Action of some ganglion-stimulating substances on the secretion of saliva from the submandibular gland.
(17/69)
An attempt has been made to determine whether the ganglionic actions of pilocarpine and of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343) contribute to their effect on salivary secretion. Salivary flow was measured from the submandibular glands of spinal cats. Destruction of the superior cervical ganglion and adrenalectomy failed to reduce the stimulant effect of pilocarpine and McN-A-343. Substances known to interfere with the ganglionic actions of pilocarpine (cocaine, methadone and choline 2:6-xylyl ether bromide) likewise failed to modify the response. It is concluded that stimulation of autonomic ganglia and of the adrenal medulla does not contribute to the salivary secretion observed after intravenous injections of pilocarpine and of McN-A-343. Dimethylphenylpiperazinium, a nicotine-like ganglion-stimulating substance, causes salivary flow by stimulating the adrenal medulla as well as parasympathetic ganglion cells; stimulation of the superior cervical ganglion by this substance does not contribute to the salivary response. (+info)
PARTICIPATION OF AN UNUSUAL GANGLIONIC PATHWAY IN THE MEDIATION OF THE PRESSOR EFFECT OF PHYSOSTIGMINE IN THE RAT.
(18/69)
In spinal rats physostigmine failed to produce a pressor response even after treatment of the animals with hexamethonium, whereas noradrenaline, McN-A-343 (4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride) and AHR602 (3-acetoxy-1-benzyl-1-methylpyrrolidinium bromide) all produced large pressor effects. In rats anaesthetized with urethane, hexamethonium completely abolished the pressor effect of dimethylphenylpiperazinium but only partially blocked the pressor response to physostigmine; pressor effects of noradrenaline, McN-A-343 and AHR602 were potentiated. Combined treatment with hexamethonium and atropine and with hexamethonium and cocaine, however, completely abolished the pressor effect of physostigmine; simultaneously the pressor effects of McN-A-343 and AHR602 as well as of dimethylphenylpiperazinium were also blocked. P-286 (N-diethylaminoethyl-N-isopentyl-N'N'-di-isopropylurea) produced an early and a late block of the pressor effect of physostigmine; the initial block was due to an adrenergic blocking action while the late block was probably due to a dual action of the drug in abolishing the effects of both the nicotinic and non-nicotinic ganglion stimulants. Pressor responses to physostigmine, McN-A-343, AHR602 and dimethylphenylpiperazinium were abolished immediately after ganglion-blocking doses of nicotine. It is suggested that an unusual ganglionic pathway participates in the mediation of the pressor response to physostigmine in the rat, especially when the established ganglionic pathways are blocked. (+info)
The role of endothelium in the phenylephrine-induced oscillatory responses of rabbit mesenteric arteries.
(19/69)
Phenylephrine-induced oscillatory contractions in rabbit mesenteric arteries were investigated in vitro. Adrenergic, cholinergic, or histamine antagonists as well as cyclooxygenase and lipoxygenase inhibitors had no effect on this phenylephrine-induced oscillation. The removal of extracellular calcium ions or treatment with a calcium antagonist reduced the amplitude and frequency of the oscillation. Removal of the endothelium or treatment with inhibitors of the synthesis or the target enzyme of endothelium-derived relaxing factor (EDRF) also reduced the amplitude and frequency of the oscillation. In a perfusion bioassay, the perfusate from an endothelium-intact arterial segment induced oscillation of an endothelium-denuded arterial ring recipient. These results suggest that phenylephrine-induced oscillation is mediated by an endothelium-derived factor such as EDRF and depends on the influx of extracellular calcium ions. (+info)
PM-induced cardiac oxidative stress and dysfunction are mediated by autonomic stimulation.
(20/69)
Epidemiological studies show that increases in particulate air pollution (PM) are associated with increases in cardiopulmonary morbidity and mortality. However, the mechanism(s) underlying the cardiac effects of PM remain unknown. We used pharmacological strategies to determine whether oxidants are implicated in PM-dependent cardiac dysfunction and whether PM-induced increase in autonomic stimulation on the heart mediates cardiac oxidative stress and toxicity. Adult Sprague-Dawley rats were exposed to either intratracheal instillation of urban air particles (UAP 750 microg) or to inhalation of concentrated ambient particles (CAPs mass concentration 700+/-180 microg/m3) for 5 h. Oxidative stress and cardiac function were evaluated 30 min after UAP instillation or immediately after exposure to CAPs. Instillation of UAP led to significant increases in heart oxidants measured as organ chemiluminescence (UAP: 38+/-5 cps/cm2, sham: 10+/-1 cps/cm2) or thiobarbituric acid reactive substances (TBARS, UAP: 76+/-10, Sham 30+/-6 pmol/mg protein). Heart rate increased immediately after exposure (UAP: 390+/-20 bpm, sham: 350+/-10 bpm) and returned to basal levels over the next 30 min. Heart rate variability (SDNN) was unchanged immediately after exposure, but significantly increased during the recovery phase (UAP: 3.4+/-0.2, Sham: 2.4+/-0.3). To determine the role of ROS in the development of cardiac malfunction, rats were treated with 50 mg/kg N-acetylcysteine (NAC) 1 h prior to UAP instillation or CAPs inhalation. NAC prevented changes in heart rate and SDNN in UAP-exposed rats (340+/-8 and 2.9+/-0.3, respectively). To investigate the role of the autonomic nervous system in PM-induced oxidative stress, rats were given 5 mg/kg atenolol (beta-1 receptor antagonist), 0.30 mg/kg glycopyrrolate (muscarinic receptor antagonist) or saline immediately before exposure to CAPs aerosols. Both atenolol and glycopyrrolate effectively prevented CAPs-induced cardiac oxidative stress (CL(ATEN): 11+/-1 cps/cm2, CL(GLYCO): 10+/-1 cps/cm2, TBARS(ATEN): 40+/-6 pmol/mg protein, TBARS(GLYCO): 38+/-6 pmol/mg protein). These data indicate that PM exposure increases cardiac oxidants via autonomic signals and the resulting oxidative stress is associated with significant functional alterations in the heart. (+info)
Ability of short-time Fourier transform method to detect transient changes in vagal effects on hearts: a pharmacological blocking study.
(21/69)
Conventional spectral analyses of heart rate variability (HRV) have been limited to stationary signals and have not allowed the obtainment of information during transient autonomic cardiac responses. In the present study, we evaluated the ability of the short-time Fourier transform (STFT) method to detect transient changes in vagal effects on the heart. We derived high-frequency power (HFP, 0.20-0.40 Hz) as a function of time during active orthostatic task (AOT) from the sitting to standing posture before and after selective vagal (atropine sulfate 0.04 mg/kg) and sympathetic (metoprolol 0.20 mg/kg) blockades. The HFP minimum point during the first 30 s after standing up was calculated and compared with sitting and standing values. Reactivity scores describing the fast and slow HFP responses to AOT were calculated by subtracting the minimum and standing values from the sitting value, respectively. The present results, obtained without controlled respiration, showed that in the drug-free condition, HFP decreased immediately after standing up (P < 0.001) and then gradually increased toward the level characteristic for the standing posture (P < 0.001), remaining lower than in the sitting baseline posture (P < 0.001). The magnitudes of the fast and slow HFP responses to AOT were abolished by the vagal blockade (P < 0.001) and unaffected by the sympathetic blockade. These findings indicate that HFP derived by the STFT method provided a tool for monitoring the magnitude and time course of transient changes in vagal effects on the heart without the need to interfere with normal control by using blocking drugs. (+info)
Cardiac regulation in the socially monogamous prairie vole.
(22/69)
Social experiences, both positive and negative, may influence cardiovascular regulation. Prairie voles (Microtus ochrogaster) are socially monogamous rodents that form social bonds similar to those seen in primates, and this species may provide a useful model for investigating neural and social regulation of cardiac function. Cardiac regulation has not been studied previously in the prairie vole. Radiotelemetry transmitters were implanted into adult female prairie voles under anesthesia, and electrocardiographic parameters were recorded. Autonomic blockade was performed using atenolol (8 mg/kg ip) and atropine methyl nitrate (4 mg/kg ip). Several variables were evaluated, including heart rate (HR), HR variability and the amplitude of respiratory sinus arrhythmia. Sympathetic blockade significantly reduced HR. Parasympathetic blockade significantly increased HR, and reduced HR variability and the amplitude of respiratory sinus arrhythmia. Combined autonomic blockade significantly increased HR, and reduced HR variability and respiratory sinus arrhythmia amplitude. The data indicate that autonomic function in prairie voles shares similarities with primates, with a predominant vagal influence on cardiac regulation. The current results provide a foundation for studying neural and social regulation of cardiac function during different behavioral states in this socially monogamous rodent model. (+info)
Experimental and clinical basis for the use of statins in patients with ischemic and nonischemic cardiomyopathy.
(23/69)
5-Hydroxytryptamine induces electrogenic secretion and simultaneously activates a modulating inhibitory neural circuit in rat small intestine in vitro.
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5-Hydroxytryptamine (5-HT) induces electrogenic secretion across rat jejunum and ileum in vitro expressed as an increase in the short-circuit current. Enhancement of this secretory response by previous serosal addition of atropine (1 microM), hexamethonium (0.2 microM) or yohimbine (0.2 microM), especially in the ileum, indicated that 5-HT simultaneously activates an anti-secretory, inhibitory, enteric, neural, cholinergic-adrenergic pathway (ENCAP). A similar inhibitory ENCAP activated by 5-HT has previously been characterized in rat colon in vitro. (+info)