Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In freely moving rats, intracerebroventricularly (i.c.v.) injected tetrahydroaminoacridine (10, 25, 50 microg) increased blood pressure and decreased heart rate in a dose- and time-dependent manner. Intravenous (i.v.) tetrahydroaminoacridine (1 and 3 mg/kg) also increased blood pressure. Atropine sulphate (10 microg; i.c.v.) pretreatment greatly attenuated the blood pressure response to i.c.v. tetrahydroaminoacridine while mecamylamine (50 microg; i.c.v.) failed to change the pressor effect. Neither atropine sulphate nor mecamylamine pretreatment affected the bradycardia induced by tetrahydroaminoacridine. However, the bradycardic response was completely blocked by atropine methylnitrate (2 mg/kg; i.p.) pretreatment. The pressor response to i.c.v. tetrahydroaminoacridine was associated with a several-fold increase in plasma levels of vasopressin, adrenaline and noradrenaline, but not of plasma renin. Pretreatment with prazosin (0.5 mg/kg; i.v.) attenuated the pressor effect without changing the bradycardia. Vasopressin V1 receptor antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl1,O-Me-Tyr2-A rg8]vasopressin (10 microg/kg; i.v.) pretreatment also partially inhibited the pressor response to i.c.v. tetrahydroaminoacridine and abolished the bradycardia. Tetrahydroaminoacridine's cardiovascular effects were completely blocked when rats were pretreated with prazosin plus vasopressin antagonist. The data show that tetrahydroaminoacridine increases blood pressure in normotensive freely moving rats by activating central muscarinic cholinergic transmission. Increases in plasma catecholamines and vasopressin are both involved in this response. The tetrahydroaminoacridine-induced reduction in heart rate appears to be due to the increase in vagal tone and plasma vasopressin.
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PMID:Cardiovascular effects of centrally injected tetrahydroaminoacridine in conscious normotensive rats. 961 49

The role of neurally born acetylcholine in the central modulation of cardiovascular short-term variability was assessed using a pharmacological probe physostigmine, a cholinesterase inhibitor that can act centrally also. Experiments were performed in instrumented conscious rats. Equidistant sampling at 20 Hz of systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and heart rate (HR) allowed direct spectral analysis. Spectra were analysed in the whole, very-low frequency (VLF), low-frequency (LF) and high-frequency (HF) domains. Physostigmine, but not neostigmine, increased SAP, LF SAP and HF SAP variability while neostigmine, but not physostigmine, decreased HR without affecting HR variability. Atropine methyl nitrate prevented neostigmine-induced bradycardia and potentiated the effects of physostigmine on DAP, LF DAP and HF DAP variability. Atropine sulphate, hexamethonium, phentolamine and metoprolol inhibited physostigmine-induced increase of SAP and LF SAP. Pre-treatment of rats by quinapril prevented physostigmine-induced increase of SAP, but not of LF SAP, while the V(1a) antagonist prevented the increase of HF SAP. The results suggest that central cholinergic neurons facilitate but do not create LF SAP and HF SAP variability. The effect of physostigmine on LF SAP seems to be mediated via central muscarinic sites and the peripheral sympathetic system, while non-muscarinic central sites and vasopressin pathways subserve the increase of HF SAP.
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PMID:Central cholinergic modulation of blood pressure short-term variability. 1648 50