the decrease in heart rate (ED50 1.05 +/- 0.25 and 0.198 +/- 0.03 mg.kg-1, respectively) was shifted to the right of that for the inhibition of cholinesterase activity (ED50 0.094 +/- 0.03 and 0.032 +/- 0.01 mg.kg-1, respectively). The decrease in cholinesterase activity reached a plateau at a cumulative dose of 0.56 +/- 0.08 and 0.32 +/- 0.08 mg.kg-1, respectively. In contrast, there did not appear to be a plateau in the bradycardic effect. The bradycardia produced by pyridostigmine and physostigmine was blocked by hexamethonium (ED50 10 +/- 1.3 and 15.3 +/- 2.4 mg.kg-1, respectively), pirenzepine (ED50 68 +/- 16 and 138 +/- 32 micrograms.kg-1, respectively), gallamine (56 +/- 11 and 67 +/- 17 micrograms.kg-1, respectively), pancuronium (32 +/- 10 and 30 +/- 4 micrograms.kg-1, respectively), and AFDX-116 (31 +/- 4 and 28 +/- 4 micrograms.kg-1, respectively). CONCLUSION: The bradycardia produced by reversible anticholinesterase drugs containing a carbamyl group is not clearly related to the degree of cholinesterase activity, and has a low sensitivity to nicotinic and muscarinic M1 and a high sensitivity to muscarinic M2 receptor antagonists.

Different properties of the bradycardia produced by neostigmine and edrophonium in the cat.

PURPOSE: The bradycardia produced by neostigmine and edrophonium was examined according to its relation to cholinesterase inhibition and to its sensitivity to block by muscarinic receptor antagonists. For comparison, the ability of muscarinic antagonists to block the bradycardia produced by electrical stimulation of the vagus nerve was determined. METHODS: Cats were anaesthetized, vagotomized and propranolol-treated. Heart rate was continuously recorded. Erythrocyte cholinesterase activity of arterial blood was measured using a radiometric technique. The right vagus nerve was isolated for electrical stimulation. The muscarinic antagonists used were atropine, glycopyrrolate, pancuronium, gallamine, and AFDX-116. RESULTS: Neostigmine produced a dose-dependent decrease in cholinesterase activity which reached a plateau at a cumulative dose of 0.16 mg.kg-1 (ED50 0.009 +/- 0.003 mg.kg-1). Neostigmine produced a dose-dependent decrease in heart rate with the dose-response relationship (ED50 0.1 +/- 0.01 mg.kg-1; P = 0.0006) shifted to the right of that for the inhibition of cholinesterase activity. In contrast to the anticholinesterase effect, the bradycardic effect did not reach a plateau and continued to increase even at doses at which the cholinesterase inhibition was maximal. The maximal decrease in heart rate when the heart was still in sinus rhythm was by 81 +/- 13 bpm (49 +/- 7% of baseline), which was produced by a dose of 0.32 mg.kg-1. Edrophonium produced dose-dependent decreases in cholinesterase activity and heart rate, which were highly correlated (correlation coefficient r = 0.99, P < 0.0001). The ED50 of the reduction in heart rate (0.9 +/- 0.18 mg.kg-1) and cholinesterase activity (0.89 +/- 0.12 mg.kg-1) produced by edrophonium were similar. Moreover, the reduction in heart rate and cholinesterase activity produced by edrophonium reached a plateau at the same dose (6.4 mg.kg-1). At this dose, heart rate decreased by 22 +/- 2 bpm (14.6 +/- 0.9% of baseline). Compared to the bradycardia produced by stimulation of the vagus nerve, that produced by neostigmine was blocked by muscarinic antagonists at significantly lower doses while that produced by edrophonium was blocked at similar doses. CONCLUSIONS: The neostigmine-induced bradycardia is poorly correlated with cholinesterase inhibition compared to that produced by edrophonium, and has a higher sensitivity to muscarinic receptor antagonists compared to that produced by edrophonium or vagus nerve stimulation. These results are consistent with the hypothesis that the neostigmine-induced bradycardia is, in part, the result of neostigmine directly activating cholinergic receptors within the cardiac parasympathetic pathway. The bradycardia produced by edrophonium may be accounted for solely by an anticholinesterase action.

Neostigmine decreases heart rate in heart transplant patients.

PURPOSE: This study evaluated the effect of neostigmine on heart rate in cardiac transplant patients. METHODS: Neostigmine (2.5-50 micrograms.kg-1) was administered to ASA 1 or 2 patients with normally innervated hearts (controls), and to patients who had undergone recent (< six months before study) or remote (> six months before study) cardiac transplantation. RESULTS: Baseline heart rate was 66 +/- 3 beats.min-1 in controls (n = 10, mean +/- SEM), which was slower than that observed in recently (95 +/- 4 beats.min-1, n = 15, P < 0.001) and in remotely (88 +/- 3 beats.min-1, n = 16, P < 0.001) transplanted patients. Neostigmine produced a dose-dependent decrease in heart rate in all patients. Controls were the most sensitive to neostigmine, with a 10% decrease in heart rate produced by an estimated dose of 5.0 +/- 1.0 micrograms.kg-1. The recently transplanted group was the least sensitive, with the maximum dose producing only an 8.3 +/- 0.9% reduction. The response to neostigmine of the remotely transplanted patients was variable. The estimated dose to produce a 10% decrease in heart rate in this group was 24 +/- 6 micrograms.kg-1 which was greater than that for controls (P = 0.008). Administration of atropine (1.2 mg) reversed the neostigmine-induced bradycardia in all three groups. Reversal of the bradycardia consisted of a transient peak increase in heart rate in controls to 145 +/- 6% of baseline, a value which was greater than that observed in recent (103 +/- 1%, P < 0.001) and in remote (109 +/- 3%, P < 0.001) transplants. CONCLUSIONS: Neostigmine produces a dose-dependent bradycardia in heart transplant patients. Some remotely transplanted patients may be particularly sensitive to the bradycardic effects of neostigmine.

Neostigmine-induced bradycardia following recent vs remote cardiac transplantation in the same patient.

PURPOSE: This report describes the effects of neostigmine on heart rate in the same patient following recent and remote cardiac transplantation. CLINICAL FEATURES: Eighty-six months following the first transplant, neostigmine 5.0 micrograms.kg-1 i.v. produced a 10% reduction in heart rate which was reversed by atropine 1.2 mg. For 24 months prior to this initial study, the patient experienced angina, suggesting cardiac afferent reinnervation. Three months after the second heart transplant, a second study showed that a six-fold increase in the dose of neostigmine, 30.0 micrograms.kg-1, only produced a 3.5% reduction in heart rate which was reversed by atropine 1.2 mg. CONCLUSIONS: These observations indicate that neostigmine produces bradycardia following cardiac transplantation, and suggest that a greater response may be observed in remotely than in recently transplanted patients.

Characteristics of sympathetic preganglionic neurones in the lumbar spinal cord of the cat.

1. In anaesthetized cats extracellular recordings have been made from antidromically identified sympathetic preganglionic neurones, located in the 2nd and 3rd lumbar segments, with axons projecting into the left lumbar sympathetic chain beyond the L4 ganglion. Sympathetic preganglionic neurones have been characterized with respect to: axonal conduction velocities, firing patterns in relation to ECG and phrenic nerve activity, responses to noxious stimuli applied to the ipsilateral hindlimb and ionophoretically applied 5-HT. 2. Two hundred and ninety-seven sympathetic preganglionic neurones were studied. Their axonal conduction velocities (0.5-13.9 m/s) were in the B and C fibre range. Sixty-eight had on-going activity and the remainder were quiescent. Of the 229 quiescent sympathetic preganglionic neurons, 111 were activated by the ionophoretic application of glutamate. 3. Of the 100 sympathetic preganglionic neurones analysed for an ECG-related pattern of discharge, forty-nine had no, and fifty-one had an ECG-related pattern of discharge. Both sympathetic preganglionic neurones with on-going activity and glutamate activated cells exhibited ECG-related patterns of discharge. 4. Only six of fifty sympathetic preganglionic neurones had a respiratory-related activity pattern. Three had maximal discharge during expiration and three during inspiration. 5. Forty-one sympathetic preganglionic neurones were examined for their response to noxious stimulation of the ipsilateral hindlimb. Ten had their activity decreased (seven glutamate-activated, three with on-going activity), seven had their activity increased (four glutamate-activated and three with on-going activity) and twenty-four were unaffected. These results demonstrate that both sympathetic preganglionic neurones with on-going activity and glutamate-activated neurones can be influenced by noxious input. Ten sympathetic preganglionic neurones had properties consistent with them having a skin vasoconstrictor function and three with muscle vasoconstrictor function. 6. Ionophoretic application of 5-HT in the vicinity of fifty-one sympathetic preganglionic neurones caused increases in the discharge of 53%, decreases in the firing of 12% and did not affect the discharge of 35%. 7. Sympathetic preganglionic neurones which had excitatory responses to 5-HT showed only decreased discharge or no response to noxious stimulation of the ipsilateral hindlimb. Conversely, sympathetic preganglionic neurones which had discharge decreased by 5-HT had primarily excitatory responses to noxious inputs. 8. It is concluded that lumbar sympathetic preganglionic neurones consist of a heterogeneous population with respect to their physiological properties and their responses to ionophoretically applied 5-HT: both may be related to function.

[3H]prazosin binding in the intermediolateral cell column and the effects of iontophoresed methoxamine on sympathetic preganglionic neuronal activity in the anaesthetized cat and rat.

The autoradiographic localization of [3H]prazosin (alpha 1-adrenoceptor ligand) binding sites was determined in cat spinal cord sections. High levels of [3H]prazosin binding were found in the intermediolateral cell column (IML) at thoracic and lumbar levels. The iontophoresis of the alpha 1-adrenoceptor agonist methoxamine onto sympathetic preganglionic neurones (SPNs) in anaesthetized cats and rats caused excitation of 8 cat SPNs and 13 rat SPNs. These results suggest an excitatory role for some of the catecholaminergic innervation of the IML.

Effects of spinal cord transection on sympathetic discharge in decerebrate-unanesthetized cats.

Previous experiments in our laboratory have shown that discharge of splenic, mesenteric, and splanchnic nerves is well maintained after spinal cord transection in chloralose-anesthetized cats (8, 9, 11). The primary purpose of this investigation was to determine if maintained sympathetic discharge could be observed after spinal transection in the absence of chloralose anesthesia. In cats anesthetized with alphaxalone-alphadolone, changes in splanchnic discharge, blood pressure, and heart rate caused by decerebration and removal of the forebrain were observed. This procedure decreased blood pressure, increased heart rate, and had no immediate effect on sympathetic discharge or its rhythm (assessed by power density spectral analysis). One hour after decerebration and termination of anesthesia, splanchnic discharge had increased by approximately 36%. Next, effects of spinal cord transection on discharge of splanchnic, mesenteric, and renal nerves were observed in the decerebrate-unanesthetized cats. Splanchnic discharge decreased by 50%, mesenteric nerve discharge was unchanged, and renal nerve discharge decreased by 97%. Therefore, splanchnic nerve discharge was not as well maintained in decerebrate-unanesthetized cats as it had been in chloralose-anesthetized animals, and the remaining splanchnic discharge appeared to affect mesenteric nerves preferentially. Finally, spectral analysis of the splanchnic discharge demonstrated that before cord transection, most of the signal was in the 0- to 6-Hz frequency range, whereas after transection the proportion of signal in this frequency range was significantly reduced and the proportion in higher frequencies (7-25 Hz) was significantly increased. This loss of low-frequency rhythmicity is consistent with findings in our previous studies in chloralose-anesthetized cats.

Tonic influences from the rostral medulla affect sympathetic nerves differentially.

Tonically active neurons in the rostral ventrolateral medulla (RVLM) that project to the autonomic regions of the spinal cord are essential for maintenance of arterial blood pressure at normal levels. Microinjection of glycine into the RVLM in anesthetized cats to inhibit the tonic discharge of these neurons caused variable initial responses in renal and mesenteric nerve discharge and arterial blood pressure. These initial responses were consistently followed by more prolonged decreases in renal and mesenteric nerve discharge and decreases in arterial blood pressure. The tonic influences of neurons in the RVLM were found to be distributed unequally to sympathetic nerves because activity of renal nerves was decreased significantly more than that of mesenteric nerves. The variable nerve and cardiovascular responses during the first 1-3 min after glycine injection were not solely due to loading or unloading of baroreceptors because similar initial responses were seen in vagotomized and sinoaortic denervated cats. Additionally, when muscimol was microinjected into the same sites, only consistent and prolonged decreases in nerve discharge and blood pressure occurred. The inhibitory actions of muscimol on RVLM neurons caused significantly greater decreases in renal than mesenteric nerve activity. Together, these findings demonstrate that the tonic discharge of neurons in the RVLM has unequal influences on renal and mesenteric nerves.

Characteristics of ongoing and reflex discharge of renal postganglionic neurons.

Characteristics of basal and reflex firing of single renal postganglionic fibers are reviewed to ascertain whether subpopulations of renal neurons can be distinguished. Moreover, characteristics of renal neurons are contrasted with those of sympathetic neurons innervating vascular and nonvascular tissues of the spleen and small intestine. Attempts to distinguish functional subtypes of renal neurons based on their responses to excitatory or inhibitory influences led to no clear conclusions. Responses of the renal population of neurons differed from those of the splenic and mesenteric populations of postganglionic neurons. Our findings provided no concrete answers about the neural mechanisms by which different functions of the kidney may be regulated selectively. This question continues to require careful and insightful investigation.

Ventrolateral medullary neurones: effects on magnitude and rhythm of discharge of mesenteric and renal nerves in cats.

1. Discharge of whole mesenteric and renal nerves was recorded in eighteen chloralose-anaesthetized, artificially respired cats. 2. Inhibition of tonic activity of neurones within the rostral ventrolateral medulla (RVLM blockade) by bilateral application of glycine caused significant reductions in discharge of renal and mesenteric nerves, arterial blood pressure and heart rate. The decrease in discharge of renal nerves was significantly greater than that of mesenteric nerves. 3. During the response to glycine application, the spinal cord was transected at the first cervical segment. The magnitude of renal nerve discharge after transection was not different from that during blockade of the RVLM. On the other hand, mesenteric nerve activity increased following spinal cord transection, returning to control levels. 4. Power spectral analysis revealed that mesenteric and renal nerves discharged with periodicities ranging from 1 to 6 Hz. Application of glycine to the RVLM reduced the slow rhythm in firing of mesenteric and renal nerves similarly. Transection of the spinal cord resulted in further reduction in the rhythmicity in discharge of both nerves. 5. The results indicate that excitatory drive from the RVLM is crucial for the maintenance of on-going discharge of renal, but not of mesenteric nerves. However, such inputs are apparently essential to maintain the slow rhythm in firing of both nerves.

Multi- and single-fibre mesenteric and renal sympathetic responses to chemical stimulation of intestinal receptors in cats.

1. In cats anaesthetized with alpha-chloralose and artificially respired, stimulation of intestinal receptors with bradykinin caused greater reflex excitation of mesenteric than of renal efferent multifibre nerve activity and significant pressor responses. 2. Activity of all nerve bundles used in this study was inhibited by stimulation of pressoreceptors. Increases in systemic arterial pressure caused inhibition of activity of renal nerves which was significantly greater than that of mesenteric nerves. 3. Spinal transection caused significant decreases in tonic renal nerve activity without altering the ongoing discharge rate of mesenteric nerves. Stimulation of intestinal receptors in spinal cats still caused significant increases is discharge of mesenteric and renal nerves, indicating that this reflex contains a spinal component. 4. Recordings of activity of individual fibres within mesenteric (21) and renal (23) nerves provided information regarding the basis for the multifibre responses to stimulation of intestinal receptors. The same proportion of fibres from both nerves was excited, but the increase in activity of mesenteric fibres was significantly greater than that of renal fibres. 5. Mesenteric fibres could be classified into two groups, based on their sensitivity to pressoreceptor influences. Fibres that exhibited pressoreceptor-independent discharge had the greatest responses to stimulation of intestinal receptors. 6. Following spinal transection the majority of mesenteric fibres continued to fire, whereas most renal fibres became quiescent. 7. The non-uniform pattern of neuronal excitation to chemical stimulation of intestinal receptors was manifest after spinal transection, demonstrating that exclusively spinal pathways can mediate this differential response pattern. 8. These results support the hypothesis that viscero-sympathetic reflexes may be organized to cause preferential excitation of neural activity directed to the organ from which the reflex originates.

Capsaicin treatment attenuates the reflex excitation of sympathetic activity caused by chemical stimulation of intestinal afferent nerves.

Sympathetic reflexes elicited by stimulation of visceral receptors have been well investigated, but the central neurotransmitters mediating these reflexes are largely unknown. Therefore, experiments were done to evaluate the role of substance P in the central transmission of a sympathoexcitatory reflex elicited by stimulation of intestinal receptors. Activity of mesenteric and renal nerves was recorded electrophysiologically in chloralose/urethane-anesthetized rats. Stimulation of intestinal receptors by serosal application of 0.5-1.0 microgram bradykinin increased mesenteric nerve activity by 100 +/- 21%, renal nerve discharge by 33 +/- 9%, and systemic arterial pressure by 10 mm Hg. Chronic capsaicin treatment (cumulative dose 950 mg/kg) caused a 52% depletion of substance P-like immunoreactivity from dorsal root ganglia and a significant attenuation of these reflexes. Mesenteric nerve activity increased by 48 +/- 6% in the capsaicin-treated rats. Bradykinin did not cause significant changes in renal nerve activity or systemic arterial pressure in these rats. The excitation of mesenteric nerve activity was significantly greater than the increase in renal nerve activity int he untreated and capsaicin-treated rats; capsaicin treatment affected responses of both nerves similarly. Capsaicin treatment did not have generalized effects on sympathetic reflexes, as mesenteric and renal nerve activities were decreased by baroreceptor activation similarly in the untreated and capsaicin-treated rats. These results suggest that the central transmission of the reflex response to intestinal receptor stimulation is mediated in part by substance P or other capsaicin-sensitive peptides.

Central actions of angiotensin II oppose baroreceptor-induced sympathoinhibition.

Angiotensin II causes increased arterial pressure which may be mediated, in part, by effects on central sympathetic neurons or by interference with central or peripheral components of the baroreceptor reflex. This investigation was undertaken to determine actions of angiotensin II on sympathetic splanchnic efferent and carotid sinus afferent activity in chloralose-anesthetized cats. Neural responses during increases in arterial pressure caused by intracarotid or intravenous administration of angiotensin II were compared with responses to equivalent increases in arterial pressure induced by intravenously injected dextran or phenylephrine. Intracarotid injections of angiotensin II caused variable splanchnic sympathetic responses consisting of increased, decreased, or unchanged activity. In contrast, intravenous infusions of dextran or phenylephrine consistently inhibited sympathetic activity. Carotid sinus afferent activity was increased similarly by intracarotid angiotensin II and intravenous dextran or phenylephrine. Sympathetic and baroreceptor afferent responses to intravenously injected angiotensin II were not significantly different from responses to dextran or phenylephrine. These data demonstrate that angiotensin II can act centrally to excite sympathetic outflow or to interfere with inhibitory influences of arterial baroreceptors.