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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of PAF has been examined in anaesthetized guinea-pigs. Intravenous (i.v.) administration of PAF (10 ng kg-1) did not modify the respiratory response but decreased the arterial blood pressure. A high dose of PAF (200 ng kg-1) caused marked bronchoconstriction and concomitant hypertension. The cyclooxygenase inhibitors aspirin (5 mg kg-1) and indomethacin (5 mg kg-1) and the thromboxane A2 (TXA2) receptor antagonist BM-13.177 (1 mg kg-1) failed to inhibit the peak bronchoconstrictive response but significantly inhibited the prolonged response following peak response. These inhibitors also attenuated PAF-induced hypertension. On the other hand, the lipoxygenase inhibitors phenidone (10 mg kg-1) and NDGA (5 mg kg-1) and the leukotriene (LT) receptor antagonist FPL-55712 (2 mg kg-1) affected neither bronchoconstriction nor hypertension induced by PAF. However, when aspirin was given in combination with NDGA, phenidone or FPL-55712, the peak and the following prolonged bronchoconstriction were significantly inhibited. The suppression of PAF-induced hypertension by aspirin was not further inhibited by the combination of these inhibitors. These results indicate that in anaesthetized guinea-pigs PAF-induced bronchoconstriction is composed of a dual response, a direct action (peak response) and an indirect action (prolonged response). The latter may be produced by the generation of TXA2 and lipoxygenase products, while PAF-induced hypertension is indirectly mediated by the generation of TXA2.
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PMID:Pharmacological modulation of platelet activating factor (PAF)-induced bronchoconstriction and hypertension in anaesthetized guinea-pigs. 290 7

Systemic administration of platelet activating factor (PAF; acetyl glyceryl ether phosphorylcholine) reduces renal blood flow, but the mechanism responsible for that effect has not been defined. To address that problem, we determined the effects on renal blood flow of PAF administered directly into the renal artery in pentobarbital (30 mg/kg)-anesthetized dogs. Bolus injections of PAF (0.2-0.8 microgram) caused transient renal vasoconstriction, reducing renal blood flow by 20 to 60% without altering systemic blood pressure; lyso-PAF (1 microgram) had no effect. The effects of PAF on renal blood flow were not altered by alpha-adrenergic blockade (phentolamine, 3 mg/kg) or by angiotensin II receptor blockade ([Sar1,Ala8]angiotensin II, 6 micrograms/kg/min), but they were increased in magnitude and duration by meclofenamate (5 mg/kg), a cyclooxygenase inhibitor. Methysergide (3 mg/kg), a serotonin antagonist, slightly reduced PAF effects, but a specific blocker of vascular serotonin receptors did not. Renal venous plasma platelet density was not altered by infusion of PAF into the renal artery at a dose (1-2 micrograms/min) that caused a sustained 20% renal blood flow decrease. Alprazolam, a benzodiazepine that competitively inhibited PAF-induced aggregation in canine platelet-rich plasma, also inhibited the renal vasoconstrictor action of PAF (0.8 mg/min, into the renal artery) but did not alter renal vasoconstrictor effects of norepinephrine or angiotensin II.
Hypertension 1987 Mar
PMID:Platelet activating factor vasoconstriction of dog kidney. Inhibition by alprazolam. 381 22

Two patients with severe postural hypotension associated with upper motor neuron and cerebellar impairment (Shy-Drager syndrome) have been studied. Head-up tilt and lower body negative pressure application caused marked falls in arterial pressure; in one patient, paradoxical vasodilatation was observed. Ice application did not increase arterial pressure or calculated forearm vascular resistance. Intravenous atropine in one patient increased heart rate by 18 beats per min, a cardioacceleratory response similar to exhausting recumbent exercise in that patient. 24 hr urinary catecholamine excretion was low, but aldosterone secretory rate was normal in the more severely afflicted patient. A prolonged elevation of plasma renin activity was noted when post-tilt hypertension occurred. When head-up tilt was not followed by this hypertensive period, plasma renin activity response to tilting was normal. Intra-arterial norepinephrine and tyramine both elicited a vasoconstrictor response. Intra-arterial infusions of norepinephrine and tyramine were repeated after administration of the monoamine oxidase inhibitor tranylcypromine. Norepinephrine was potentiated 4.1- and 0.5-fold in the two patients; tyramine was potentiated 3.7-and 1.1-fold in the two patients, respectively. A therapeutic program of tranylcypromine and tyramine (in the form of cheddar cheese) resulted in substantial clinical improvement. It is concluded that in at least some patients with idiopathic postural hypotension, norepinephrine is present in postganglionic sympathetic fibers. A therapeutic program of tyramine and a monoamine oxidase inhibitor may be of value when more conventional modes of therapy fail.
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PMID:Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy. 543 69

Progressive autonomic failure is a clinical syndrome of autonomic dysfunction that may occur in isolation as in idiopathic orthostatic hypotension (IOH) or in association with a central neurologic disorder, multiple system atrophy (MSA). MSA and IOH can be distinguished on the basis of biochemical and pharmacologic tests. Plasma norepinephrine levels are low in IOH and normal in MSA; neither group increases the plasma norepinephrine level adequately in response to postural change. Both MSA and IOH manifest an exaggerated pressor response to administered norepinephrine. However, only patients with IOH have true adrenergic receptor supersensitivity. The autonomic dysfunction in IOH primarily involves the peripheral autonomic neurons whereas the defect in MSA is the failure to activate appropriately an intact distal sympathetic nervous system. Neuropathologic studies reveal a multisystem degeneration in MSA; the few postmortem examinations of the central nervous system in IOH reveal lesions confined to the intermediolateral columns of the spinal cord. Orthostatic hypotension may be treated with a number of medications although supine hypertension limits the usefulness of these drugs. Further development and testing of a sympathetic neural prosthesis may help to resolve this therapeutic dilemma. Only the parkinsonian features in MSA respond to treatment with anticholinergic drugs.
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PMID:Multiple system atrophy. Clinical aspects, pathophysiology, and treatment. 653 71

Synthetic platelet-activating factor (PAF-acether) was shown to act as a shock inducer when a dose of 9 or 36 nmol . kg-1 was injected i.v. into dogs anesthetized with 30 mg . kg-1 i.v. sodium pentobarbitone. Nine nmol . kg-1 PAF-acether caused portal vein and pulmonary artery hypertension but only transiently; blood TXB2 and 6 keto PGF1 alpha levels rose; there was a lasting fall of 77% in systemic blood pressure, cardiac output fell by 86%, heart rate by 17%, plasma volume by 43%, and femoral artery blood flow by 66%, whereas the hematocrit rose by 33%. A dose of 36 nmol . kg-1 PAF-acether reduced coronary artery blood flow by 56%, diminished myocardial O2 consumption, raised O2 extraction and caused metabolic acidosis leading to death in 2 out of 7 animals. All these changes displayed the typical features of common acute circulatory collapse with distributive and hypovolemic etiologies, suggesting that PAF-acether might be an endogenous mediator in the early and late stages of shock.
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PMID:Acute circulatory collapse caused by platelet-activating factor (PAF-acether) in dogs. 668 72

1. Pretreatment with intravenous WEB-2086 (0.5 mg/kg; an antagonist of the actions of platelet activating factor; PAF) with or without indomethacin (2 mg/kg) failed to prevent or modify the fall in blood pressure following unclipping of the renal artery of anaesthetized two-kidney, one-clip hypertensive rats. 2. The same medications given to two other groups of rats 60 min after unclipping when the blood pressure had fallen to stable levels failed to reverse the fall. 3. Despite evidence that both prostanoids and PAF can be detected in increased amounts in renal venous blood after unclipping, they do not appear to mediate the reduction in blood pressure in this model of reversible hypertension.
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PMID:WEB-2086 and indomethacin do not modify blood pressure fall on unclipping hypertensive rats. 795 50

Thirty-seven men with angiography or ultrasound confirmed peripheral arterial occlusive disease were divided into two groups. Group 1 included 24 patients treated with one daily infusion of 10 g of phosphocreatine in 200 ml of solvent for 10 days. Group 2 included 13 patients who were given 0.9% NaCl in the same scheme. Groups were comparable in: duration of intermittent claudication, maximal walking distance, Ketle index, cholesterol, triglycerides, frequency of ischemic heart disease, hypertension, diabetes, smoking. Patients were examined 4 times: before starting, on second day, after treatment period, and 1 month after. Treadmill-test; ADP-, PAF-, 5-HT-induced platelet aggregation; D-dimer; PAI-1 activity; blood viscosity at high and low shear rate; hematocrit were performed. After treatment maximal walking distance significantly increased in patients of Group 1. Mechanisms of this effects include positive influence of phosphocreatine on platelet aggregation, blood rheology, coagulation and fibrinolytic systems.
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PMID:The effect of exogenous phosphocreatine on maximal walking distance, blood rheology, platelet aggregation, and fibrinolysis in patients with intermittent claudication. 807

Experiments were performed in pentobarbital-anesthetized rats, to study the mechanism of the acute pulmonary edema induced by Tityus serrulatus scorpion venom. In control rats injection of venom (50 micrograms/100 g, i.v.) induced arterial hypertension and lung edema (lung/body index or LBI equal to 1.01 +/- 0.09). In rats pretreated with heparin (100 IU/100 g 30 min previously) the venom induced similar hypertensive effects, but no edema was detected (LBI = 0.63 +/- 0.06, P > 0.05). Similarly, in rats pretreated with the PAF antagonist BN-52021 (0.5 mg/100 g, i.v., 30 min previously), the venom-induced hypertension was not modified but the acute pulmonary edema was prevented (LBI = 0.67 +/- 0.08, P > 0.05). It is concluded that PAF plays an important role on the genesis of pulmonary edema induced by scorpion venom in the rat. It is suggested that the inhibitory action of heparin could be related to a decrease in the vascular permeability in the lungs.
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PMID:Heparin or a PAF antagonist (BN-52021) prevents the acute pulmonary edema induced by Tityus serrulatus scorpion venom in the rat. 826 52

Orthostatic hypotension and related neurologic symptoms are frequently encountered in clinical practice. The maintenance of appropriate blood pressure and heart rate responses upon assuming the upright posture are dependent upon: 1. intact mechanical (venous valves) mechanisms, 2. functioning arterial and cardiopulmonary baroreceptors, 3. normal peripheral neural pathways, 4. normal central neural integration, and 5. appropriate neurohormonal secretion. Dysfunction at one or more of these loci may facilitate the occurrence of orthostatic hypotension and syncope. In general, the mechanisms of orthostatic hypotension may be divided into three categories. In the first category, processes interfere with normal compensatory responses to upright posture. Examples of this mechanism include age related autonomic changes, diabetic neuropathy and central nervous system disease such as Shy-Drager syndrome. The second principal mechanism involves overwhelming otherwise normal reflexes by an intense orthostatic stimulus. An obvious example of this mechanism is syncope related to hemorrhage. A final category of orthostatic hypotension relates to interference with reflex responses by drugs that may limit vasoconstriction, heart rate or cardiac output adjustments or exaggerate venous pooling. These are commonly used medications such as vasodilators, beta-adrenergic blockers and nitrates. The treatment of orthostatic hypotension revolves around the recognition of underlying causes or contributing factors amenable to correction or avoidance. Other helpful treatment options include nocturnal head-up tilting and mineralocorticoids, both of which help to expand blood volume. Many other therapeutic agents have been tried in small and selected patient populations, often with disappointing results. While many of the drugs available (phenylephrine, ephedrine, tyramine, dihydroergotamine) can improve upright blood pressure, side effects are common, and supine hypertension is problematic in many patients. Interventions of this type should be carefully initiated in a monitored setting. The carotid sinus is an important component of a neural control system responsible for heart rate and blood pressure homeostasis. Excessive heart rate and blood pressure responses to distortion of the carotid sinus are the basis for the carotid sinus syndrome (CSS). Patients with CSS tend to be elderly males and local pathology in the neck is frequently involved. Atherosclerotic coronary artery disease and hypertension are important clinical correlates. Two major categories of carotid sinus hypersensitivity (CSH) are recognized: cardioinhibitory and vasodepressor. Cardioinhibitory CSH is the most common, and in its purest form consists of sinus bradycardia or arrest, asystole or AV block during carotid sinus massage. This vagally-mediated response is eliminated by atropine. Cardiac pacing is nearly universally successful in preventing severe symptoms.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Alterations in reflex function contributing to syncope: orthostatic hypotension, carotid sinus hypersensitivity and drug-induced dysfunction. 833 Aug 51

Recent advances in our understanding of the pathophysiology of cardiovascular regulation and the metabolism of catecholamines have enabled us to develop an improved system of classification of autonomic disorders. Patients with autonomic impairment, clinically unassociated with other neurological abnormalities, are considered to have the Bradbury-Eggleston syndrome (idiopathic orthostatic hypotension, pure autonomic failure). Individuals whose autonomic failure is accompanied by degeneration in other neurological systems are classified as having the Shy-Drager syndrome (multiple system atrophy with autonomic failure). Patients in whom a deficiency of the enzyme dopamine-beta-hydroxylase is present from birth have many features suggestive of the Bradbury-Eggleston syndrome but manifest normal sweating and biochemically have an elevated plasma and urinary dopamine level. Recognition of these individuals is of particular importance because they are uniquely responsive to treatment with oral dihydroxyphenylserine (L-DOPS). A fourth disorder is baroreflex failure; this disorder is usually due to surgery, trauma, radiation or other injury to the ninth or tenth cranial nerves or the medullary nuclei which their fibers innervate. Patients with baroreflex failure have oscillations between hypertension and hypotension, but these alterations are poorly correlated with posture. Very high levels of plasma norepinephrine are found during the hypertensive phase of baroreflex failure. Baroreflex failure is generally responsive to treatment with clonidine. In conclusion, the diagnosis and therapy of autonomic disorders has improved due to the more precise taxonomy now current.
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PMID:Classification of autonomic disorders. 837 Oct 2


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