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

1. Seven latent hypertensive patients and seven matched controls were subjected to standardized mental stress and orthostatic provocation. 2. Mental stress increased blood pressure by approximately 25%, heart rate by 25 beats/min, plasma glycerol by 50% and plasma cyclic AMP by 25% in both groups. Plasma glucose and renin activity were unchanged. Plasma noradrenaline and adrenaline were essentially unchanged during stress. 3. There was an insignificant tendency towards higher noradrenaline levels in latent hypertensive subjects and two of these subjects displayed an exaggerated noradrenaline response to standing. 4. Our results indicate that the physiological responses to mental stress are caused by selective neuronal activation, rather than by generalized sympatho-adrenal activation. Latent hypertension does not seem to be associated with adrenergic hyperactivity or receptor supersensitivity, except possibly in individual cases.
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PMID:Sympatho-adrenal and cardiovascular response to mental stress and orthostatic provocation in latent hypertension. 23 22

The effect of the beta-adrenoblocker propranolol on adrenaline-stimulated lipolysis was studied in the adipose tissue of spontaneously hypertensive rats (SHR) and control rats. The lipolytic activity was estimated from the increase in glycerol concentration in the incubation medium in vitro. The adipose tissue of SHR responded to adrenaline similarly to that of control rats, but the concentration of adrenaline inducing the half-maximum response (KA) was 2 times less for SHR than KA for normotensive controls. Under propranolol effect this parameter was increased more significantly in SHR than in controls. These data indicate higher sensitivity of SHR adipose tissue to propranolol that may well be relative to alteration of the properties of beta-adrenergic receptors of adipose tissue in this form of hypertension.
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PMID:[Effect of the beta-adrenoblocker propranolol on adrenaline-stimulated lipolysis in the adipose tissue of spontaneously hypertensive rats]. 54 Jan 41

Studies were performed in nine male patients with moderate hypertension. Treatment with metoprolol, 50--150 mg three times daily for 4--17 weeks, had no effect on the plasma level of glycerol, free fatty acids, triglycerides or glucose under basal conditions, neither in the supine nor in the upright position. Submaximal work, performed postprandially, increased plasma glycerol before medication but not during metoprolol, in spite of a marked increase in plasma noradrenaline. The work load employed caused no change in free fatty acids, triglycerides or glucose, neither before medication nor during metoprolol.
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PMID:Effect of metoprolol on blood glycerol, free fatty acids, triglycerides and glucose in relation to plasma catecholamines in hypertensive patients at rest and following submaximal work. 63 34

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.
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PMID:Neurohypophyseal vasopressor principle: vasopressor hormone as well as antidiuretic hormone? 73 54

2 women complaining of headaches were found to have benign intracranial hypertension with increased rCBV (regional cerebral blood volume) of 85% and reduced rCBF (regional cerebral blood flow) of 10%. A lumbar puncture was done showing a small rCBV reduction of 13% but no significant change in rCBF. The patients were also administered 1.5 gm/kilogram body weight of glycerol 3 times a day. After 18 weeks of glycerol treatment, headaches and papilledema disappeared, rCBV and rCBF returned to normal levels, and cerebrospinal fluid pressure was reduced. It is believed that all 3 intracranial compartments may be involved in producing intracranial pressure in benign intracranial hypertension patients although it is difficult to determine the varying degrees to which each factor may be involved. The intracranial pressure may be increased due to venous engorgement and increased CBV. Because of undesirable side effects after long term use of deramethasone and diuretics like furosemide, oral glycerol therapy is used for prolonged therapy without adverse reactions.
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PMID:Increased cerebral blood volume in benign intracranial hypertension. 117 96

The authors present their results regarding the use of a buffered solution of glycerol 30%-sodium ascorbate 20% (GLIAS) for the treatment of brain oedema and intracranial hypertension. GLIAS was perfused intravenously in 80 patients with several types of brain oedema. In every patients serum and urinary osmolarity, diuresis, main blood and urine parameters, and ICP were monitored. Following GLIAS infusion an increase in plasma osmolarity was observed, changing the average basal value plus 13.4% after 15 min., 10.5% after 30'. At the same time there was a reduction of ICP and improvement in cerebral compliance. In each case there was a decrease in intracranial hypertension and brain oedema without significant collateral effects.
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PMID:Brain oedema and intracranial hypertension treatment by GLIAS. 141 43

Intensive therapy of a patient with status asthmaticus must lead to a reduction of vital threat by improving respiratory and cardiac functions. Because of the bronchodilating effect of ketamine, analgesic sedation with ketamine and benzodiazepines is extremely useful for prolonged ventilation. At the beginning of this treatment it can be necessary to supplement the continuous intravenous infusion of ketamine and diazepam or ketamine and midazolam with small bolus doses of up to 3.5 mg/kg/h of ketamine. Experience has shown that the combination of ketamine and midazolam has better controllability. In some of our patients the bronchodilating effect of ketamine was not sufficient and therefore ventilation with halothane was necessary at least intermittently. In contrast to halothane, ketamine can be combined with vasodilators and sympathomimetics as our own experience has shown. The combined application of ketamine with glycerol trinitrate or sodium nitroprusside is indicated in the event of pulmonary or general hypertension. The use of sympathomimetics--mainly beta-sympathomimetics--antagonizes the negative inotropic effect of ketamine, improves the circulatory system and leads to a direct bronchodilating effect. Progress in treatment was mainly achieved by continuous intravenous infusions of terbutaline (Bricanyl). Aminophylline is very compatible with ketamine, but because of its stimulating effect the use of aminophylline seems to be reasonable only during weaning from the ventilator. Control of the usually deep analgesic sedation and an accompanying optimum drug therapy are only possible with complete cardiorespiratory monitoring including invasive blood pressure measurement and catheterization of the pulmonary artery. In our clinic 24 patients with status asthmaticus were treated. Sixteen asthmatic patients were treated with analgesic sedation using ketamine and benzodiazepines, three of them without intubation and ventilation. In spite of the life-threatening situation and reanimation before admission to the intensive care unit, only one patient died. Our experience has shown that intensive therapy including analgesic sedation with ketamine and benzodiazepines, optimized by application of sympathomimetics and vasodilators, is suitable for overcoming the life-threatening situation of patients with status asthmaticus.
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PMID:[The treatment of status asthmaticus using ketamine--experimental results and clinical experience]. 141 80

Hypertension-hypervolemia therapy (HHT) is widely employed for treatment against vasospasm after subarachnoid hemorrhage (SAH). A few investigations have been reported to establish the fact that HHT results in a high incidence of congestive heart failure and pulmonary edema as well as deterioration of brain edema. From the point of view that the cerebral circulation is not independent of the systemic circulation, the authors investigated the effect of HHT on the systemic circulation of patients with SAH. In 72 patients, intracranial pressure (ICP), pulmonary catheter wedge pressure (PCWP), pulmonary arterial pressure (PA), central venous pressure (CVP), arterial pressure (AP), cardiac index (CI), arterial blood gas (ABGS), electrocardiogram (ECG), serum and urine electrolytes were monitored postoperatively. Furthermore, among these patients, the flow (Flow), volume (Volume) and velocity (Velocity) of the cortical vessels were monitored by means of a Laser Doppler in 25 patients. A cisternal or spinal drain was placed in all of the patients. Elevation of PCWP and CVP and Flow were observed when 300ml of 10% glycerol was administered within a period of 30 minutes, whereas administration of the same dose of glycerol over a period of 60 or 120 minutes caused no significant changes on these parameters. Elevation of PCWP and CVP and decrease of CI and Flow, occasionally associated with premature ventricular contraction (PVC), were observed in some patients when 100ml of 25% albumin was administered. However, administration of the same dose of albumin over a period of 120 or 240 minutes did not cause deterioration of the cardiac function. These facts could be explained by Guyton's law in which massive transfusion causes cardiac dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Serious pitfalls which can be encountered in a course of hypertension-hypervolemia therapy for vasospasm]. 157 56

In a double-blind randomized crossover study of 10 patients with mild essential hypertension, the influence of antihypertensive treatment with the angiotensin-I converting enzyme inhibitor enalapril (a single dose of 10 mg.day-1) on submaximal endurance exercise performance at a work rate eliciting a heart rate of 150 beats/min was studied. Resting and exercise blood pressure were significantly reduced during enalapril therapy. Heart rate was unaffected. Submaximal endurance exercise performance was reduced by 12% (p = 0.06). Plasma lactate concentrations were significantly increased and serum nonesterified fatty acid concentrations were decreased during exercise in patients receiving enalapril treatment. Plasma glucose and potassium levels and serum glycerol concentrations were not influenced by enalapril treatment. Because the impairment of endurance performance during enalapril treatment is relatively small compared with the reductions caused by other antihypertensive agents, such as beta-adrenoceptor blocking agents or diuretics, it is of minor clinical importance for most physically active patients with hypertension.
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PMID:Submaximal endurance exercise performance during enalapril treatment in patients with essential hypertension. 165 Dec 1

These studies were designed to investigate whether the centrally mediated pressor effects of hypertonic sodium chloride (NaCl) solutions are triggered in response to changes in the cerebrospinal fluid (CSF) osmolality and whether the chloride ion plays a role in these effects. In Inactin anesthetized, vagotomized rats, alterations in the arterial pressure to cerebroventricular administration (i.c.v.) of various concentrations of NaCl, sodium nitrate (NaNO3), glycerol, creatinine, lithium chloride (LiCl), lithium nitrate (LiNO3) and choline chloride were evaluated. The pressor effects of NaCl were significantly greater than those produced by either glycerol, creatinine and/or NaNO3 solutions. Central effects of NaCl were identical to that of LiCl; likewise, NaNO3 and LiNO3 produced essentially similar increases in the blood pressure. In other words, the two chloride salts produced significantly greater increases in the arterial pressure than the nitrate salts. Choline chloride also produced significant increases in the blood pressure both before and after pretreatment with hemicholinum (i.c.v.). In a separate series of experiments, pretreatment of rats with a vasopressin antagonist (i.v.), significantly attenuated the pressor effects of NaCl, NaNO3 and that of choline chloride whereas after autonomic ganglionic blockade with chlorisondamine, pressor responses of only NaCl, but not those of NaNO3 or choline chloride were significantly inhibited. These data indicate that elevation of either Na+ or Cl- in the CSF facilitates vasopressin secretion and that Na+ and Cl- ions function synergistically in the central nervous system (C.N.S.) to enhance sympathetic activity. The present studies demonstrate that the circumventricular structures in the C.N.S. that participate in the regulation of blood pressure are more responsive to changes in concentrations of Na+ and Cl- rather than to net changes in the CSF osmolality. The data further suggest that the chloride ion contributes to the central pressor effects of NaCl and may play a role in the pathophysiology of salt-dependent hypertension.
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PMID:Studies on the role(s) of cerebrospinal fluid osmolality and chloride ion in the centrally mediated pressor responses of sodium chloride. 182 60


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