European journal of pharmacology
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The effect of haloperidol, pimozide and amphetamine on acetylcholine (ACh) output from the cerebral cortex was investigated in unanaesthetized, freely moving and urethane-anaesthetized rats and guinea pigs. Haloperidol (1 mg/kg i.p.) decreased ACh output only in the anaesthetized rats and increased it only in unanaesthetized guinea pigs. ⋯ Amphetamine (1 mg/kg i.p.) in all cases, stimulated ACh output. In rats with a septal lesion, the effect of amphetamine on ACh output was suppressed but that of pimozide was still present.
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It is likely that substance P is a neurotransmitter at the first afferent synapse. These synapses may mediate pain sensations from thermal, mechanical or chemical (bradykinin) stimulation of nociceptors. Correlation of the responsiveness of dorsal horn neurones to iontophoretic application of a substance P analogue and mechanical or chemical stimulation of the hind limb suggested that sensitivity to substance P was shown by cells responding to chemical but not mechanical noxious stimulation.
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The effect of naloxone on nitrous oxide analgesia in man has been investigated. The paradoxical response so obtained indicates the possibility of a dural system mediating the pain response in man. These results support previous animal experiments indicating that nitrous oxide analgesia is mediated by the opiate receptors.
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Changes in systolic blood pressure (SBP), heart rate (HR), heart rate and plasma renin concentration (PRC) have been compared in three different groups of rats between the ages of 5 and 20 weeks. The groups were: spontaneously hypertensive rats (SHRs), atenolol-treated SHRs (200 mg/kg/day orally throughout the 15 weeks) and normotensive rats of the same strain (WKYs). Treatment with atenolol markedly inhibited the onset of genetic hypertension, reduced HR and PRC from the outset and diminished the heart weight/body weight ratio. Comparison of changes in these parameters in atenolol-treated SHRs, control SHRs and WKYs strongly suggests that the mechanism of atenolol's preventive action against hypertension development in SHRs primarily involves its effects on heart and on the renin--angiotensin system.