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PubMed2006

Vardenafil increases coronary flow response to hypercapnic acidosis in isolated guinea pig heart.

The hypothesis was tested that vardenafil, a PDE5 inhibitor, specifically enhances coronary vasodilation during acidosis. In isolated constant pressure perfused guinea pig hearts, infusion of vardenafil (<or= 1 microM) increased coronary flow concentration-dependently 34 % above baseline. In parallel, cGMP release increased (0.44 +/- 0.094 vs. 0.14 +/- 0.017 pmol/min x g at 0.5 microM vardenafil vs. baseline). Flow increases occurred in the absence of changes in heart function (LVP, heart rate, dP/dt(max), heart rate - pressure product). Infusion of the NO synthase blocker L-NMMA (100 microM) caused a rightward shift of the dose-response curve of vardenafil. To test whether vardenafil treatment may enhance metabolic coronary vasodilation, arterial pCO(2) was raised from 38 to 61 mmHg, which resulted in a steady state flow increase of 18.8 +/- 4.5%. Infusion of vardenafil, given at a threshold flow enhancing concentration, doubled the coronary flow response during hypercapnic acidosis to 38.4 +/- 4.2 % (p=0.004). This flow amplification during acidosis was not shared by the K(ATP) channel opener cromakalim, indicating a specific effect of vardenafil on flow control during myocardial acidosis. We conclude that vardenafil specifically relaxes coronary resistance vessels through NO/cGMP-dependent pathways and increases the coronary flow response toward hypercapnic acidosis. This finding further supports the importance of the NO-cGMP axis in mediation of this flow response.

Acidosis↗
PubMed1996

Effect of metabolic alkalosis and metabolic acidosis on urinary kallikrein excretion of anaesthetized rats: evidence for a role of blood pH as regulator of renal kallikrein secretion.

The effect of altering the acid-base status on urinary kallikrein excretion of barbiturate-anaesthetized rats was investigated. Alkalosis was induced in a group of rats by intravenous (i.v.) infusion of NaOH at 0.45 mmol x h(-1) for 30 min. Acidosis was induced in two groups of rats by i.v. infusion of HCl at 1.5 mmol x h(-1) for 30 min (uncompensated acidosis) or 0.15 mmol x h(-1) for 3 h (compensated acidosis), respectively. Time controls received 0.45 mmol x h(-1) NaCl. Rats with alkalosis excreted less kallikrein than their controls (P < 0.05). Rats with uncompensated acidosis excreted more active kallikrein (P < 0.05), whereas rats with compensated acidosis excreted similar amounts when compared with their respective controls. In rats with uncompensated acid-base derangements, the urinary kallikrein excreted per millilitre of glomerular filtrate was correlated with blood H+ activity (r = 0.99, P < 0.01). Arterial blood pressure, haematocrit, glomerular filtration rate, urine flow rate and Na+ and K+ excretions of experimental and control animals did not differ. Thus, renal kallikrein secretion into the tubular fluid appears to be regulated by blood proton activity. This, along with our previous demonstration that kallikrein inhibits HCO3- secretion into the tubular lumen (Renal Physiol 17:301-306, 1994; J Physiol (Lond) 488:163-170, 1995), indicates that this enzyme is part of a feedback loop regulating acid-base balance.

Acidosis↗
PubMed1979

Familial absorptive hypercalciuria and renal tubular acidosis.

Hypercalciuria was considered as a secondary condition when associated with familial renal tubular acidosis. Later studies suggested that hypercalciuria could lead to renal tubular acidosis and nephrocalcinosis. Selected members of a family spanning five generations were studied. Renal tubular acidosis was present in eight subjects in three consecutive generations. Increased 24-hour urinary calcium excretion was present in nine subjects in three consecutive generations, alone in the younger generation, and in combination with renal tubular acidosis and nephrocalcinosis in the older generation. Calcium loading tests showed the absorptive nature of hypercalciuria in nine of 18 subjects studied. This report suggests that in this family the absorptive hypercalciuria is an autosomal dominant genetic defect with complete penetrance and variable expressivity which leads to renal tubular acidosis and nephrocalcinosis.

Acidosis, Renal Tubular↗
PubMed1982

Hyperkalemic hyperchloremic metabolic acidosis in sickle cell hemoglobinopathies.

This report describes the occurrence of hyperkalemic hyperchloremic metabolic acidosis in six patients with sickle cell hemoglobinopathies. Three patients had sickle cell anemia, two had sickle cell trait and one had S-C disease. In all patients, decreased renal potassium excretion was demonstrated by the finding of a fractional potassium excretion lower than that of control subjects with comparable glomerular filtration rates. Two patterns of impaired urinary acidification were discerned. Four patients had a urinary pH above 5.5 in the presence of systemic acidosis and, thus, were classified a having distal renal tubular acidosis. The remaining two patients had very low rates of ammonium excretion despite intact capacity to lower urinary pH below 5.5 during systemic acidosis; this pattern was ascribed to selective aldosterone deficiency. Sickle cell hemoglobinopathies should be included in the differential diagnosis of hyperkalemic hyperchloremic metabolic acidosis.

Acidosis, Renal Tubular↗
PubMed1975

Acetazolamide, metabolic acidosis, and intraocular pressure.

In order to investigate whether or not there is a causal relationship between the metabolic acidosis and the ocular hypotension induced by acetazolamide, we undertook to correlate over a period of time the blood-acidifying and ocular-hypotonizing effects of administering the lowest intravenous effective dose of acetazolamide; to treat the metabolic acidosis induced by acetazolamide by means of the intravenous introduction of bases, and pulmonary hyperventilation (respiratory alkalosis); to evaluate the effects on the intraocular pressure (IOP) by neutralizing the acetazolamide-induced metabolic acidosis by means of a continuous infusion of sodium bicarbonate; to determine the relationship between the metabolic acidosis induced by blood-acidifying agents, which do not inhibit carbonic anhydrase, and the IOP; and to determine the changes in the acid-base status of the aqueous humor induced by acetazolamide and other blood-acidifying drugs. We found that the hypertonic buffering solution of sodium bicarbonate could reduce the IOP by itself through an osmotic mechanism. On the basis of our results, we believe that a causal relationship exists between the metabolic acidosis induced by acetazolamide, and by other drugs that have a blood-acidifying effect as the result of other mechanisms, and ocular hypotension, bothin the animal and in the glaucomatous patient.

Acetazolamide↗
PubMed1996

Increased resistance to acute respiratory acidosis in isolated cardiac muscle following chronic hypoxia-induced hypertrophy.

OBJECTIVES: Hypertrophied myocardium is more sensitive to ischaemic dysfunction and damage. The objective of this study was to determine the effect of respiratory acidosis on cardiac muscle function following hypoxia-induced right ventricular hypertrophy, and to ascertain the role of Na(+)-H+ antiporter, which is known to be associated with cell growth. METHODS: Wistar rats were maintained at 10% O2 for 1 or 4 weeks. Experiments were performed on right ventricular papillary muscles stimulated at 1 Hz, and developed tension was recorded. The effect of respiratory acidosis was examined by equilibrating the perfusing solution with increasing levels of CO2, and the role of the Na(+)-H+ antiporter was determined by preincubation with the inhibitor 5-(N,N-hexamethylene) amiloride (HMA). Data were analysed by comparison of the slope of the semi-log plot of normalised tension against pH. RESULTS: Right ventricular hypertrophy was apparent after both 1 and 4 weeks of hypoxia. Respiratory acidosis reduced developed force in preparations from all groups, but the relationship between log tension and pH in the 4-week hypoxia group was less steep than in controls (4-week hypoxia 0.736 (0.057); control 0.947 (0.067); P < 0.01). In the 1-week hypoxia group however the relationship was steeper (1.243 (0.090); P < 0.01). HMA increased the slope in all groups, and under these conditions the control and 4-week hypoxia groups were not significantly different (control 1.134 (0.080); 4-week hypoxic 1.083 (0.087); P > 0.05). CONCLUSIONS: The increased resistance to respiratory acidosis of hypertrophied cardiac muscle following 4 weeks of hypoxia was abolished by HMA. This implies that it is related to increased activity of the Na(+)-H+ antiporter. The mechanism underlying the decreased resistance to acidosis following 1 week of hypoxia is unclear, but is unlikely to involve the Na(+)-H+ antiporter.

Acidosis, Respiratory↗
PubMed1991

Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis.

Carbonic anhydrase II (CA II) deficiency in man is an autosomal recessive disorder manifest by osteopetrosis, renal tubular acidosis, and cerebral calcification. Other features include growth failure and mental retardation. Complications of the osteopetrosis include frequent bone fractures, cranial nerve compression symptoms, and dental malocclusion. The anemia and leukopenia seen in the recessive, lethal infantile form of osteopetrosis are not seen in CA II deficient patients. The renal tubular acidosis usually includes both proximal and distal components. Symptoms of metabolic acidosis respond to therapy, but no specific treatment is available for the osteopetrosis or cerebral calcification. We review here the role of carbonic anhydrases in bone resorption and renal acidification, and discuss clinical features and laboratory findings which distinguish CA II deficiency from other disorders producing osteopetrosis, renal tubular acidosis, or brain calcification. Methods to evaluate patients with pure proximal renal tubular acidosis for deficiency of CA IV are also discussed.

Acidosis, Renal Tubular↗
PubMed1989

Effects of metabolic acidosis and diabetes on the abundance of specific renal mRNAs.

1. The effects of exogenously (NH4Cl ingestion) and endogenously (streptozotocin-diabetes) generated chronic metabolic acidosis on the abundance of rat renal mRNAs have been examined. 2. Total RNA was translated in vitro and the translation products analyzed by two-dimensional gel electrophoresis. 3. The translation product identified as phosphoenolpyruvate carboxykinase (PEPCK) increased 3.5-fold in both acidosis and diabetes. 4. This increase was not observed in diabetic rats treated with NaHCO3. 5. The abundance of one other translation product increased in acidosis. 6. That of 10 others increased in diabetes, several of which were elevated regardless of acid-base status. 7. The abundance of one translation product decreased in acidosis and diabetes but not in NaHCo3 treated diabetic rats, indicating acid-base regulation of this product. 8. The results establish that the acidosis response is limited to a small number of renal mRNAs and confirm that renal PEPCK is primarily regulated by changes in acid-base status. 9. They also indicate that diabetes affects the abundance of specific renal mRNAs through mechanisms independent of acid-base status.

Acidosis↗
PubMed1984

Effects of 'DIDS', an anion transport blocker, on CSF [HCO3-] in respiratory acidosis.

During acute respiratory acidosis increments in cisternal cerebrospinal fluid (CSF) [HCO3-] approximate decrements in CSF [Cl-] with CSF [Na+] remaining unchanged; the mechanisms mediating this reciprocal anionic relationship are unclear. In the present study we investigated the effects of DIDS (4,4'-diisothiocyano-disulfonic stilbene), a known inorganic anion exchange blocker, on CSF ionic regulation in acute respiratory acidosis. In two groups of anesthetized paralyzed dogs we injected either mock CSF (group I, n = 8) or mock CSF containing DIDS (group II, n = 9) into the lateral cerebral ventricles. After 45 min, acute respiratory acidosis was induced for 6 h. During acute respiratory acidosis, CSF PCO2 rose in average by 38 mm Hg in both groups; increments in CSF [HCO3-], however, were significantly lower by about 2 mEq/L in DIDS-treated animals than in controls throughout the experimental period. Such differences were not due to changes in CSF lactate concentration which were similar in both groups. Furthermore, CSF [Na+] remained unchanged in both groups. Since disulfonic stilbene derivatives combine selectively with the carrier involved in anion transport and inhibit inorganic anion exchange, the data in the present study suggest that in the central nervous system a DIDS-inhibitable carrier is involved in the rise of CSF [HCO3-] observed during acute respiratory acidosis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1993

Glucocorticoids and the renal Na-H antiporter: role in respiratory acidosis.

We examined the role of glucocorticoids in the activity of the renal brush border Na-H antiporter under baseline conditions (5% CO2 gassing) and during respiratory acidosis (10% CO2 gassing) in cultured monolayers of a proximal tubule suspension (primary cultures of the proximal tubule). Primary cultures of the proximal tubule showed an adaptive increase in renal brush border Na-H antiporter activity in response to respiratory acidosis in presence but not in the absence of physiologic concentrations of hydrocortisone in the medium. The effect of hydrocortisone to increase the activity of the renal brush border Na-H antiporter in respiratory acidosis could also be elicited by dexamethasone. Deletion of hydrocortisone from the medium also impaired the baseline activity of the Na-H antiporter. The effect of hydrocortisone to increase the activity of the Na-H antiporter under baseline conditions and during respiratory acidosis was elicited by physiologic concentrations of the hormone and 100-fold increase in concentration did not further increase the activity of the Na-H antiporter. These results demonstrate that the presence of physiologic concentrations of glucocorticoids are necessary for the baseline activity of the renal brush border Na-H antiporter and its adaptive increase in response to respiratory acidosis.

Acidosis, Respiratory↗
PubMed1995

Neonatal cerebral arterial flow velocity waveforms in term infants with and without metabolic acidosis at delivery.

To define the effects of acid base status at delivery on neonatal cerebral artery flow velocity waveform patterns obtained using Doppler ultrasound during the first week of life, a longitudinal comparative study of neonates born at term with and without evidence of metabolic acidosis in the umbilical artery was undertaken. Eighty-two appropriate for gestational age infants delivered after uncomplicated pregnancies with non-acidotic umbilical artery blood gases and in whom no neonatal complications were noted were studied to establish reference values of neonatal cerebral arterial vascular resistance index (RI) in normal term infants during the first week of life. A further 189 infants were grouped according to the presence and severity of metabolic acidosis at delivery, and also the presence of high risk features in the antenatal period. In the normal non-acidotic infants, over the first 24 h of life, there was a significant fall in the cerebral arterial resistance index (RI) in all the vessels examined, after which a steady state value was attained with no significant changes in vascular resistance index being noted during the remainder of the study period. The fall in RI between 12 and 24 h of age was consistent in all study groups. Infants with metabolic acidosis at delivery had blood flow patterns compatible with decreased resistance to flow in both anterior and middle cerebral arteries which persisted throughout the first week of life. This reduction in cerebral vascular resistance was most marked in those infants with severe metabolic acidosis. The majority of severely acidotic infants had a benign clinical outcome in the first week of life and all infants had normal cerebral ultrasound scans during the neonatal period. These findings suggest that metabolic acidosis at birth is associated with changes in neonatal cerebral arterial vascular resistance during the first week of life, and in the presence of benign clinical course the significance of this observation with regard to neurodevelopmental outcome requires evaluation.

Acidosis↗
PubMed1995

Renal tubular acidosis complicated with hypokalemic periodic paralysis.

Three Chinese girls with hypokalemic periodic paralysis secondary to different types of renal tubular acidosis are presented. One girl has primary distal renal tubular acidosis complicated with nephrocalcinosis. Another has primary Sjögren syndrome with distal renal tubular acidosis, which occurs rarely with hypokalemic periodic paralysis in children. The third has an isolated proximal renal tubular acidosis complicated with multiple organ abnormalities, unilateral carotid artery stenosis, respiratory failure, and consciousness disturbance. The diagnostic evaluation and emergent and prophylactic treatment for these three types of renal tubular acidosis are discussed.

Acidosis, Renal Tubular↗
PubMed1988

The effects of metabolic acidosis and alkalosis on the response to sympathomimetic drugs in dogs.

Sympathomimetic drugs are commonly used in many circumstances to increase cardiac output, blood pressure, and myocardial contractility. However, factors such as acidosis or alkalosis are known to influence the action of these drugs. This study looked at the response to the administration of epinephrine, norepinephrine, dopamine, dobutamine, isoproterenol, and glucagon at normal pH and under acidotic (pH 7.2 +/- 0.01) and alkalotic (pH 7.59 +/- 0.01) conditions in 17 dogs. Acidosis was produced with an infusion of hydrochloric acid and alkalosis by infusion of sodium bicarbonate. The infusions were given over one hour followed by a 15- to 30-minute stabilization period. With the administration of each sympathomimetic drug at each pH level, hemodynamic parameters and measurements of myocardia; contractility were recorded. Epinephrine increased cardiac output at normal pH, but decreased cardiac output under conditions of both acidosis and alkalosis; the net change from values at pH 7.40 was nearly 3 L/min. The only other drug to demonstrate this reversal of cardiac output, though to a lesser degree, was dopamine, 10 microg/kg/min, and only in the alkalotic state. Dobutamine was the only drug that decreased contractility under acidotic conditions, while all other drugs caused an increase. In sum, epinephrine was the only drug markedly affected by metabolic acidosis and alkalosis. Isoproterenol's hemodynamic effects were altered the least by changes in acid-base balance. Alkalosis had an equally adverse effect on the cardiovascular system as compared with acidosis.

Acidosis↗
PubMed1994

The use of dichloroacetate in the treatment of overwhelming hypoxic acidosis.

Overwhelming hypoxic acidosis due to poor tissue oxygen delivery from low cardiac output, pulmonary failure, and other causes has devastating effects postoperatively on patient outcome. Whereas conventional therapeutics often can not reverse the downward spiral of these patients, dichloroacetate (DCA) has been shown to be beneficial. This study investigated the metabolic and hemodynamic effects of DCA given after the onset of overwhelming hypoxic acidosis in a canine model. A hypoxically ventilated canine model of severe induced acidosis was established and dogs surviving the development of acidosis were randomized to receive DCA or sodium chloride (NaCl) treatment. Dogs receiving DCA after development of hypoxic lactic acidosis showed no further change in metabolic parameters during the 90-minute treatment period (pH, 7.24 to 7.23; HCO3, 17.7 to 18 mmol/L; lactate, 2.04 to 1.05 mM/L); whereas animals receiving an equivalent sodium load showed progressive, significant deterioration in all parameters (pH, 7.24 to 7.12; HCO3, 16.8 to 13.2 mM/L; lactate, 2.05 to 3.55 mM/L). Myocardial blood flow was significantly increased by hypoxia in all dogs. Finally, cardiac output and stroke volume were significantly increased at 90 minutes by DCA versus control. Myocardial oxygen utilization efficiency (LV work/M VO2) was improved during DCA treatment. DCA, a carboxylic acid, increases pyruvate dehydrogenase activity, thereby enhancing lactate use a metabolic substrate. DCA had an ameliorative metabolic effect, and benefitted myocardial performance without a direct inotropic effect. DCA treatment appears to enhance myocardial performance on a metabolic and not primarily inotropic basis, does not increase the "cost" of myocardial work, and warrants further study.

Acidosis, Lactic↗
PubMed2005

Role of phosphorylation of Thr(17) residue of phospholamban in mechanical recovery during hypercapnic acidosis.

OBJECTIVES: To assess the time course of phosphorylation of phospholamban residues, the underlying mechanisms determining these phosphorylations, and their functional impact on the mechanical recovery during acidosis. METHODS: Langendorff perfused rat hearts were submitted to 30 min of hypercapnic acidosis. Contractility, relaxation, and phosphorylation of phospholamban residues, immunodetected by specific antibodies, were determined. RESULTS: Acidosis produced a mechanical impairment followed by a spontaneous recovery, most of which occurred within the first 3 min of acidosis (early recovery). During this period, contractility and relaxation recovered by 67+/-9% and 77+/-11%, respectively, from its maximal depression, together with an increase in the Ca(2+)-calmodulin-dependent protein kinase II (CaMKII)-dependent phosphorylation of Thr(17). The CaMKII inhibitor KN-93, at 1, 5 and 10 microM, decreased Thr(17) phosphorylation to basal levels and produced a similar impairment of the early relaxation recovery (50%). However, only 5 and 10 microM KN-93 inhibited the early contractile recovery and completely blunted the late mechanical recovery. Inhibition of the reverse mode of the Na(+)/Ca(2+) exchanger by KB-R7943 decreased Thr(17) phosphorylation but accelerated the early contractile recovery. CONCLUSIONS: CaMKII-dependent Thr(17) phosphorylation significantly increased at the beginning of acidosis, is responsible for 50% of the early relaxation recovery, and is linked to the activation of the reverse Na(+)/Ca(2+) mode. The early contractile recovery and the late mechanical recovery are dependent on CaMKII but independent of the phosphorylation of the Thr(17) residue of phospholamban. The reverse Na(+)/Ca(2+) mode has an additional negative effect that opposes the early mechanical recovery.

Acidosis↗
PubMed2006

Ca2+/calmodulin-dependent protein kinase: a key component in the contractile recovery from acidosis.

Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca(2+) responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca(2+) levels and Ca(2+) transient amplitude. Recent experimental evidence indicates that activation of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca(2+) transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca(2+) handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca(2+) uptake and SR Ca(2+) load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.

Acidosis↗
PubMed2004

Acidosis-induced protein tyrosine phosphorylation depends on Ca2+ influx via voltage-dependent Ca2+ channels in SHR aorta.

The contractile response to acidosis in isolated aorta from spontaneously hypertensive rat (SHR) depends upon tyrosine phosphorylation of phosphatidylinositol 3 kinase (PI3-kinase) and Ca2+ influx via voltage-dependent Ca2+ channels (VDCC). In this study, verapamil, a VDCC inhibitor, was shown to markedly inhibit acidic pH-induced contraction, whereas the residual contraction in the presence of verapamil was unaffected by the PI3-kinase inhibitor, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one hydrochloride (LY-294002). Interestingly, the LY-294002-insensitive component of contraction was further inhibited by verapamil in the presence of LY-294002. Western blotting revealed that acidosis stimulated tyrosine phosphorylation of p85, which was abolished when tissues were pretreated with tyrphostin 23, a tyrosine kinase inhibitor, verapamil or EGTA. In fura-2-loaded aortic strips, acidosis induced a rise in intracellular Ca2+ ([Ca2+]i) that was partially inhibited by LY-294002. The residual increase in [Ca2+]i caused by acidosis in the presence of LY-294002 was abolished by verapamil. These findings suggest that acidosis-induced Ca2+ influx through VDCC is the upstream event leading to the tyrosine phosphorylation of PI3-kinase, which in turn contributes to the enhancement of Ca2+ entry to some extent in SHR aorta.

Acidosis↗
PubMed2005

Acidosis-induced relaxation of human internal mammary artery is due to activation of ATP-sensitive potassium channels.

Metabolic acidosis is associated with various clinical situations including diabetes mellitus and renal diseases. The aim of this study was to investigate the effects of acidosis on the resting as well as precontracted human left internal mammary artery. The vessels were obtained from the patients undergoing coronary artery bypass grafting surgery at The Aga Khan University Hospital, Karachi. Left internal mammary artery was cut into rings and isometric tension recording experiments were performed. Decrease in pH of the bathing solution from 7.4 to 6.8 had no effect on the resting tension of left internal mammary artery, whereas, acidic pH markedly relaxed the contractions to 24.8 mM KCl and 300 nM phenylephrine. Interestingly, when the KCl- or phenylephrine-contracted rings were treated with 3 microM glibenclamide; an inhibitor of ATP-sensitive potassium (K(ATP)) channels, the relaxant effect of acidosis was abolished. Similarly, acidosis failed to cause relaxation of 100 nM endothelin-1-induced contraction in Ca2+-free bathing solution or in the presence of a voltage-dependent Ca2+ channel inhibitor, verapamil (10 microM), whereas, endothelin-1-induced contraction was attenuated by acidosis in Ca2+-containing normal solution. From all these data, it is concluded that under the acidic pH conditions, opening of K(ATP) channels occurs; resulting in the hyperpolarization, decrease in Ca2+ influx via voltage-dependent Ca2+ channels and subsequent relaxation of human left internal mammary artery.

Acidosis↗