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

In eight male patients with normal liver and kidney function fibrinolytic components were measured in arterial blood and in renal and hepatic vein blood, obtained during catheterization for analysis of hypertension. Blood samples were collected simultaneously from veins und corresponding arteries before and 5 minutes after the completion of intravenous injection of desmopressin (DDAVP), 0.4 micrograms/kg body weight over a 10 minute period. DDAVP induced a rise in t-PA antigen and activity, and in von Willebrand factor, accompanied by a decrease in free PA-inhibitor level. We failed to detect a significant rise in plasma urokinase activity. The concentrations of fibrinogen, plasminogen, alpha 2-antiplasmin, antithrombin III and coeruloplasmin did not change either. Renal production of t-PA under basal conditions was inferred from a negative arterio-venous (A-V) difference in t-PA-activity and in t-PA-antigen levels but this could not be confirmed by orthogonal regression analysis of the same data. A-V differences of other fibrinolytic factors were negligible. In the hepatic vessels a significant positive A-V difference of t-PA-activity and of t-PA-antigen levels was a uniform finding. After DDAVP, when plasma levels were elevated, the mean A-V difference was proportionally higher, consistent with a constant fractional elimination rate. Free PA-inhibitor was virtually absent from arterial blood after DDAVP, but appeared in hepatic vein blood, indicating either production of the inhibitor by the liver or dissociation of a circulating complex of t-PA and its inhibitor in the liver. The blood levels of the other investigated components did not show any change upon passage through the liver.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal and hepatic handling of endogenous tissue-type plasminogen activator (t-PA) and its inhibitor in man. 314 78

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3 to 6.8 mM), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mM), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/hr), high plasma aldosterone (32 to 100 ng/dl), normal GFR (131 +/- 2.5 ml/min/1.73 m2). During hyperkalemic period, urine was highly acidic (pH 4.6 to 5.0), urinary NH4 excretion (13 mumoles/min) and urinary net acid excretion (24 mumoles/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, maximal tubular HCO3 reabsorption (Tm HCO3) was markedly diminished (19 mmoles/liter GF), fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized, was 20%. Urine-minus-blood PCO2 increased normally (31 mmHg) during NaHCO3 infusion, and urinary pH remained maximally low (less than 5.3) when buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while urinary pH remained maximally low (4.9 to 5.2), Tm HCO3 returned to normal value (24.8 mmoles/liter GF), and FE HCO3 became nil. The renal handling of K was improved with acute NaHCO3 loading and normalized after DDAVP nasal insufflation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type II pseudohypoaldosteronism: proximal tubular acidosis and distal tubular hyperkalemia corrected by DDAVP]. 408 72

The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.
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PMID:Vasopressin as a possible contributor to hypertension. 632 16

The aim of the present study was to investigate whether the presence of arginine vasopressin (AVP) is necessary for the establishment of high blood pressure in spontaneously hypertensive rats (SHR). For this purpose we crossbred SHR of the stroke-prone substrain (SHRSP) with rats homozygous for hypothalamic diabetes insipidus of the Brattleboro strain (DI) which are unable to synthetize AVP. The successful introduction of the DI gene into the SHRSP strain (SHRDI) was demonstrated by the following observations: In 10-month-old rats, water intake was similarly elevated in SHRDI as in DI rats (137 +/- 6.5 vs 125 +/- 10.5 ml per 24 hours). AVP was undetectable in the plasma, in the hypothalamus, and in the pituitary of SHRDI and DI rats. Urine osmolality and urinary concentration of sodium and potassium were markedly reduced. SHRDI and DI did not adequately concentrate their urine during an 8-hour period of water deprivation, but both strains of rats responded well with a fall in urine output and a rise in urine osmolality to subcutaneous administration of the non-pressor analog of AVP, DDAVP. Mean arterial blood pressure was markedly increased in SHRDI as well as in SHRSP (184 +/- 9.7 vs 197 +/- 5.2 mm Hg). Thus, we have developed a new line of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus. From this finding it is concluded that AVP is not essential for the development and maintenance of spontaneous hypertension of rats.
Hypertension
PMID:Development of a new strain of spontaneously hypertensive rats homozygous for hypothalamic diabetes insipidus. 682 22

The intraventricular administration of vasopressin or DDAVP (desmopressin acetate) increased the brain water content from 78.2% to 79.2-79.5%. This was achieved without an accompanying water load. The applied water load alone did not increase the water content of the brain. There was no significant difference in the water content of the brain between animals treated with intraventricular vasopressin and intravenous water load and animals receiving only intraventricular vasopressin. The water content of the olfactory bulbs of the control animals was 3.8% higher than that of the hemispheres. While the water content of the hemispheres increased by 1.3%, that of the olfactory bulbs did so by 1.7% subsequent to the intraventricular administration of DDAVP. Measurement of the brain electrolyte content was not conclusive as to the mechanism of water permeability changes. The possible mechanism is discussed. Although no tissue or cerebrospinal fluid concentrations of vasopressin enabling comparison with clinical pathological conditions have been measured, it is suggested that increased secretion of vasopressin into the cerebrospinal fluid in conditions such as subarachnoid hemorrhage or intracranial hypertension of various origins might play a role in edema formation.
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PMID:Brain water accumulation after the central administration of vasopressin. 713 57

1. Homozygous Brattleboro rats with hereditary hypothalamic diabetes insipidus (DI) developed one-kidney, one-clip (1K-1C) and two-kidney, one-clip (2K-1C) Goldblatt renal hypertension. 2. However, the systolic blood pressure (SBP) in 1K-1C Brattleboro rats was significantly lower than in non-DI hypertensive 1K-1C Long-Evans (LE) rats. 3. Treatment with the synthetic antidiuretic analogue of vasopressin, DDAVP (1-desamino-8-D-arginine vasopressin), increased the SBP in the DI rats to the same level as in 1K-1C Long-Evans. This elevation of SBP was associated with increased extracellular fluid volume in the DI rats after DDAVP. 4. The results suggest that vasopressin is not essential for the development of renal hypertension but the absolute levels of blood pressure achieved in 1K-1C hypertension are volume-dependent and thus influenced by the water-retaining properties of vasopressin.
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PMID:Importance of antidiuretic properties of vasopressin in experimental renal hypertension. 732 74

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension. 795 85

Vasovagal reflexes, such as hypotension and bradycardia, are induced by rapid hemorrhage and mimic neurocardiogenic reflexes in mammals. We examined the role of vasopressin in the neurocardiogenic responses to mild, rapid hemorrhage (1 mL/100 g for 30 seconds) and severe hemorrhage (1 mL/100 g body wt for 30 seconds repeated three times at 11-minute intervals) in homozygous Brattleboro and Long-Evans rats. Mild, rapid hemorrhage induced severe bradycardia and hypotension only in Long-Evans rats. Exogenous vasopressin (1.85 pmol/kg per minute for 1 hour) restored both the bradycardic and hypotensive responses in Brattleboro rats. DDAVP, a vasopressin V2-receptor agonist (0.19 pmol/kg per minute for 24 hours), did not affect the cardiovascular responses to hemorrhage in Brattleboro rats, although it maintained urine production within normal limits. However, OPC-31260 (21.6 mumol/kg IV), a vasopressin V2-receptor antagonist, attenuated both the hypotensive and bradycardic responses to hemorrhage in Long-Evans rats. A vasopressin V1-receptor antagonist attenuated bradycardia and delayed the recovery of arterial pressure after hemorrhage but did not affect the hypotension that occurred immediately after hemorrhage in Long-Evans rats. Methylatropine also attenuated both the bradycardic and hypotensive responses induced by hemorrhage, but propranolol had no effect on the cardiovascular responses to hemorrhage in Long-Evans rats. The recovery of arterial pressure after repeated hemorrhage was less adequate in Brattleboro rats than in Long-Evans rats. Our results suggest that the neurocardiogenic responses to hemorrhage, especially hypotension, may be related to vasodilation induced by a V2-receptor-mediated mechanism and by the vagal reflex, both of which are substantiated by the existence of vasopressin. The coexistence of V1- and V2-receptor mechanisms may be necessary for the hypotensive response to hemorrhage. We found that a V2-receptor antagonist attenuated the hypotension mediated by the so-called neurocardiogenic reflex.
Hypertension 1996 Jan
PMID:Role of vasopressin in neurocardiogenic responses to hemorrhage in conscious rats. 859 76

Haemodialysis (HD) patients are at an increased risk of bleeding because of uraemic bleeding tendency and systemic anticoagulation caused by intermittent heparinization. Additional risk factors may be aspirin or coumarin use for the prevention of fistula thrombosis, diffuse intravascular coagulation, recent trauma, postsurgical state, inadequate control of hypertension, gastrointestinal lesions, diabetic retinopathy, renal cystic disease, and uraemic pericarditis. In HD patients with an active bleeding focus blood transfusion, desmopressin acetate (DDAVP), conjugated oestrogens, and dialysis treatment can limit the bleeding risk. Strategies to reduce the bleeding risk conveyed by systemic anticoagulation during HD are regional heparin anticoagulation and minimal heparinization. In our opinion, dialytic modalities that completely preclude systemic anticoagulation, i.e. peritoneal dialysis (PD), heparin-free HD, and HD with regional anticoagulation with prostacyclin, mesilates, or citrate, are indicated for patients who are actively bleeding, or who are within 3 days from a bleeding episode, or a surgical or accidental wound, or who are less than 2 weeks from cerebral or retinal haemorrhage, and for patients with incompletely treated proliferative diabetic retinopathy or uraemic pericarditis.
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PMID:The bleeding risk in chronic haemodialysis: preventive strategies in high-risk patients. 871 39

Under water restriction, arginine vasopressin (AVP) is released and promotes water reabsorption in the distal nephron, mainly through AVP V2-receptors. It has been proposed that renal kinins counteract the hydro-osmotic effect of AVP. We hypothesized that kinins acting through B2 receptors antagonize the urinary concentrating effect of AVP. To test this, bradykinin B2 receptor knockout mice (B2-KO) and 129/SvEv mice (controls) were placed in metabolic cages and urine collected for 24 hours (water ad libitum). After that, urine was again collected from the same mice during 24 hours of water restriction. Urinary volume (UV), urinary osmolarity (UOsm), and urinary Na+ (UNaV) and K+ (UKV) excretion were determined. On water restriction, UV in controls decreased by approximately 25%, whereas in B2-KO mice there was almost a 60% drop in urinary output (P=0.001 versus controls). In the controls, water restriction increased UOsm by 347 mOsm/kg H2O, approximately 14% above baseline (NS), whereas in knockout mice the increase was 3 times that seen in the controls: >1000 mOsm/kg H2O (P=0.001 versus controls). Compared with normohydration, UNaV and UKV in the water-restricted state increased more in controls than in B2-KO mice. This difference in electrolyte excretion could be explained by greater dehydration in the controls (dehydration natriuresis). In a second protocol, we tried to mimic the effect of endogenous AVP by exogenous administration of an AVP V2-receptor agonist, desmopressin (DDAVP). To suppress endogenous AVP levels before DDAVP administration, mice were volume-overloaded with dextrose and alcohol. UOsm was 685+/-125 and 561+/-58 mOsm/kg H2O in water-loaded controls and B2-KO mice, respectively. After DDAVP was injected subcutaneously at a dose of 1 microgram/kg, UOsm increased to 1175+/-86 mOsm/kg H2O (Delta+490 mOsm) in the controls and 2347+/-518 mOsm/kg H2O (Delta+1786 mOsm) in B2-KO mice (P<0.05 versus controls). We concluded that water restriction or exogenous administration of an AVP V2-receptor agonist has a greater urinary concentrating effect in B2-KO mice than in controls, suggesting that endogenous kinins acting through B2 receptors oppose the antidiuretic effect of AVP in vivo.
Hypertension 1999 Jun
PMID:An enhanced effect of arginine vasopressin in bradykinin B2 receptor null mutant mice. 1037 29


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