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

The best definition of risk factors for renal injury, irrespective of the aetiological agent, comes from observations in patients with acute renal failure. From such observations, two subdivisions have evolved, i.e., acute insults and host risk factors. Acute renal insults include: hypertension, sepsis, use of nephrotoxic drugs (e.g., aminoglycoside antibiotics and contrast media), haemoglobinuria or myoglobinuria, liver disease and extracellular volume depletion. Host risk factors include: advanced age, hypertension, gout and hyperuricaemia, diabetes mellitus, chronic renal failure and use of diuretics. Furthermore, the mechanism of acute renal injury can be correlated with different risk factors: for a tubular toxic agent, acting either directly on the cells or haemodynamically, a dose-dependency is characteristic; while for immunologically mediated injury, genetic predisposition is more important. The identification of risk factors for chronic toxic injury is confounded by the possibilities of multiple episodes of subclinical renal injury, the distinct possibility that a major component of the ageing process may be a loss of renal reserve, and a progressive body burden, of, e.g., cadmium, which may deplete intrinsic protective mechanisms. However, clinically relevant risk factors can alert the clinician to exercise additional caution when prescribing medications that are potentially nephrotoxic. Such factors include dehydration, pre-existing renal disease, age, co-existing diseases that cause renal ischaemia, gender, concomitantly administered drugs, and electrolyte abnormalities.
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PMID:Risk factors for toxic nephropathies. 265 33

Recently, there has been an explosion of knowledge on vasopressin, including its neuro-anatomy, biochemistry and physiology. Recent work demonstrates extensive extra-hypothalamic vasopressinergic projections from the SON and PVN. Of particular importance are projections to the cardiovascular medullary centres. Conversely, the SON and PVN receive reciprocal catecholaminergic innervation from autonomic medullary centres. Vasopressin should now be regarded as a peptide hormone with important peripheral effects, as well as a neuropeptide acting as a neurotransmitter or neuromodulator with important CNS actions. The central and peripheral vasopressin systems are not only anatomically differentiated, but, although integrated, may also function independently. There is an important interaction between the central vasopressin system and the autonomic nervous system. Vasopressin has multiple and diverse actions on the cardiovascular system, including direct vasoconstriction, antidiuresis and hence volume control, central actions on cardiovascular neural centres, modulation of the baroreflex and direct cardiac effects. It also acts in concert with the sympathetic nervous system and the renin-angiotensin system as an integrated neurohormonal system in the control of blood pressure. Vasopressin appears to have an important role as a vasoconstrictor agent whenever volume is threatened, such as in dehydration, haemorrhage, adrenal insufficiency and orthostasis. It seems unlikely that vasopressin acts as a direct vasoconstrictor agent in the pathogenesis of any form of experimental or human hypertension. Although plasma vasopressin levels have been reported to be elevated in most forms of hypertension, this correlates best with the severity of hypertension. Furthermore, the levels are not elevated to the pressor range, so that increased vascular reactivity and sensitivity has to invoked. This does not appear to be specific for vasopressin. However, vasopressin may be indirectly involved through volume maintenance or interactions within the CNS. Indeed, its volume retaining properties have probably been underestimated. Whereas in acute situations the vasoconstrictor properties may be of some importance, it is difficult to sustain long-term hypertension without maintenance of an adequate plasma volume. Vasopressin's central actions on the cardiovascular medullary centres, the baroreflex, the autonomic nervous system and catecholamine metabolism may also be involved in some hypertensive processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vasopressin in circulatory control and hypertension. 293 70

Hypertension developed within 5 weeks in uninephrectomized rats administered deoxycorticosterone acetate (DOCA, 30 mg/kg, s.c., weekly) and given isotonic saline to drink. Chronic dietary administration of tryptophan (50 g/kg food) reduced intake of saline solution and prevented the elevation of systolic blood pressure induced by treatment with DOCA alone. Treatment with tryptophan also protected against the reduction in urinary concentrating ability during a 24 h dehydration that is characteristic of DOCA-treated rats. Other tests were carried out to assess the responsiveness to the beta-adrenergic agonist, isoproterenol. The tests included measurement of drinking and heart rate following acute administration of isoproterenol. The characteristically depressed drinking response of DOCA-treated rats to acute administration of isoproterenol was returned to that of untreated controls by chronic treatment with tryptophan. However, the reduced chronotropic response of the heart of DOCA-treated rats to administration of isoproterenol was unaffected. The cardiac hypertrophy characteristic of DOCA-treatment was attenuated significantly by chronic treatment with tryptophan. These results suggest that tryptophan provides significant protection against the development of DOCA-induced hypertension, polydipsia, and cardiac hypertrophy in rats. The mechanism by which tryptophan protects is unknown and requires additional study.
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PMID:Prevention of DOCA-induced hypertension in rats by chronic treatment with tryptophan. 295 Oct 40

Chronic subcutaneous (s.c.) infusion (osmotic minipump) of L-5-hydroxytryptophan (L-5-HTP, 4.2 to 12.6 mg/day) to uninephrectomized, deoxycorticosterone acetate-salt-treated (DOCA) rats (1.36 mg/kg per day via s.c. silastic implants) reduced their exaggerated intake of isotonic saline significantly (12.6 mg/day), prevented the elevation of blood pressure (4.2 to 12.6 mg/day), prevented cardiac hypertrophy (12.6 mg/day), and provided modest protection against reduction of urinary concentrating ability, characteristic of DOCA-treated rats during a 24-h dehydration. The exaggerated dipsogenic response of DOCA-treated rats to administration of angiotensin II (AII, 50 and 100 micrograms/kg, s.c.) was also reduced by treatment with L-5-HTP (4.2 and 8.4 mg/day). The specific binding of AII to its receptors in membranes from the diencephalon of the brain was increased significantly above control level by chronic treatment with DOCA, but was returned to control level by concomitant treatment with L-5-HTP. Daily urinary excretion of dopamine, increased by treatment with DOCA, was unaffected by treatment with L-5-HTP (6.3 mg/day). Daily urinary excretion of epinephrine was increased by treatment with L-5-HTP (6.3 and 12.6 mg/day). These results suggest that chronic administration of L-5-HTP provides significant protection against the development of DOCA-induced hypertension, polydipsia, polyuria, and cardiac hypertrophy in rats. The mechanism by which L-5-HTP protects is unclear and remains to be established.
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PMID:Chronic treatment with L-5-hydroxytryptophan prevents the development of DOCA-salt-induced hypertension in rats. 296 66

The authors examined 30 patients with intracranial hypertension caused by brain tumor who received 1 g/kg mannitol for dehydration. It was found that dehydration improves the function of the brain in the stage of subcompensation but makes it worse in the stage of decompensation. This has an effect both on the patients' general condition and on the EEG. The response of the healthy hemisphere to the administration of mannitol differed significantly from that of the involved hemisphere. Indications were determined for prescribing dehydration therapy according to the clinical stage of intracranial hypertension.
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PMID:[EEG changes in response to dehydration depending on the extent of intracranial hypertension]. 314 64

Minoxidil (Loniten), a potent predominant arteriolar vasodilator, provides prompt and effective reduction of blood pressure in many patients with severe hypertension. Minoxidil results, however, in profound reflex tachycardia and increased plasma volume almost always necessitating concomitant use of beta-adrenergic blocking agents and diuretics. Hypertrichosis and massive fluid retention are troublesome adverse reactions that may require discontinuation of minoxidil and initiation of an alternative antihypertensive agent. When minoxidil is discontinued, diuretic dosage requires re-evaluation and possible tapering to prevent volume depletion. Volume depletion is a risk factor in patients with persistent peripheral edema, sodium deprivation or dehydration; these states may interfere with physiologic mechanisms that maintain adequate cerebral perfusion upon standing, triggering orthostatic hypotension and potential syncope. Hypertension clinic visits should routinely include supine followed by sitting and standing blood pressure determinations to ensure detection of orthostatic hypotension. Described in the article is a case study in which a patient developed severe orthostatic hypotension one month after minoxidil was discontinued. Pathophysiologic mechanisms are discussed.
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PMID:Orthostatic hypotension occurring after discontinuation of long-term minoxidil therapy. 317 16

In a prospective study of postoperative complications, strokes occurred in 6 out of 2463 patients (0.2%) who underwent non-cardiac, non-carotid artery surgery. The patients who experienced cerebrovascular accidents, including three cases of transient ischemic attack, were significantly older than the rest of the group (mean age 79 years versus 65 years) and had manifestations of atherosclerosis in at least one organ preoperatively. Significant predictors of risk for postoperative cerebrovascular accidents were previous cerebrovascular disease, heart disease, peripheral vascular disease, and hypertension. Cerebrovascular accidents occurred late in the postoperative period, 5-26 days after surgery, and were not directly related to surgery and anesthesia. They were more frequent after acute than after elective operations. Precipitating factors for some of the stroke incidents were rapid atrial fibrillation and postoperative dehydration.
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PMID:Postoperative cerebrovascular accidents in general surgery. 321 96

The authors reviewed the effect of low dose dopamine administration (1-5 micrograms/kg/min) in neurosurgical patients with acute renal failure (5 cases) or hypernatremia (7 cases) in whom cerebral dehydration therapy for intracranial hypertension was thought to be causative of these disorders. Cases with hypernatremia (serum sodium over 155 mEq/l) were considered in the stage of impending acute renal failure as in the majority of cases serum creatinine levels were mildly elevated while urinary sodium was markedly diminished. Associated with systemic hypovolemia, in cases with acute renal failure (with serum creatinine over 3.5 mg/dl and urinary output of less than 20 ml/hr for more than 4 hour duration) the urinary sodium levels were less than 20 mEq/l. In all the cases treated by low dose dopamine, urinary output and sodium increased within 6 hours and in the following 24 hours stabilized urinary output with its elevated sodium (some 100 mEq/l) was obtained. As the result, elevated urea-nitrogen or serum sodium was rather easily washed out and the patients were kept adequately hydrated afterwards. Any complications such as aggravation of cerebral edema or convulsive disorder were not associated with this regime. The authors, therefore, would emphasize that low dose dopamine administration resulting in sodium diuresis and increase in renal blood flow is a practical way of method in treating patients with hypernatremia or acute renal failure caused by hyperosmolar agent infusion in their acute stage.
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PMID:[Renal protection in acute neurosurgical diseases--effect of a low dose dopamine with reference to acute renal failure and hypernatremia in patients with dehydration]. 322 69

Many recent investigations of the mechanism of volume-expansion natriuresis fail to appreciate that the observed renal sodium excretion may not be dependent on an increase in intravascular volume, but rather on the infused sodium load or extracellular fluid volume expansion. With this in mind, the natriuresis of isotonic volume expansion, hypertonic saline infusion, and dehydration have a common basis: they present a relative or absolute sodium load. Lesions of forebrain periventricular tissue prevent the natriuretic response to these three states of body fluid imbalance. In this review we discuss the evidence for a common central nervous system-mediated natriuretic mechanism in response to disturbances of fluid and electrolyte balance. We also propose a role for pars intermedia-derived, proopiomelanocortin-derived peptides as humoral mediators of renal sodium excretion. Evidence from our laboratory, as well as others, provides data for a testable hypothesis to explain central nervous system-mediated natriuresis, as well as an explanation of how central nervous system lesions or neurochemical perturbations affect the renal response to body fluid imbalance.
Hypertension 1987 Nov
PMID:The natriuretic response to hydromineral imbalance. 331 6

Relative polycythaemia is a general term which includes patients with a normal red cell mass but a contraction of the plasma volume as the cause for the polycythaemia. The relative polycythaemias can broadly be divided into two groups. Firstly, relative polycythaemia may be due to a primary loss of plasma volume due to dehydration, capillary leak or hypo-oncotic pressure. Secondly, relative polycythaemia may be due to a primary contraction of the vascular compartment (i.e. reduced venous compliance). It is this second group which is the least understood and is analysed in detail in this review. In general, this group of polycythaemias is secondary to exogenous or endogenous stress and is mediated via the sympathetic nervous system. Hypoxia, smoking, neurological disorders, myocardial infarction and acute psychological stress have all been demonstrated as possible factors. In many cases of chronic stress polycythaemias aetiological factors may be identified, whereas in others the term idiopathic is probably appropriate. There appears to be a relationship between the idiopathic stress polycythaemias, hypertension and psychological stress. Other patients may have primarily a disorder of blood volume control involving the autonomic nervous system and its receptors. The haemorheological significance of relative polycythaemia and its management are discussed. Treatment is generally dictated by the underlying cause. In stress polycythaemias the stimulus should be removed as far as possible. However, in some patients with chronic idiopathic stress polycythaemia, regular venesection may be required to maintain the venous haematocrit at an appropriate level.
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PMID:The contracted plasma volume syndromes (relative polycythaemias) and their haemorheological significance. 332 61


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