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

This study characterizes the response to dietary calcium in DOCA-salt hypertension. Body weight, systolic blood pressure, and total serum calcium levels were compared among normotensive control rats, DOCA-salt hypertensive rats treated with calcium carbonate (CaCO3) augmentation, and DOCA-salt hypertensive rats without supplementary dietary calcium. Dietary calcium augmentation prevented the rise of blood pressure that is normally produced by DOCA-salt. Attenuation in systolic blood pressure was independent of weight loss or total serum calcium and may be linked to alterations in calcium homeostasis that are seen in both human and experimental hypertension. Thus this study provides important data that may assist in further explicating the role that alterations in calcium homeostasis play in DOCA-salt hypertension. Further, these data may also be important in the identification of a nonpharmacological intervention for testing in humans.
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PMID:Effect of supplemental dietary calcium on the development of DOCA-salt hypertension in weanling rats. 786 48

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

There are two types of diabetes mellitus. Type I, insulin-dependent diabetes (IDDM), which becomes manifest before the age of 40, is the result of an absolute deficiency of insulin. Type II, the non-insulin-dependent diabetes (NIDDM), develops in the elderly and is caused by a relative insulin deficiency. Patients with type-I diabetes are prone to the development of ketoacidosis, while type II causes hyperglycaemic, hyperosmolar, nonketotic coma. Apart from these acute metabolic alterations, the long-term complications of diabetes are of concern to the anaesthesiologist. Hypertension, coronary artery disease, renal insufficiency and autonomic neuropathy are common and can result in myocardial ischaemia, cardiovascular instability and gastroparesis, with an increased risk of aspiration. Limited movement of the atlanto-occipital joint can cause difficult intubation. To avoid perioperative metabolic catastrophy, blood glucose concentration should be kept between 6.7 and 10 mmol.l-1 (120-180 mg.dl-1). Hypoglycaemia can result in neurological damage, whereas hyperglycaemia causes impaired wound healing and susceptibility to infections and worsens ischaemic damage to the myocardium and brain. Perioperative diabetes management depends on the severity of the surgical procedure and the type of diabetes. All type-I diabetics, whatever operation being performed, need insulin. The intravenous route is recommended as it allows better adjustment. After determination of the fasting blood glucose level, insulin is given at a dosage of 0.5-1 U.h-1 (at gluc < 11.1 mmol.l-1), 1.5-2 U.h-1 (at gluc 11.1-16.7 mmol.l-1) or 3 U.h-1 (at gluc > 16.7 mmol.l-1). In addition, 5-10 g glucose.h-1 is given. In type-II diabetes the oral antidiabetic drug is withheld. During minor surgery the blood glucose concentration is monitored frequently, and if necessary insulin (with gluc > 13.9 mmol.l-1) or glucose is given. In most cases of major surgery insulin therapy will be necessary. Administration should follow the guidelines listed for type-I diabetes. Whether the intravenous or the subcutaneous route is used for insulin, repeated glucose determinations are mandatory. If ketoacidosis develops the volume depletion is treated with normal saline. For hyperglycaemia and acidosis insulin (3-6 U.h-1) with 10-20 mmol.h-1 potassium phosphate is given. Bicarbonate is only indicated when the serum pH is lower than 7.1. It must be borne in mind that perioperative management of diabetes does not end with postanaesthesia care.
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PMID:[Anesthesia and diabetes mellitus]. 804 63

In physiological conditions, the regulation of acid-base balance in brain maintains a noteworthy stability of cerebral pH. During systemic metabolic acid-base imbalances cerebral pH is well controlled as the blood/brain barrier is slowly and poorly permeable to electrolytes (HCO3- and H+). Cerebral pH is regulated by a modulation of the respiratory drive, triggered by the early alterations of interstitial fluid pH, close to medullary chemoreceptors. As blood/brain barrier is highly permeable to Co2, CSF pH is corrected in a few hours, even in case of severe metabolic acidosis and alkalosis. Conversely, during ventilatory acidosis and alkalosis the cerebral pH varies in the same direction and in the same range than blood pH. Therefore, the brain is better protected against metabolic than ventilatory acid-base imbalances. Ventilatory acidosis and alkalosis are able to impair cerebral blood flow and brain activity through interstitial pH alterations. During respiratory acidosis, [HCO3-] increases in extracellular fluids to control cerebral pH by two main ways: a carbonic anhydrase activation at the blood/brain and blood/CSF barriers level and an increase in chloride shift in glial cells (HCO3- exchanged for Cl-). During respiratory alkalosis, [HCO3-] decreases in extracellular fluids by the opposite changes in HCO3- transport and by an increase in lactic acid synthesis by cerebral cells. The treatment of metabolic acidosis with bicarbonates may induce a cerebral acidosis and worsen a cerebral oedema during ketoacidosis. Moderate hypocapnia carried out to treat intracranial hypertension is mainly effective when cerebral blood flow is high and vascular CO2 reactivity maintained. Hypocapnia may restore an altered cerebral blood flow autoregulation. Instrumental hypocapnia requires a control of cerebral perfusion pressure and cerebral arteriovenous difference for oxygen, to select patients for whom this kind of treatment may be of benefit, to choose the optimal level of hypocapnia and to avoid any deleterious effect. If hypocapnia is maintained over several days, an adaptation of CSF pH may limit the therapeutic effect on the cerebral blood flow and the intracranial pressure.
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PMID:[Acid-base equilibrium and the brain]. 809 67

Previous studies that have evaluated the Na(+)-H+ antiporter in cells from hypertensive subjects were generally performed under conditions in which HCO3-CO2, the physiological buffer system, was absent from the assay media. The objective of this study was to evaluate the activity of the Na(+)-H+ antiporter and that of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchangers in cells assayed in the presence of HCO3-CO2 in the media. Lymphocytes from 6- to 8-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) rats were obtained from the thymus gland and assayed immediately after isolation. The activity of the Na(+)-H+ antiporter after stimulation by cell acidification (pHi approximately 6.4) was similar in SHR and WKY rats (18.67 +/- 1.03 and 16.12 +/- 0.92 mmol H+/L per minute, respectively). Recovery from cell alkalinization was effected by an Na(+)-independent Cl(-)-HCO3- exchanger, with maximal activity at an alkaline pHi (approximately 7.7). The stimulated activity of this Na(+)-independent Cl(-)-HCO3- exchanger was also not different between SHR and WKY cells (2.65 +/- 0.25 and 2.55 +/- 0.32 mmol H+/L per minute, respectively). Acute chloride removal produced a rise in pHi that was Na(+)-dependent and sensitive to 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) but resistant to ethylisopropylamiloride (EIPA), reflecting the activity of an Na(+)-dependent Cl(-)-HCO3- exchanger. 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, and high pHi, Na(+)-independent Cl(-)-HCO3- exchanger), the Na(+)-dependent Cl(-)-HCO3- exchanger had its maximal activity near steady-state pHi (approximately 7.1). No significant differences were found in the stimulated activity of this exchanger between cells from SHR and WKY rats (2.23 +/- 0.26 and 2.50 +/- 0.43 mmol H+/L per minute, respectively). The kinetic properties of the Na(+)-dependent and Na(+)-independent Cl(-)-HCO3- exchanger, examined as a function of external Cl-, were also virtually identical in cells from SHR and WKY rats. We conclude that in lymphocytes from SHR and WKY rats, the activity of the two Cl(-)-HCO3- exchangers, like that of the Na(+)-H+ exchanger, is dependent on the prevailing pHi. The Na(+)-dependent Cl(-)-HCO3- exchanger has its highest activity near steady-state pHi, suggesting an important role in the cell defense against intracellular acidosis under physiological conditions.(ABSTRACT TRUNCATED AT 400 WORDS)
Hypertension 1994 Apr
PMID:Regulation of intracellular pH in the spontaneously hypertensive rat. Role of bicarbonate-dependent transporters. 814 20

Severe ketonuria developed during sedation with propofol in a 12 year old girl with brain injury. Deep sedation with propofol (5.1 mg/kg/h) was required because of agitation and severe intracranial hypertension; as a part of our management protocol, glucose intake was restricted to 5 Kcal/h. After 18 hours of propofol infusion there was intense ketonuria (8+ by Ketostix) without any evidence of metabolic acidosis (pH, HCO3- and anion gap were within normal values). At this time, indirect calorimetry (Deltatrac) confirmed that energy expenditure was principally based on fat consumption (70% of energy expenditure). Lowering the propofol infusion rate and increasing glucose intake reduced fat consumption to 39% within 8 hours: at this time, Ketostix was negative for ketone bodies. This case illustrates a potential risk of ketonuria during prolonged sedation with propofol (a 10% solution of intralipid), particularly if glucose intake is restricted. Monitoring urinary ketone bodies is recommended under these circumstances.
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PMID:Massive ketonuria during sedation with propofol in a 12 year old girl with severe head trauma. 820 21

Acid-base status and renal acid excretion were studied in the Dahl/Rapp salt-sensitive (S) rat and its genetically salt-resistant counterpart (R). S rats developed hypertension while on a very high salt diet (8%) and while on a more physiological salt diet (1%) and remained normotensive while on a very low salt diet (0.08%). Under the high salt diet, intracellular pH measured in freshly isolated thymic lymphocytes using 2',7'-bis (carboxyethyl)-5 (6)-carboxyfluorescein acetomethyl ester, a pH-sensitive dye, was lower in S than in R rats both when measured in the presence of HCO3/CO2 (7.32 +/- 0.02 vs. 7.38 +/- 0.02, respectively, P < 0.05) and in its absence (7.18 +/- 0.04 vs. 7.27 +/- 0.02, respectively, P < 0.05). Under the high salt diet, net acid excretion was higher in S than R rats (1,777 +/- 111 vs. 1,017 +/- 73 muEq/24 h per 100 g body wt, respectively, P < 0.001), and this difference was due to higher rates of both titratable acid and ammonium excretion. Directionally similar differences in intracellular pH and net acid excretion between S and R rats were also observed in salt-restricted animals. In S and R rats placed on a normal salt intake (1%) and strictly pair-fed to control food intake as a determinant of dietary acid, net acid excretion was also higher in S than in R rats (562 +/- 27 vs. 329 +/- 21 muEq/24 h per 100 g, respectively, P < 0.01). No significant difference in either blood pH or bicarbonate levels were found between S and R rats on either the 0.08%, 1%, or 8% salt diets. We conclude that renal acid excretion is augmented in the salt-sensitive Dahl/Rapp rat. Enhanced renal acid excretion may be a marker of increased acid production by cells from subjects with salt-sensitive hypertension.
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PMID:Renal acid excretion and intracellular pH in salt-sensitive genetic hypertension. 848 83

Calcium intake has been implicated as being an important factor in the development and treatment of hypertension. The mechanisms underlying the relationship between calcium and blood pressure are not yet clearly defined. Experimental studies have documented an inverse association between calcium intake and blood pressure level. For 15 years it has been shown that calcium supplementation is effective in lowering blood pressure in hypertensive rats and, on the other hand, calcium deprivation results in increased blood pressure levels. Enriched calcium diets decrease blood pressure in genetic hypertension displayed by spontaneously hypertensive rats (SHR), stroke-prone SHR, Lyon hypertensive rats or Dahl salt-sensitive rats and, in volume-dependent hypertension induced by saline and mineralocorticoid or angiotensin II administration in Wistar or Sprague-Dawley rats. Efficacy is observed with calcium carbonate added in the diet and with calcium chloride or calcium gluconate in drinking water. Compared with the normal level in the diet (0.5% to 1%), calcium supplementation represents mainly a fourfold increase whose effect is more intense in young weaning animals treated for a long-lasting period (4 to 10 weeks).
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PMID:Blood pressure effects of calcium intake in experimental models of hypertension. 858 13

We evaluated changes in erythrocyte sodium transport systems, platelet pH, and calcium concentration induced by low and high salt intakes in a group of 50 essential hypertensive patients classified on the basis of their salt sensitivity. Patients received a standard diet with 20 mmol NaCl daily for 2 weeks supplemented in a single-blind fashion by placebo tablets the first 7 days and NaCl tablets the following 7 days. Salt sensitivity, defined as a significant rise (P <.05) in 24-hour mean blood pressure obtained by ambulatory blood pressure monitoring, was diagnosed in 22 (44%) patients. The remaining 28 (56%) were considered to have salt-resistant hypertension. In the entire group of hypertensive patients, high salt intake promoted a significant increase (P <.05) in the maximal rate of erythrocyte NA(+)-Li(+) countertransport (from 271 +/- 19 to 327 +/- 18 microM/(L cells/h) and of the Na(+)-dependent HCO3(-)-CL(-) exchanger (from 946 +/- 58 to 1237 +/- 92 microM/L cells/h) as well as in platelet pH (from 7.15+/-0 0.01 to 7.19+/-0.02 and calcium concentration (from 49+/-2 to 57 +/-2 nmol/L). Depending on salt sensitivity, high salt intake promoted opposing changes in some of the sodium transport systems studied. Salt-sensitive patients increased the maximal rate of the erythrocyte Na(+)-K(+) pump (fom 7.0 +/- 0.4 to 8.8 +/- 0.4 mmol/(L cells/h), Na(+)-K(+)-Cl(-) cotransport (from 416 +/- 37 to 612 +/- 41 micromol/(L cells/h), Na(+)-Li(+) countertransport (from 248 +/- 20 to 389 +/- 17 micromol/(L cells/h) at the end of the high salt period. Conversely, salt-resistant patients decreased the Na(+)-K(+) pump (from 8.0 +/- 0.4 to 6.9 +/- 0.3 mmol/(L cells/h) and Na(+)-K(+)-Cl(-) cotransport (from 578 +/- 53 to 481 +/- 43 micromol/(L cells/h). We conclude that modulation of erythrocyte sodium transport systems by high salt intake depends on salt sensitivity. The Na(+)-K(+) pump, Na(+)-K(+)-Cl(-) cotransport, and Na(+)-Li(+) countertransport increase in salt-sensitive patients, whereas the activity of these sodium transport systems tends to decrease in salt-resistant patients. Independent of salt sensitivity, high salt intake promotes a significant increase in the erythrocyte Na(+)-dependent HCO3(-)-Cl(-) exchanger, platelet pH, and calcium concentration in essential hypertensive patients.
Hypertension 1996 Apr
PMID:Erythrocyte sodium transport, intraplatelet pH, and calcium concentration in salt-sensitive hypertension. 861 69

We describe a case of a 26 year old patient affected by a rare syndrome characterized by hyperkalemia, arterial hypertension and normal glomerular filtration rate (Gordon's syndrome), probably due to a renal tubular defect in the reabsorption of sodium or chloride. The patient, who had hyperkalemia since the age of 4 years, was referred to our Centre because of hypertension not well controlled with antihypertensive treatment. After drug therapy wash-out, we confirmed the existence of hypertension (180/100 mm Hg; ambulatory BP monitoring: 24-h mean BP = 151/91 mm Hg; 7 am-11 pm = 157/95; 11 pm-7 am: 133/82) and blood and urine tests showed hyperkalemia (6.6 mEq/L), hyperchloremia (115 mEq/L), mild metabolic acidosis (pH = 7.35, HCO3 = 19 mEq/L), low levels of plasma renin activity ( < 0.2 ng/ml/h), slight increase of plasma (1.08 nM/L) and daily urine aldosterone (129 nM) and normal serum creatinine (1.1 mg/dl) and glomerular filtration rate (91 ml/min). These data allowed to exclude the presence of renal failure and hyporeninemic hypoaldosteronism, which are the most common diseases with hypertension and hyperkalemia, and suggested the diagnosis of Gordon's syndrome. After 1 month of treatment with chlorthalidone (12.5 mg o.i.d) we observed the normalization of BP (130/80 mm Hg; ambulatory BP monitoring: 24-h BP: 132/76 mm), serum potassium (5,1 mEq/L) and the other blood and urine tests. These results were confirmed 6 months later and at present the patient has good clinical conditions.
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PMID:[Hypertension, hyperpotassemia and normal glomerular filtration (Gordon's syndrome): a case report]. 868 60


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