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

Although total diversion of portal blood flow has been considered to be the main factor leading to encephalopathy following nonselective shunt (NSS), increased intestinal absorption of cerebral toxins secondary to mesenteric venous decompression could also play a role. Conversely, the low frequency of encephalopathy after the distal splenorenal shunt (DSRS) may be due to preservation of both hepatic portal perfusion and mesenteric venous hypertension. Portal hemodynamics, intestinal absorption of D-xylose, ammonia metabolism, and clinical encephalopathy were assessed preoperatively and in the early and late postoperative periods in cirrhotic patients selected for the DSRS (n = 12) and NSS (n = 10). Preoperatively, NSS patients had significantly less hepatopetal portal blood flow (P = 0.03) and lower D-xylose absorption (P = 0.004) than DSRS patients. DSRS resulted in no significant alterations in hepatic portal perfusion, portal pressure, D-xylose absorption, fasting blood ammonia (NH3), or tolerance to an oral dose of ammonium chloride. In contrast, NSS resulted in complete portal diversion and decompression and significant enhancement of D-xylose absorption on both the early (P = 0.02) and late (P = 0.03) postoperative evaluations. Early and late postoperative levels of MH3 were significantly higher in NSS patients. Encephalopathy was more frequent after NSS (80%) than after DSRS (17%, P = 0.003). When all patients were considered, preoperative to early DSRS (17%, P = 0.003). When all patients were considered, preoperative to early postoperative change in NH3 correlated with change in D-xylose absorption (r = 0.52, p = 0.02), and there were significantly more individuals with a greater than 2 gm increase in D-xylose absorption who developed encephalopathy (83%) than patients with no or minimal increase in D-xylose absorption (33%, P = 0.04). The results of this study suggest that altered intestinal absorption may be one of many factors determining postshunt cerebral function.
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PMID:Portal hemodynamics, intestinal absorption, and postshunt encephalopathy. 687 34

A 13-year-old girl with severe hypertension (240/140 mm Hg), short stature, marked hyperkalemia (8.6 mEq/liter), and renal tubular acidosis was studied. Renal parenchymal and renovascular diseases as well as endocrinologic causes of hypertension were ruled out by appropriate studies. The hypertension was associated with sodium retention, increased plasma volume, suppressed plasma renin activity, and decreased urinary excretion of aldosterone. Impaired renal excretion of potassium was demonstrated by sodium sulfate infusion when the patient was fed a high-sodium diet but a significant kaliuresis occurred when the test was performed on a low-sodium diet suggesting that renal sodium retention may play a role in the defect in potassium excretion. The renal tubular acidosis was associated with normal distal acidification but a low bicarbonate threshold (19 mmoles/liter) and marked suppression of urinary ammonium excretion. The hypertension, hyporeninemia, and hypoaldosteronism as well as the hyperkalemia and acid-base abnormalities were completely reversed by dietary sodium restriction or the administration of thiazides or furosemide. It is concluded that an unusual avidity for sodium chloride reabsorption by the renal tubules leading to extracellular volume expansion and renin-aldosterone suppression plays a significant pathogenic role in this syndrome and may explain the hypertension and biochemical abnormalities discussed.
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PMID:Severe hypertension, hyperkalemia, and renal tubular acidosis responding to dietary sodium restriction. 706 87

A study of renal function of 51 patients with gout and an equal number of normouricaemic controls revealed significant differences. A relative impairment of the glomerular filtration rate and urine concentrating ability in the gouty subjects could not be wholly explained on the basis of aging or hypertension. Renal dysfunction was generally mild and was not associated with specific clinical characteristics higher levels of uric acid excretion, or hypertriglyceridaemia. Gout patients excreted urine with a significantly lower pH. This was associated with a relatively high excretion of titratable acid and a deficit of ammonium excretion, which was accentuated by ingestion of an acid load. Urate clearance was significantly reduced in gout, even when expressed as a fraction of the glomerular filtration rate.
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PMID:Renal impairment and gout. 743 72

A 16-month-old boy ingested liquid zinc chloride/ammonium chloride soldering flux. He developed severe local burns, metabolic acidosis, hepatic damage, hyperamylasemia, lethargy, and hypertension. Peak measured plasma zinc was 1,199 micrograms/dL. Because of persistent signs of systemic toxicity, he was chelated with dimercaprol (BAL) and EDTA. Although clinical improvement was noted coincident with the initiation of chelation, there was no apparent increase in urinary zinc excretion. Scarring in the gastric antrum necessitated an antrectomy. The child recovered without other apparent complications.
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PMID:Acute zinc chloride ingestion in a child: local and systemic effects. 771 Jan 73

Acute hyperammonemia causes cerebral edema, elevated intracranial pressure and loss of cerebral blood flow (CBF) responsivity to CO2. Inhibition of glutamine synthetase prevents these abnormalities. If the loss of CO2 responsivity is secondary to the mechanical effects of edema, one would anticipate loss of responsivity to other physiological stimuli, such as hypoxia and changes in mean arterial blood pressure (MABP). To test this possibility, pentobarbital-anesthetized rats were subjected to either hypoxic hypoxia (PaO2 approximately 30 mm Hg), hemorrhagic hypotension (MABP approximately 70 and 50 mm Hg), or phenylephrine-induced hypertension (MABP approximately 125 and 145 mm Hg). CBF was measured with radiolabeled microspheres. Experimental groups received intravenous ammonium acetate (approximately 50 mumol min-1 kg-1) for 6 h to increase plasma ammonia to 500-600 microM. Control groups received sodium acetate plus HCl to prevent metabolic alkalosis. The increase in CBF during 10 min of hypoxia after 6 h of ammonium acetate infusion (84 +/- 19 to 259 +/- 52 ml min-1 100 g-1) was similar to that after sodium acetate infusion (105 +/- 20 to 265 +/- 76 ml min-1 100 g-1). Cortical glutamine concentration was elevated equivalently in hyperammonemic rats subjected to normoxia only or to 10 min of hypoxia. With severe hypotension, CBF was unchanged in both the ammonium (80 +/- 20 to 76 +/- 24 ml min-1 100 g-1) and the sodium (80 +/- 14 to 73 +/- 16 ml min-1 100 g-1) acetate groups. With moderate hypertension, CBF was unchanged. With the most severe hypertension, significant increases in CBF occurred in both groups, but there was no difference between groups. We conclude that hypoxic and autoregulatory responses are intact during acute hyperammonemia. The previously observed loss of CO2 responsivity is not the result of a generalized vasoparalysis to all physiological stimuli.
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PMID:Preservation of cerebral blood flow responses to hypoxia and arterial pressure alterations in hyperammonemic rats. 767 76

We examined the interaction among changes in pHi, [Ca2+]i, myosin light-chain phosphorylation, and contraction in arterial smooth muscle stimulated by histamine, NH4+, Tris+, and/or changes in extracellular pH (pHo). We loaded swine carotid medial tissues with 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein to measure pHi or aequorin to measure [Ca2+]i. Incubation of tissues in NH4+ increased pHi, [Ca2+]i, myosin phosphorylation, and force. Washout of NH4+ decreased pHi and transiently further increased in [Ca2+]i and force. Incubation of tissues in a similar concentration of Tris+ or increasing pHo also increased pHi; however, there were only modest changes in [Ca2+]i and force. Increasing extracellular pH coincidentally with washout of NH4+ prevented the decrease in pHi but did not affect the NH4+ washout-induced contraction. These data suggest that NH4+ altered [Ca2+]i and contraction by mechanisms other than its effects on pHi. The type of pH buffer did not affect the [Ca2+]i, myosin phosphorylation, or stress response to histamine stimulation. The time course of changes in pHi was much slower than the time course of histamine-induced changes in [Ca2+]i, myosin phosphorylation, and stress. Addition of 10 mmol/L NH4+ concurrently with histamine aborted the histamine-induced decrease in pHi and significantly slowed the histamine-induced increase in [Ca2+]i, myosin phosphorylation, and stress. There was little effect on histamine-induced increases in [Ca2+]i, myosin phosphorylation, or contraction when three other protocols aborted the histamine-induced decrease in pHi. These data show that incubation in NH4+ can alter [Ca2+]i and contraction in both unstimulated and histamine-stimulated smooth muscle. However, these effects were not caused by NH4(+)-dependent changes in pHi.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1995 Apr
PMID:pHi, [Ca2+]i, and myosin phosphorylation in histamine- and NH4(+)-induced swine carotid artery contraction. 772 87

This article reviews work from this laboratory dealing with acid-base status and intracellular pH (pHi) regulation in rat genetic models of hypertension. With freshly isolated thymic lymphocytes, pHi and its regulation were examined in the spontaneously hypertensive rat (SHR). In this rat model, pHi was found to be reduced as compared with that of lymphocytes from normotensive Wistar-Kyoto (WKY) rats. The activity of the Na+/H+ antiporter assessed after stimulation by acute cell acidification was similar in lymphocytes from SHR and WKY rats both in the nominal absence of HCO3- and in media containing HCO3- (22 mM). The kinetic properties of the Na+/H+ antiporter, examined as a function of pHi with the Hill kinetic model, revealed no significant differences between lymphocytes from SHR and WKY rats. The kinetic properties of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchangers, examined as a function of external Cl-, were also virtually identical in lymphocytes from SHR and WKY rats. Unlike the Na(+)-H+ exchanger and the Na(+)-independent Cl(-)-HCO3- exchanger, which had their highest activities at extremes of pHi (low pHi, Na(+)-H+ exchanger; high pHi, Na(+)-independent Cl(-)-HCO3- exchanger), the Na(+)-dependent Cl(-)-HCO3- exchanger had its maximal activity near steady-state pHi. In Dahl/Rapp salt-sensitive rats with hypertension, the pHi of thymic lymphocytes was also reduced as compared with that of normotensive salt-resistant animals. In this model, renal net acid excretion in salt-sensitive rats was augmented as compared with that of salt-resistant rats. The increase in renal acid excretion was due to an increase in both ammonium and titratable acid excretion and was observed while animals were placed on high, normal and low salt diets. The findings of intracellular acidosis and enhanced renal acid excretion suggest that cellular acid overproduction is augmented in salt-sensitive hypertension.
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PMID:Acid-base status and intracellular pH regulation in lymphocytes from rats with genetic hypertension. 787 40

We designed the present study to clarify whether the intracellular pH change by ammonium chloride influences endothelium-dependent relaxation in thoracic aorta of 9-week-old Sprague-Dawley rats. Intracellular alkalinization with 3 mmol/L ammonium chloride, which did not affect resting vascular tone, attenuated acetylcholine-induced relaxation but not nitroglycerin vasodilation. Acetylcholine relaxation was more inhibited by a shorter duration of treatment. Thus, change in intracellular pH may be important in the effect because the alkalinizing effect of ammonium chloride disappears gradually. In support of this, the proton ionophore nigericin abolished the effect. Also, amiloride shortened the effect of ammonium chloride, suggesting that intracellular pH plays a role: sodium-proton antiport antagonizes the disappearance of ammonium chloride-induced intracellular alkalinization. The synthesis of vasoconstrictor prostaglandins, such as thromboxane A2, may be stimulated during acetylcholine treatment, resulting in the attenuation of acetylcholine relaxation, because the relaxation was abolished by treatment with the phospholipase A2 inhibitor quinacrine, cyclooxygenase inhibitor indomethacin, prostaglandin H2/thromboxane A2 receptor antagonist S1452, and thromboxane A2 synthase inhibitor dazmegrel. Phospholipase A2 may contribute to the effect of intracellular alkalinization, which is compatible with the fact that the optimal pH of phospholipase A2 is neutral to alkaline. In addition, superoxide dismutase attenuated the effect of ammonium chloride. In conclusion, intracellular alkalinization by ammonium chloride attenuated acetylcholine-induced relaxation, possibly through the interrelated production of both thromboxane A2 and superoxide radicals.
Hypertension 1994 Aug
PMID:Inhibitory effect of ammonium chloride on acetylcholine-induced relaxation. 803 43

Brain edema, leading to intracranial hypertension and brain herniation, is a major cause of death in fulminant liver failure. Astrocyte swelling is a prominent neuropathological feature in experimental fulminant liver failure. It has been postulated that the osmotic effects of glutamine, generated in astrocytes from ammonia and glutamate in a reaction catalyzed by glutamine synthetase, could mediate brain swelling. Normal rats and rats that received a portacaval anastomosis were infused with ammonium acetate or a sodium acetate control; brain water in cerebral cortex was measured with the gravimetry method, intracranial pressure by means of a cisterna magna catheter and cortical amino acids using high-performance liquid chromatography. Although brain edema was detected in both groups receiving ammonia, it was of a greater magnitude in portacaval anastomosis rats (80.94% + 0.17% vs. 80.24% + 0.09%, p < 0.01), resulting in the development of intracranial hypertension. When portacaval anastomosis rats were infused with ammonium acetate and pretreated with 150 mg/kg methionine-sulfoximine, an inhibitor of glutamine synthetase activity, brain edema was ameliorated and intracranial pressure did not rise. A dose-dependent reduction in brain glutamine levels was seen with increasing doses of methionine-sulfoximine; however, brain edema did not decrease beyond the 150 mg/kg dose, suggesting that the increase in brain water was not solely a result of glutamine accumulation. We conclude that brain edema of a magnitude that results in intracranial hypertension is more likely to develop in rats after portacaval anastomosis receiving a continuous ammonia infusion. The osmotic effects of glutamine appear to mediate, but only in part, the increase in brain water seen in this preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ammonia-induced brain edema and intracranial hypertension in rats after portacaval anastomosis. 818 74

Reduced extracellular pH and bicarbonate levels recently have been reported in normotensive salt-sensitive subjects. To assess the possible role of altered renal acid-base handling in the perturbation of acid-base status in these individuals, we measured the renal acid-base excretion after an acute oral administration of either an alkali or acid load in normotensive salt-sensitive and salt-resistant men. Twenty-four young (22 to 29 years old), healthy male volunteers were placed on a low-salt diet (20 mmol NaCl per day) for 2 weeks with either 220 mmol NaCl or placebo added to the low-salt diet for 1 week each in a randomized single-blind crossover order. Salt sensitivity was defined as a significant drop in mean arterial pressure (> 3 mm Hg, mean of 60 readings taken on the seventh day of each diet, P < .05) during the low-salt diet. On the fifth and seventh days of each week, subjects were given an oral load of either sodium citrate (0.7 mmol/kg) or ammonium chloride (2.2 mmol/kg), respectively, in a randomized order, and arterial and urinary acid-base status was assessed at baseline and followed for 8 hours thereafter. According to the above definition, 13 subjects were considered salt sensitive. During the high-salt diet, mean arterial pressure was higher in the salt-sensitive than in the salt-resistant group (P < .01). Cumulative urinary bicarbonate excretion after the administration of sodium citrate was lower in the salt-sensitive than in the salt-resistant subjects during both the low-salt (46%, P < .001) and high-salt (32%, P < .01) diets.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 Dec
PMID:Renal acid-base excretion in normotensive salt-sensitive humans. 824 21


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