Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of these experiments were to study the interactions of N-methyl-D-aspartate (NMDA) with baroreceptor reflexes induced by transient carotid clamping. Adult male Sprague-Dawley rats were anesthetized with urethane. Bilateral common carotid artery occlusion resulted in a reversible and reproducible hypertension in the vagotomized animals. This hypertensive reaction was blocked by intraventricular injection of NMDA antagonists, such as 2-amino-7-phosphono-heptaneoate (AP-7) and phencyclidine (PCP). We also found that blood pressure-sensitive neurons of the rostral ventrolateral medulla (RVLM) could be classified into two groups, on the basis of their responses to norepinephrine given intravenously. Using pressure microejection and single unit recording, we observed that clamping of the common carotids resulted in excitation of type I neurons. This evoked excitation, similar to that induced by NMDA, was blocked by locally applied AP-7. However, the carotid occlusion-induced responses of type II neurons were not blocked by AP-7. In conclusion, the present data suggest that NMDA receptors are involved in hypertensive responses during carotid occlusion, perhaps involving a site in the rostral ventrolateral medulla.
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PMID:NMDA antagonists attenuate hypertension induced by carotid clamping in the rostral ventrolateral medulla of rats. 189 54

In recent years, more and more attention has been paid to the studies about the cardiovascular function of phencyclidine (PCP) receptor, but very little about the cardiovascular function of central PCP receptor. In this study, we observed the effects of PCP on the blood pressure (BP) and heart rate (HR) by injecting the agonist or antagonist of PCP receptor into cerebral ventricle (icv) or spinal subarachnoid space (ith), to find out the cardiovascular function of central PCP receptor. It was found that icv PCP (250 nmol) elicited a slow and long lasting hypotension or fast and long lasting bradycardia. ith PCP elicited sharp hypotension and bradycardia immediately, with dose-dependent response. The hypotension and bradycardia of ith PCP (150 nmol) were significantly antagonized by ith 15 nmol dextrorphan. TCP, an agonist of PCP receptor, also elicited sharp hypotension and bradycardia immediately. However, subcutaneous injection (sc) of PCP (10 mg/kg) elicited hypertension and had no effect on HR. The results mentioned above indicate that central PCP receptors have the inhibitory effect on cardiovascular system. The cardiovascular effect of sc PCP may be the effect of combination of central and peripheral PCP receptors.
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PMID:[Cardiovascular effect mediated by phencyclidine receptor in central nervous system]. 216 62

Although hypertension can be associated with phencyclidine (PCP) use, subarachnoid hemorrhage (SAH) is a rare result. The radiological and pathological findings are reported of a patient with acute SAH who had chromatographic evidence of PCP in his blood. The occurrence of SAH in a patient who uses PCP may be caused by a disrupted arterial vessel wall and/or vasospasm due to the pharmacological action of the drug on the cerebral vasculature.
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PMID:Pathological and radiological correlation of subarachnoid hemorrhage in phencyclidine abuse. Case report. 361 76

The inhalation of toxic gases or vapours is capable of resulting in pulmonary oedema (P.O.), the mechanism of which corresponds, on the basis of a number of hemodynamic studies carried out, to that which characterises the so-called "lesional" pulmonary oedema, which is different from so-called "hemodynamic" oedema. Classically PAP, PCP and P wedge pressure have virtually normal values (normalisation of pulmonary arterial hypertension by correction of hypoxemia). CI and SWILV are normal or increased and pulmonary resistances are virtually normal. The origin of the oedema is thus related to an increase in alveolo-capillary permeability. The inhalation of toxic gases or vapours with a caustic or irritant action, or containing particles, however, usually adds on an obstructive syndrome, similar to a severe asthmatic attack. Under such conditions, the marked reduction in intrathoracic pressure during inspiration definitely favours pulmonary oedema by decreasing intra-alveolar pressure and by the accumulation of blood in the pulmonary circulation, and is capable of masking pulmonary arterial hypertension. Raised pressure, related to expiratory effort, on the contrary, decreases venous return and may result in collapse of the capillaries. Whilst the principal mechanism of PO by the inhalation of toxic gases or vapours is related to an increase in alveolo-capillary permeability, it is nevertheless important not to under-estimate the role of variations in intra-thoracic pressures which may constitute a provoking or at least aggravating element.
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PMID:[Pulmonary edema of toxic origin. Hemodynamic data]. 611 Dec 79

Although barbiturates are often effective as therapeutic agents in several types of brain ischemia, there is no consensus as to their mechanisms of action. Exactly why other intravenous anesthetics such as ketamine are not effective therapies in brain ischemia is not known. Structural analogs of ketamine such as phencyclidine (PCP) not only exert potent hallucinogenic properties and are widely abused drugs, but often result in hypertensive encephalopathies and death. In view of the paucity of information on the cerebral circulatory actions of barbiturates, ketamine and PCP (and analogs), in-vivo (microcirculatory) and in-vitro studies were undertaken. Barbiturates, in anesthetic concentrations (e.g., 10(-5) to 10(-4) M), were found to exert direct vasodilator actions on cerebral arterial smooth muscle; these relaxant actions appear to be related to inhibition of calcium ion (Ca2+) influx in cerebral vessels. The latter may be important in the salutory actions of barbiturates in brain ischemia, head trauma and cerebrovasospasm. Unlike barbiturates, ketamine was found to exert spasmogenic actions on cerebral arteries, which may aid in explaining the inability of this anesthetic to be of therapeutic value in brain ischemia. PCP and its analogs, as well as other hallucinogenic molecules (e.g., LSD, mescaline) produced spasms in cerebral arterioles, venules and arteries in concentrations which mimic their hallucinogenic potencies. Distinct PCP-like receptors which subserve contraction appear to exist on large as well as microscopic cerebral blood vessels. Spasms induced by PCP, its analogs and ketamine can be readily reversed or prevented completely by calcium channel blockers. The latter agents could be quite useful, clinically, in prevention of cerebral infarction, hypertension and fatality associated with PCP (and analogs) intoxication.
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PMID:Effects of barbiturates, phencyclidine, ketamine and analogs on cerebral circulation and cerebrovascular muscle. 640 Apr 29

PCP (10 mg/kg, s.c.) causes hypertension that is associated with decrease or tendency to decrease the levels of epinephrine and norepinephrine in the hypothalamus and the brainstem regions. If this represents a decreased catecholaminergic activity, then this may enhance sympathetic activity and contribute to the PCP-induced hypertension.
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PMID:Effect of phencyclidine (PCP) on blood pressure and catecholamine levels in discrete brain nuclei. 649 20

Coronary morphology, risk factors, long-term prognosis, and progression of coronary arteriosclerosis were investigated in 679 (649 mean and 30 women) post-infarction patients under 40 years of age. These patients represented 80% of 844 MI patients under 40 who were referred to our hospital in the years 1973-1980; 20% had refused coronary angiography; 465 patients were followed up for 1-7 years (mean 3.5 years). In 164 patients, a second coronary angiography was performed 3.8 years after the first angiogram, which was done an average 3 months after the acute episode. The main results were as follows: 8.4% of the patients had zero-vessel disease and 3.7% had a normal coronary angiogram. The majority had single-vessel disease (57.3%). The prevalence of zero-vessel disease decreased with age while that of multivessel disease increased. With increasing vessel involvement, the prevalence of hypercholesterolemia, hypertriglyceridemia, and hypertension increased. A history of smoking was equally common in patients with zero-, single-, double-, and triple-vessel disease. In women the combination of smoking and the use of oral contraceptive drugs was frequently seen. In one-quarter of the zero-vessel disease patients, the infarction occurred during unusually intense physical exercise. The statistical analysis of the survival data using the proportional hazards model (univariate analysis) showed the variables heart volume/body wt., ventricular arrhythmias, PCP at rest, PCP max, work capacity, ventricular function, and number of diseased vessels to be of prognostic importance. Multivariate analysis using this model revealed the following independent variables to be relevant to prognosis: heart volume/body wt., ventricular arrhythmias, ventricular function, and number of diseased vessels. After an average of 3.8 years since the first coronary angiography, 28.6% of the patients showed a significant progression of coronary arteriosclerosis (at least two degrees of stenosis according to the AHA classification). In the subgroup of patients with multilocular disease in the first angiogram, progression was 10 times as frequent as in a group with initial unilocular disease (34.3% vs 3.6%). Patients with progression had continued to smoke significantly more often than patients without progression (38.4%) vs 14.5%). Regression of coronary angiographic findings was significantly more frequent in the group of patients with initial unilocular disease than in those with multilocular disease in the first angiogram (28.6% vs 10.6%). Regression might be explained as recanalization and organization of a thrombus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myocardial infarction at a young age (under 40 years). 669 76

Activation of the sympathetic system by phencyclidine (PCP) should result in catecholamine release from the adrenals. However, adrenalectomy does not reduce PCP-induced hypertension. In an attempt to rectify this inconsistency, the direct effects of PCP on the bovine adrenal medulla were examined. At (3 X 10(-6) M), PCP reduced the acetylcholine-(ACh)-induced catecholamine release by 50%. Surprisingly, barium-induced secretion of catecholamines was also reduced by PCP. ACh-induced catecholamine release was not altered by 10(-3)M 4-aminopyridine (4 AP), the potassium channel blocker. Thus, calcium antagonist actions of PCP and consequent block of catecholamine secretion from adrenal medulla may explain the lack of effect of adrenalectomy on PCP-induced hypertension. Possible contributions of calcium and/or potassium channel blockade to other manifestations of PCP overdosage are discussed.
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PMID:Block by phencyclidine of acetylcholine and barium induced adrenal catecholamine secretion. 688 80

The aim of this study was to assess the possible role of a central cholinergic component phencyclidine (PCP)-induced hypertension. Sprague-Dawley rats, lightly anesthetized with urethane, exhibited a dose related pressor response following 0.1-1.0 mg/kg PCP i.v. After i.v. atropine pretreatment, the PCP dose-response curve was shifted to the right, and the magnitude of the pressor responses was reduced by about 50%. In addition, atropine reduced the incidence of apneusis, but had no effect on the bradycardia that accompanied the pressor responses. Methylatropine (i.v.) did not reduce the PCP pressor responses, nor did it prevent the apneusis induced by PCP. These results suggest that in addition to its direct pressor effects the activation of central cholinergic systems contribute significantly to the cardiovascular and respiratory toxicity induced by PCP.
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PMID:Reduction by atropine of phencyclidine hypertension and apneusis. 707 Feb 2

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17


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