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

Over the past three years, high-dose barbiturate therapy has been used in the treatment of 60 patients with head injury (N = 45), encephalitis (N = 8), acute focal cerebral ischemia (stroke, N = 4), and global anoxia secondary to drowning (N = 3). High-dose barbiturates appear to be useful adjuncts in the control of intracranial hypertension refractory to other methods of therapy. Administration of barbiturates to patients with this problem will often reduce the requirement for osmotic agents, thereby facilitating medical management by avoiding hyperosmolality and fluid and electrolyte depletion. In a carefully controlled intensive care setting the risk of barbiturate therapy is low, though the costs and demands on personnel are great. Survival appeared to be improved in aptients with ,head injury and encephalitis. Although the ultimate outcome was not altered in patients with stroke or near-drowning, intracranial hypertension did not occur until barbiturate therapy was withdrawn. This experience provides an ethical basis to justify further randomized studies for determining whether or not barbiturates materially improve the neurological outcome following cerebral ischemic and traumatic insults.
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PMID:High-dose barbiturate therapy in humans: a clinical review of 60 patients. 53 17

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
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PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80

This study was designed to explore factors involved in the regulation of Na-K pumps in erythrocytes and blood pressure in anephric Sprague-Dawley female rats. Twenty-four hours following bilateral nephrectomy, the rats were given a 1-h infusion of 1 ml of either 0.9% or 5.4% saline, or 5% or 30% glucose. At the completion of the infusion, tail blood pressure was determined and blood was drawn for the measurement of the ouabain-furosemide-sensitive sodium efflux rate constant in erythrocytes. Infusion of 5.4% saline or 30% glucose caused a significant reduction in the erythrocyte sodium efflux rate constant, more pronounced with the former, and an elevation in blood pressure. Nephrectomy or infusion of 0.9% saline or 5% glucose had no effect on either parameter. These findings suggest that in anephric rats (1) extracellular fluid hyperosmolality rather than extracellular fluid volume expansion inhibits the Na-K pump in all cells; (2) a Na-K pump inhibitor is involved in the genesis of hypertension.
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PMID:Regulation of Na+-K+ pump activity in erythrocytes and blood pressure in anephric rats. 285 34

There is conflicting evidence for the existence of a renal sodium excretory deficit in the salt-sensitive hypertensive Dahl S (DS) rat strain. While presentation of acute sodium loads, in vivo or in vitro, suggests that DS kidneys cannot excrete sodium as efficiently as kidneys from the salt insensitive genetic control Dahl R (DR) rat strain, metabolic studies of Dahl rats on a high-sodium diet are unable to differentiate between DS and DR rats. The natriuretic response to acute sodium loads is dependent on the integrity of structures in or near the anteroventral 3rd ventricle (AV3V) region. Therefore, it was thought that an AV3V-dependent chronic sodium challenge might also uncover an excretory defect in DS rats. We have investigated the renal response of inbred Dahl S (SS/Jr) and Dahl R (SR/Jr), and Sprague-Dawley rats to 48 h of dehydration; a manoeuvre which produces hyperosmolality and hypernatremia, with its renal response dependent on the integrity of the AV3V. Inbred Dahl S, Dahl R and Sprague-Dawley rats showed identical renal electrolyte excretory responses to both dehydration and rehydration. These results are discussed in terms of the mechanism of salt-induced hypertension and dehydration natriuresis.
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PMID:Dehydration natriuresis in Dahl S rats: no evidence for renal excretory deficit. 337 1

A 24 year old man developed partial central diabetes insipidus with impaired thirst and an elevated osmotic threshold to the release of arginine vasopressin (AVP). Plasma AVP was present in inappropriately small concentrations despite severe hyperosmolality. In addition, marked hypertension accompanied this disorder and all abnormalities, including the hypertension, responded to 1-desamino-8-D-arginine vasopressin therapy. Several lines of evidence suggest this disorder may be a disturbance of hypothalamic function.
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PMID:Essential hypernatremia: disordered thirst and blood pressure control. 386 42

The anteroventral third ventricle (AV3V) region plays an important role in fluid and electrolyte balance and cardiovascular control in the rat; however, experiments in other species have raised questions about the universality of findings in the rat. The effects of discrete lesions placed within the AV3V area on hydromineral balance, the pressor response to angiotensin II given intravenously, and the initiation of a renin-dependent model of hypertension were examined in the dog. A transpharyngeal approach to the optic chiasm enabled us to destroy only the anterior aspects of the AV3V region (aAV3V group) or to include the entire nucleus medianus (NM) as well (aAV3V + NM group). Lesions of the aAV3V caused polydipsia and transient hypernatremia and hyperosmolality. In contrast, adipsia and a sustained increase in plasma sodium levels and osmolality were observed in dogs with lesions of the aAV3V plus the entire NM. Neither lesion altered baseline arterial pressure, heart rate, plasma levels of catecholamines and vasopressin, or total plasma protein levels. Only in aAV3V + NM lesioned dogs was there a tendency for plasma angiotensin II immunoreactivity to be elevated above control values at 2 and 4 days after operation. Neither lesion attenuated the pressor response to intravenous angiotension II or the initiation of renal hypertension induced by aortic coarctation. As observed in other species, structures within the AV3V region participate in hydromineral balance in the dog; however, in the dog portions of the NM dorsal to the AV3V region are essential for the mediation of drinking behavior.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:The anteroventral third ventricle region. Participation in the regulation of blood pressure in conscious dogs. 399 35

The hyperosmolality of current ionic angiographic media gives rise to several adverse effects. Use of the first low-osmolality medium, metrizamide (Amipaque), has been inhibited by expense and by the necessity for prior mixing into solution. Hexabrix is the first of such media to be available in stable solution, and its use in angiocardiography is reported, in direct comparison with Urografin, Triosil, Cardio-Conray, and metrizamide. The low osmolality media cause significantly less discomfort than ionic media, and are better tolerated in paediatric angiocardiography. In coronary angiography Hexabrix causes comparable T wave change to Urografin and more than Triosil or metrizamide, but tends to have less effect on heart rate. The risk of exacerbating pulmonary arterial hypertension in right heart angiography appears to be reduced.
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PMID:Hexabrix--a new contrast medium in angiocardiography. 702 Jul 27

Mannitol is an osmotic diuretic used in acute oliguric renal failure, acute cerebral edema, and acute glaucoma. It is metabolically inert and is excreted through the kidneys. So once renal function is impaired, mannitol accumulates and the movement of water into the intravascular space with resultant cellular dehydration. Two patients suffered reversible acute oliguric renal failure following mannitol infusion given as treatment for intracranial hypertension. Both patients experienced nausea and vomiting and became increasingly lethargic with edema of general body. Congestive heart failure occurred. Laboratory data showed severe dilutional hyponatremia with hyperosmolality. We successfully treated them with extracorporeal ultrafiltration method (ECUM) and hemodialysis (HD). Some discussions were presented about acute renal failure following mannitol infusion.
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PMID:[Acute renal failure following mannitol infusion]. 837 73

It is now generally accepted that diabetes can alter central nervous system (CNS) function. Even in the absence of overt cerebrovascular accidents or repeated hypoglycemic reactions, uncontrolled hyperglycemia is associated with cognitive changes. These changes are documented both in patients with diabetes as well as in animal models of experimental diabetes. The cognitive impairment can be ameliorated with optimization of blood glucose control. The potential causes of CNS dysfunction in diabetes can be broadly categorized as either vascular causes including changes in the blood-brain barrier and metabolic changes. The latter causes include repeated hypoglycemic episodes, hyperglycemia, hyperosmolality, acidosis, ketosis, neuroendocrine or neurochemical changes. The other contributory causes of CNS dysfunction in diabetes include the presence of hypertension, uremia, peripheral and autonomic neuropathy and multiple drug use.
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PMID:Pathophysiology of central nervous system complications in diabetes mellitus. 935 75


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