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PubMed1984

Facilitation of ganglionic response to bethanechol by repetitive stimulation of the preganglionic nerve.

Repetitive stimulation of the preganglionic nerve of the rat superior cervical sympathetic ganglion potentiates the amplitude of asynchronous firing elicited by the muscarinic agonist, bethanechol. The amplitude of stimulus-induced facilitation is not related to frequency of stimulation and occurs with a stimulation frequency of 10 Hz or greater. Facilitation, but not the asynchronous firing is reduced by lowering the temperature of the bathing solution. Dibutryl cyclic adenosine monophosphate and theophylline had no effect on asynchronous firing but reduced stimulus-induced facilitation. Neither dibutryl cyclic guanosine monophosphate up to 1 mM nor nitroprusside had any significant effect on bethanechol-induced asynchronous firing or stimulus-induced facilitation. Tetraethylammonium caused a 200% increase in stimulus-induced facilitation. Acetylcholine, in a concentration that elicited maximum nicotinic firing, had no effect on the magnitude of bethanechol-induced asynchronous firing. Increased Ca++, Mg++ or Mn++ reduced both asynchronous firing and stimulus-induced facilitation. It is concluded that facilitation is a result of transmitter release, possibly not acetylcholine.

Acetylcholine↗
PubMed1997

Regional variation in the effects of nicotine on catecholamine overflow in rat brain.

The effects of acute, repeated intermittent and continuous administration of nicotine on the overflow of noradrenaline in the ventral hippocampus and dopamine in the nucleus accumbens and striatum have been studied. Daily injections of nicotine (0.4 mg/kg(-1) for 5 days) enhanced noradrenaline and dopamine overflow in the ventral hippocampus and nucleus accumbens respectively (P < 0.01 and P < 0.05) but not dopamine in the striatum in response to a nicotine challenge. The responses in the ventral hippocampus and nucleus accumbens were attenuated (P < 0.01) by the constant infusion of nicotine at a dose of 1 mg kg(-1) per day; the dopamine response in the striatum required a higher dose (4 mg kg(-1) per day) before desensitisation was observed. The data suggest that the dopamine projections to the striatum are less sensitive to both stimulation and desensitisation by nicotine than the catecholamine projections to the ventral hippocampus and nucleus accumbens.

Animals↗
PubMed1991

Cholinergic activation of a population of corneal afferent nerves.

The in vivo rabbit cornea was used to investigate the effect of acetylcholine on "free" nerve endings from A-delta and C-fibers in the long-ciliary (corneal) nerve. Extracellular electrophysiologic recordings were obtained from 67 corneal nerve fibers. Acetylcholine in concentrations of 10(-5) to 10(-3) M stimulated a specific population of these corneal afferents that were not activated by mechanical or thermal stimuli. Their conduction velocity was determined to be 1.14 +/- 0.34 m/s (mean +/- SD). The other three previously characterized corneal nerve populations (mechanical, mechano-heat, and cold) were not stimulated by the cholinergic agonists or antagonists. Acetylcholine sensitive afferents were also stimulated by carbachol (10(-5) to 10(-3) M) and nicotine (10(-6) to 10(-4) M) but not by bethanecol (10(-5) to 10(-3) M). Acetylcholine-induced activity was abolished by d-tubocurare (10(-4) M) and kappa-bungarotoxin (10(-6) M). The cAMP analog 8-bromoadenosine 3'5'-cyclic monophosphate activated the same population of chemosensitive C-fibers as acetylcholine. It is concluded that a specific population of C-fiber afferents exist in the rabbit cornea which are stimulated by acetylcholine possibly acting via a neuronal nicotinic receptor. Physiologically, these nerves may be involved in the production of pain following tissue injury or ischemia.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMedDate not supplied

Directional preponderance of nystagmus and excitement of autonomic nervous system.

Since autonomic nervous dysfunction is the most common predetermining factor of vertigo, the functional relationship between these two systems was studied using the rabbits. Cervical sympathectomy or electric stimulation of the superior cervical ganglion were given to the animal on one hand, and modulation of the blood pressure and electric stimulation of the hypothalamus were done, on the other. These manoeuvres rarely induced asymmetry of the vestibulo-ocular reflex (VOR). However, when other pairs of conditions were combined, such as cervical ganglion stimulation and BP modulation, or sympathectomy and hypothalamic stimulation, directional preponderance of VOR became prominent. This experimental model seems to explain the mechanism of vertigo observed.

Animals↗
PubMed1982

Evidence for increased release of prostaglandins of E-type in response to orthodromic stimulation in the guinea-pig superior cervical ganglion.

Prostaglandins of the E type (PGEs) stimulate cyclic adenosine 3',5'-monophosphate (cAMP) biosynthesis both in isolated preparations of rat, guinea-pig and rabbit superior cervical ganglia (SCG) and in calf SCG slices. Electrical stimulation of preganglionic nerve fibers of the guinea-pig SCG remarkably increased PGE release and cAMP biosynthesis. These effects were blocked by reducing the Ca2+ to Mg2+ ratio in the incubation medium. Atropine (1 microM) and phentolamine (10 microM) inhibited PGE biosynthesis and significantly reduced cAMP levels.

Animals↗
PubMedDate not supplied

Circuits and projections of cat stellate ganglion.

BACKGROUND: Although connections of stellate ganglion (SG) have been widely explored, some features of pathways and projections remain unknown, such as the source and fate of preganglionic axons present in output branches, including both synaptically interrupted and traversing pathways as well as axon composition (efferent and afferent) of these output nerves. METHODS: Circuits and central projections of cat SG were investigated using horseradish peroxidase (HRP) tracer and electrophysiologic techniques including stimulation of ganglionic branches during recording of genesis of compound action potentials in other nerves or centrally evoked responses. RESULTS: All branches of SG including vertebral nerve are mixed, i.e., they contain axons that synapse in the periphery or traverse ganglia. A novel synaptically interrupted pathway bi-directionally coursing along subclavian branches and inferior cardiac nerve was identified. Preganglionic axons traversing stellate ganglion course in communicating branch to vagus nerve and to inferior cardiac nerve, a small number of these preganglionic axons traversing stellate ganglion reach cervical sympathetic trunk via subclavian branches. For the first time, a small number of preganglionic traversing pathways were also detected in vertebral nerve. Afferent axons with somata located in C8-T7 dorsal root ganglia, identified in all branches of SG, projected centrally to neurons in thalamus and somatosensory zones of cerebral cortex and coincided with afferent projections of brachial plexus. CONCLUSIONS: Present data contribute to the morphologic description of autonomic regulation of thoracic organs, including centrally independent peripheral autonomic axon reflexes.

Animals↗
PubMedDate not supplied

Variability of responses to sinusoidal modulation.

Many studies of visual neurons make use of stimuli that are sinusoidally modulated in time, and take as the response the fundamental Fourier component of the firing. This is a study of the variability of the fundamental sinusoidal components. A theoretical analysis shows that the variance of sinusoidal components should be nearly independent of their amplitudes; this is expected despite the observation that variance of firing rate increases with increasing firing rate. However, this result applies only to the variance of the complex amplitude, defined as the complex Fourier amplitude in response to each stimulus cycle. This variance is called the complex variance. The variance of the scalar amplitude, which is simply the amplitude in response to each stimulus cycle disregarding phase (scalar variance) is expected to shrink by a factor of up to 2 1/3 as the response magnitude approaches zero. If the relationship between variance of rate and rate is linear, complex variance should be independent of amplitude. If the relationship between variance of rate and rate is characterized by a compressive nonlinearity (as has been observed), the complex variance should very slightly decrease with increased amplitude, despite the main trend of increased variance of rate with increased rate. Data from cat ganglion cells stimulated with sinusoidally modulated lights of various contrasts agree with the theory, although some individual cases show trends that may be indicative of nonlinearity in the relationship between variance of rate and rate.

Animals↗
PubMed1999

Effects of nicotine gum on coronary vasomotor responses during sympathetic stimulation in patients with coronary artery stenosis.

Smoking-cessation rates may be improved by nicotine-replacement therapy that reduces withdrawal symptoms. However, nicotine may have adverse effects on coronary circulation. The purpose of this study was to examine the short-term effects of nicotine gum chewing on the dimensions of coronary arteries of patients with coronary artery disease and on the response of coronary vessels to sympathetic stimulation caused by the cold pressor test. In 17 patients who were past chronic cigarette smokers, cross-sectional areas of 32 coronary artery stenoses and 32 adjacent apparently normal segments were measured by using quantitative coronary angiography at baseline and after a cold pressor test before and after nicotine gum chewing. The cold pressor test produces an increase in arterial pressure without any change in heart rate. These changes were similar before and after nicotine gum. Before nicotine gum, the cross-sectional area of coronary stenoses and apparently normal segments was significantly and similarly reduced during the cold pressor test (-11+/-12% and -11+/-12%, respectively; both p values <0.0001 vs. baseline). After nicotine gum, baseline cross-sectional area was not modified, and response to the cold pressor test was similar to that observed before nicotine gum (-11+/-18% and -12+/-12%, respectively; both p values <0.0001 vs. baseline). In conclusion, nicotine-replacement therapy by using nicotine gum does not reduce the surface area of normal and diseased coronary segments and does not enhance the constricting effect of sympathetic stimulation produced by the cold pressor test. Thus nicotine gum may be considered a relatively safe drug in patients who need nicotine-replacement therapy to stop smoking.

Administration, Oral↗
PubMed1997

Inhibitory effect of capsaicin on detrusor contractility: further study in the presence of ganglionic blocker and neurokinin receptor antagonist in the rat urinary bladder.

In order to understand the mechanisms by which capsaicin at high concentrations affects the micturition reflex and detrusor contractility, in vivo and in vitro whole bladder studies were conducted using ganglionic blockers and a neurokinin receptor antagonist. Thirty-eight adult rats were divided into control (normal saline cystometry) and experimental (1,000 microM capsaicin cystometry) groups. Both groups were subdivided to receive pretreatment with intravesical hexamethonium, perivesical hexamethonium, or intravesical spantide ([D-Arg1, D-Trp7,9, Leu11]-substance P). After in vivo cystometry, the bladders were removed and in vitro whole bladder contractility studies using electrical field stimulation as well as bethanechol and KCl stimulations were performed. In the bladders pretreated with perivesical hexamethonium, the amplitudes of contractions and in vitro detrusor contractility under electrical stimulation were decreased. Other bladder preparations showed no significant differences from the controls. However, when 1,000 microM capsaicin was infused into the bladders, both control and experimental bladders showed an initial excitation and a final inhibition with an elevated basal intravesical pressure and retention. Capsaicin at 100 microM did not have this effect. The results of this study conclude that blockage of perivesical ganglia or neurokinin receptors in the submucosa did not influence the depressant effects of 1,000 microM capsaicin on the micturition reflex and detrusor contractility in rats. Nonspecific toxic effects on detrusor muscle or nerves is likely when intravesical high-concentration capsaicin is administered.

Administration, Intravesical↗
PubMed1992

Effects of dopaminergic and noradrenergic mechanisms on the neuronal activity of the isolated pineal organ of the trout, Oncorhynchus mykiss.

The effects of exogenous applied catecholamines on the neuronal activity of ganglion cells of the luminance type (achromatic cells) were investigated in the photosensitive pineal organ of the trout, Oncorhynchus mykiss. Extracellular recordings were performed on neurons of the superfused isolated pineal organ. Addition of dopamine to the superfusion medium increased the spontaneous activity of more than 60% of the achromatic neurons (n = 25). The D1-dopamine antagonist SCH-23390 and D2-dopamine antagonist spiperone reversed the dopamine-induced stimulation of ganglion cells and inhibited their maintained activity, which suggests that dopamine acts via both D1- and D2-receptors. Norepinephrine, the beta-adrenergic agonist isoproterenol, and DOPA enhanced the spontaneous activity of most of the ganglion cells, whereas the beta-antagonist propranolol depressed the discharge rate and reversed the action of isoproterenol. This suggests that catecholamines might play a modulatory role in the regulation of the neural activity of pineal luminance neurons.

Animals↗
PubMed1996

The reversal of experimental hemorrhagic shock induced by nicotine and dimethylphenylpiperazinium is adrenal-dependent.

In a rat model of volume-controlled hemorrhagic shock causing the death of all control animals within 30 min, the intravenous injection of either nicotine (50 micrograms/kg) or dimethylphenylpiperazinium (DMPP) (0.5 micrograms/kg) produced a rapid and sustained reversal of the shock condition, with 100% survival 2 h after treatment. Bilateral adrenalectomy completely prevented the anti-shock effect of the two drugs, even though administered at higher doses (150 micrograms/kg in the case of nicotine; 10 micrograms/kg in the case of DMPP). It is concluded that stimulation of adrenaline release plays a fundamental role in the mechanism of action of nicotine- and DMPP-induced shock reversal.

Adrenal Glands↗
PubMed2006

Nicotine treatment induces expression of matrix metalloproteinases in human osteoblastic Saos-2 cells.

Tobacco smoking is an important risk factor for the development of severe periodontitis. Recently, we showed that nicotine affected mineralized nodule formation, and that nicotine and lipopolysaccharide stimulated the formation of osteoclast-like cells by increasing production of macrophage colony-stimulating factor (M-CSF) and prostaglandin E2 (PGE2) by human osteoblastic Saos-2 cells. In the present study, we examined the effects of nicotine on the expression of matrix metalloproteinases (MMPs), tissue inhibitors of matrix metalloproteinases (TIMPs), the plasminogen activation system including the component of tissue-type plasminogen activator (tPA), urokinase-type PA (uPA), and PA inhibitor type 1 (PAI-1), alpha7 nicotine receptor, and c-fos. We also examined the effect of the nicotine antagonist D-tubocurarine on nicotine-induced expression of MMP-1. Gene expression was examined using real-time polymerase chain reaction (PCR) to estimate mRNA levels. In addition, expression of the MMP, TIMP, uPA, tPA, and PAI-1 proteins was determined by Western blotting analysis. Nicotine treatment caused expression of MMP-1, 2, 3, and 13, but not MMP-14, to increase significantly after 5 or 10 d of culture; MMP-14 expression did not change through day 14. Enhancement of MMP-1 expression by nicotine treatment was eliminated by simultaneous treatment with D-tubocurarine. In the presence of nicotine, expression of uPA, PAI-1, or TIMP-1, 2, 3, or 4 did not change over 14 d of culture, whereas expression of tPA increased significantly by day 7. Nicotine also increased expression of the alpha7 nicotine receptor and c-fos genes. These results suggest that nicotine stimulates bone matrix turnover by increasing production of tPA and MMP-1, 2, 3, and 13, thereby tipping the balance between bone matrix formation and resorption toward the latter process.

Cell Line, Tumor↗
PubMed2005

Stimulated release of tissue plasminogen activator from artery wall sympathetic nerves: implications for stress-associated wall damage.

Recurrent stress is clinically associated with early onset hypertension and coronary artery disease. A mechanism linking emotion to pathogenic remodeling of the artery wall has not been identified. Stress stimulates acute regulated release of tissue plasminogen activator (t-PA) into the circulation, which is presently attributed to the vascular endothelium. Sympathetic neurons also synthesize t-PA and axonally transport it to the arterial smooth muscle. Unlike release by the endothelium, a stress-stimulated sympathetic discharge would potentially accelerate degradation of the wall matrix by plasmin. To assess whether sympathetic axons are the principal source of acute stress-induced arterial release of t-PA, we compared the output from small densely innervated and large sparsely innervated isolated artery segments before and after sympathetic stimulation, and after ablations. Following phenylephrine infusion densely-innervated microvessels in uveal eyecups were released over 60-fold greater amounts of active t-PA per milligram than the sparsely innervated aorta; and ten-fold more than carotid artery segments. Mesenteric artery release was 4.8-fold greater than release by the carotid artery. In vivo, uveal release of t-PA increased more than three-fold within one minute following superior cervical sympathetic ganglion electrical stimulation, and after phenylephrine, or nicotine infusions of the anterior chamber. Circulating levels of t-PA fell 70% following chemical sympathectomy. We propose that sympathetic nerves are the primary source of stress-induced release of t-PA into and from the densely innervated resistance arteries and arterioles, where dysregulated plasmin-induced proteolysis could damage the wall matrix.

Animals↗
PubMed1989

Secretory and radioligand binding studies on muscarinic receptors in bovine and feline chromaffin cells.

1. Muscarinic agonists enhanced catecholamine release from perfused cat adrenal glands with the following relative order of potencies: methacholine greater than oxotremorine greater than McN-A-343 greater than pilocarpine greater than bethanechol greater than muscarine. Because a continuous online electrochemical detection system was used to monitor catecholamine release, this sequence could be obtained at concentrations much lower (1-10 microM) and during much shorter stimulation times (3-30 s) than in previous reports. 2. All muscarinic agonists used secreted adrenaline preferentially over noradrenaline. Methacholine evoked a sustained, non-desensitizing response in the cat adrenal, which declined to basal levels of secretion immediately after Ca2+ removal: upon Ca2+ restoration secretion was restored to the previous plateau. 3. In addition to evoking a direct secretory response, low concentrations of methacholine, pilocarpine, bethanechol or muscarine clearly potentiated cat adrenal secretory responses evoked by pulses of nicotine (2 microM for 30 s) or high K+ (17.7 mM for 30 s). 4. [3H]Quinuclydinyl benzylate (QNB) specifically bound to cat adrenomedullary membranes with a saturating monophasic curve, suggesting a single binding site with a KD of 23 pM and a Bmax of 67 fmol (mg protein)-1. Preferential displacement by atropine over pirenzepine suggests that the binding site is associated to a M2-type muscarinoceptor. 5. Methacholine (3-300 microM) did not enhance the spontaneous catecholamine release from perfused bovine intact adrenal glands or superfused chromaffin cells. Neither did the drug affect secretion evoked by dimethylphenylpiperazinium (10 microM for 3 s) or K+ (35 mM for 3 s) from isolated superfused bovine adrenal chromaffin cells. 6. [3H]QNB bound to purified bovine adrenomedullary plasma membranes with a KD of 29 pM and a Bmax of 89 fmol (mg protein)-1. Displacement by pirenzepine suggests the presence of two binding sites (Hill coefficient = 0.64) with Ki1 of 39 nM and Ki2 of 2734 nM. 7. Because the ionophore A23187 enhanced K(+)-evoked secretion in both, bovine and cat adrenals, it seems that a similar cytosolic Ca2+ rise induced by muscarinic stimulation might constitute the underlying mechanism both to cause a secretory response per se as well as the potentiation of catecholamine release evoked by nicotinic or high K+ stimulation. However, it is unclear why the bovine behaves differently from the feline chromaffin cell as far as the muscarine-evoked effects are concerned.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2006

The effects of caffeine on the inducibility of atrial fibrillation.

INTRODUCTION: There is widespread belief that caffeine consumption is linked to atrial arrhythmias; however, there is a relative lack of systematic evidence to support the assertion. The purpose of this study was to investigate whether caffeine, in doses equivalent to daily use in the general population, alter the propensity for atrial fibrillation (AF) in an experimental model comparing normal and simulated predisposition to AF. METHODS AND MATERIAL: Caffeine (caffeine Na benzoate, 50:50 mixture) was administered intravenously at 1, 3, and 5 mg/kg doses in dogs producing serum levels of 2 to 4, 5 to 7, and 8 to 10 microg/mL. To simulate focal AF, premature stimulation from the right superior pulmonary vein was delivered at 2x, 4x, and 10x threshold at a rate of 180/min (S(1)-S(2) = 330 milliseconds) without and then with low-level stimulation of ganglionated plexi (GP) at the entrance of the right superior pulmonary vein. The window of vulnerability (WOV), a measure of the propensity for AF inducibility, was determined by the longest coupling interval of the premature beat (S(1)-S(2)) minus the shortest S(1)-S(2), which induced AF. The cumulative WOV is the sum of the individually determined WOV. RESULTS: At each serum level of caffeine, the cumulative WOV was lower without rather than with GP stimulation compared with control. The cumulative WOV for both the stimulated, that is, predisposed to AF, and nonstimulated, that is, normal groups, exhibited a significantly lower average as compared with that exhibited by the control group (P <or= .003-.02). CONCLUSION: These findings suggest that the presence of caffeine may result in an unexpected reduction in the propensity for AF in healthy individuals and in those with a predisposition for AF (enhanced AF inducibility caused by the stimulation of the GP).

Animals↗
PubMed2006

A preliminary study of the effects of cigarette smoking on prepulse inhibition in schizophrenia: involvement of nicotinic receptor mechanisms.

BACKGROUND: Schizophrenics exhibit deficits in prepulse inhibition (PPI) of the startle response, and have high rates of cigarette smoking. We evaluated the effects of cigarette smoking on PPI deficits in schizophrenia, and the role of nicotinic acetylcholine receptors (nAChRs) in mediating cigarette smoking-related PPI enhancement. METHODS: PPI was assessed at baseline, after overnight abstinence, and after smoking reinstatement during three separate test weeks in nicotine-dependent schizophrenia (n=15) and control (n=14) smokers pre-treated with the nAChR antagonist mecamylamine (MEC; 0.0, 5.0 or 10.0 mg/day). RESULTS: PPI was comparable between schizophrenia and control smokers after ad lib cigarette smoking. Overnight smoking abstinence significantly reduced PPI, while smoking reinstatement reversed abstinence-induced worsening of PPI deficits in schizophrenia. However, acute abstinence and reinstatement did not alter PPI in controls. PPI enhancement by smoking reinstatement in schizophrenia was dose-dependently blocked by MEC, whereas MEC had no effect on PPI in control smokers. CONCLUSIONS: These results suggest that: 1) Non-deprived smokers with schizophrenia have comparable levels of PPI to non-deprived smoking controls; 2) In schizophrenia, PPI is impaired by smoking abstinence and improved by acute smoking reinstatement, and; 3) enhancement of PPI by cigarette smoking in schizophrenia is mediated by stimulation of central nAChRs. Our findings may contribute to understanding the increased vulnerability to nicotine dependence in schizophrenia, with implications for treatment of PPI deficits in this disorder.

Acetylcholinesterase↗
PubMed1994

Effect of L-glutamic acid on acid secretion and immunohistochemical localization of glutamatergic neurons in the rat stomach.

Glutamatergic neurons in the rat stomach were localized immunohistochemically using antibodies against L-glutamate (L-Glu) as well as glutamate synthesizing enzyme, glutaminase (GLNase). Myenteric ganglia and nerve bundles in the circular muscle and the longitudinal muscle were found to contain GLU- and GLNase-positive nerve fibers, while submucosa and mucosa were devoid of glutamatergic innervation. The distribution of glutamatergic neurons and their processes in both myenteric ganglia and circular muscle is heterogeneous within the stomach. The effect of L-Glu on gastric acid secretion was investigated on an everted preparation of isolated rat stomach. L-Glu at 10(-7) and 10(-8) M alone had no effect on acid secretion. It was found that the oxotremorine-, histamine-, or gastrin-stimulated acid secretion was markedly reduced by L-Glu at 10(-8) M, whereas L-Glu had little effect on the acid secretion stimulated by dimethyl-phenylpiperazinium (DMPP) at this concentration. However, at higher concentration, e.g., 10(-7) M, L-Glu also markedly reduced DMPP-induced acid secretion. Among L-Glu receptor agonists tested, quisqualic acid (QA) is most potent, followed by kainic acid (KA) and N-methyl-D-aspartic acid (NMDA) in inhibiting oxotremorine-stimulated acid secretion. Furthermore, this inhibitory effect of L-Glu on oxotremorine-stimulated acid secretion is blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a specific non-NMDA receptor antagonist. All these results suggest that glutamatergic neurons are involved in the modulation of gastric acid secretion via ionotropic QA/KA receptors, probably through openings of Ca2+ channels.

Animals↗
PubMed2003

Enhancement of carotid chemoreceptor reflex and cardiac chemosensitive reflex in the acute phase of myocardial infarction of the anesthetized rabbit.

In the acute phase of cardiac ischemia there is an imbalance of the autonomic outflow with a depression of the baroreceptor reflex. Carotid chemoreceptor stimulation evokes an increase on arterial blood pressure and bradycardia in the anesthetized and paralyzed animal. The activation of cardiac chemosensitive fibers elicit the Bezold-Jarisch reflex comprising a decrease of arterial blood pressure and bradycardia. In the present study, we studied the modifications of the carotid chemoreceptor reflex and the Bezold-Jarisch reflex elicited during the acute phase of myocardial infarction (MI) in the anesthetized and paralyzed rabbit. Rabbits were anesthetized with pentobarbitone, paralyzed and artificially ventilated. The carotid sinus region was exposed and a cannula was inserted retrogradely through the external carotid artery into the carotid bifurcation; the carotid body was stimulated by a lobeline injection. A catheter was advanced, via the right carotid artery, to the origin of the aorta and the Bezold-Jarisch reflex was evoked by an injection of ATP. The baroreflex was provoked by an increase in after-load or by clamping the common carotid artery. Heart ischemia was provoked by ligation of the descending coronary artery. Arterial blood pressure, carotid artery pressure, heart rate and electrocardiogram were monitored. Stimulation of cardiovascular and cardiac receptors was performed before and after coronary ligation. Results show an overall increase in the cardiovascular reflex responses elicited by stimulation of chemically activated receptors and an overall decrease of the baroreceptor responses after MI. In conclusion, these data show the existence of an enhancement of the reflex cardiovascular responses to carotid chemoreceptor and cardiac chemosensitive receptors stimulation and confirmed the depression of baroreceptor reflexes following heart ischemia that could account for the imbalance of the autonomic output observed in the acute phase of myocardial infarction.

Adenosine Triphosphate↗