High blood pressure. Causes, symptoms, treatments

Emergence, persistence, and resolution of suicidal ideation during treatment of depression in old age.


Five sulfonamide inhibitors of carbonic anhydrase inhibited parathyroid hormone-induced resorption of bone in organ culture. The relative activities of the sulfonamides as resorption inhibitors were such as to suggest the presence of a functional carbonic anhydrase system in bone linked to the mechanism of bone resorption.

Acidification of luminal fluid in the proximal convoluted tubule has been modeled as a pump-leak system. Using isolated perfused rabbit proximal convoluted tubules in a HCO-3/CO2-free in vitro environment, we studied "H+ leak" by imposing pH gradients across the tubule and measuring the change in pH from perfusate to collected fluid. Active acidification was inhibited by acetazolamide with and without hypothermia. At 21 degrees C a symmetrical H+ leak with an apparent permeability coefficient of approximately 0.15 cm X s-1 was found with either a lumen-to-bath or bath-to-lumen [H+] gradient. At 37 degrees C a much higher apparent permeability coefficient was found that was dependent on luminal lactate. Phosphate movement did not affect H+ fluxes significantly. Without luminal lactate, the apparent permeability coefficient was 0.31 cm X s-1. Although this permeability coefficient is larger than other ionic permeability coefficients in this segment, it is not sufficient to account for a significant H+ leak compared with rates of acidification or bicarbonate reabsorption. To investigate the role of Na+-H+ exchange in mediating the observed H+ leak, we perfused tubules with low [Na+] solutions with and without amiloride (10(-3) M). Neither the lower [Na+] nor the presence of amiloride diminished the apparent [H+] permeability coefficient. We conclude that a H+ leak pathway independent of Na+-H+ exchange is present in the proximal convoluted tubule.

This paper attempts to further clarify the characteristics of Mecholyl- or epinephrine-stimulated glucose metabolism in the isolated monkey eccrine sweat gland with special emphasis on its relationship to increased sodium transport. The Mecholyl- or epinephrine-stimulated glucose metabolism (as estimated by either lactate or (14)CO(2) production or both) is seen only in the secretory coil and not in the duct. It is markedly suppressed in the absence of glucose, Na(+), or K(+). It is inhibited by ouabain (10(-3) M) and partially suppressed in a low-sodium (40 mM), high-potassium (100 mM) medium.2,4-dinitrophenol (10(-4) M) reverses ouabain-induced inhibition of lactate and (14)CO(2) production but only partially reverses inhibition induced by Na(+) + K(+) deprivation, indicating that metabolic inhibition by ouabain is secondary to the inhibition of sodium transport. There is no synergism between Mecholyl and epinephrine. The absence of any significant inhibitory effects by acetazolamide (Diamox) or HCO(3) (-)-free media suggests that H(+) transport may not be important in sweat gland function. In contrast to a report by Wolfe et al., human eccrine sweat glands show considerable oxidative activity ((14)CO(2) production of 0.42-0.72 nmol/gland/h). These observations are discussed in terms of the linkage between sweat gland energy metabolism and sodium transport.

Recent investigations have suggested an important role of statins in the prevention of stroke and dementia independent of their lipid-lowering properties. Using transcranial Doppler sonography (TCD), we examined acetazolamide reactivity as a marker of cerebral vasoreactivity in patients with subcortical small-vessel disease before and after pravastatin treatment.

The aim of this paper is to present the current possibilities in idiopatic intracranial hypertension (IIH) diagnostics. Optical coherence tomography belongs to these possibilities in last few years. The necesarry interdisciplinary co-operation of ophthalmologist and neurologist concerning in IIH patients is pointed out in the mentioned case reports.

A total of 105 patients underwent CSF leak repair; 39 patients (37.1%) were treated for spontaneous CSF leaks. Mean age was 57.7 years and 33 were female (85%). Average body mass index (BMI) was 38.5 kg/m(2). The most common sites were cribriform plate (51%), sphenoid lateral pterygoid recess (31%), and ethmoid roof (8%). All patients underwent endoscopic repair utilizing image guidance with multilayered closure in most cases. Five patients (12.8%) developed recurrent CSF leak with mean ICP of 27.0 cm H(2)O, compared to 25.0 cm H(2)O for those without recurrence (P = .33). All had successful rerepair at mean follow-up of 2.8 years. Acetazolamide was used in nine patients, whereas six patients underwent VPS placement for elevated ICP management. Diagnosis of benign intracranial hypertension (BIH) was statistically associated with need for acetazolamide or VPS (P < .001), whereas elevated ICP reached borderline significance (P = .049).

The function of carbonic anhydrase in H(+) secretion by the turtle bladder was studied in vitro. Dose response curves were obtained for the carbonic anhydrase inhibitors, acetazolamide and ethoxzolamide, with and without addition of CO(2) to the system. In addition, carbonic anhydrase was assayed in homogenates of mucosal cells. The activity in the homogenates was 155+/-16 U/g dry wt, of which only 11 U represented contamination from erythrocytes; after addition of 5 x 10(-6)m acetazolamide, no enzyme activity was detectable. In the intact preparation free of exogenous CO(2), the dose response curve for acetazolamide showed two plateaus of inhibition, one at 50% and one at more than 80% inhibition. At 50% inhibition (from 5 x 10(-6) to 5 x 10(-5)m acetazolamide), H(+) secretion was restored or enhanced by CO(2) addition to the same extent as bladders not exposed to acetazolamide. At concentrations of more than 1 x 10(-4)m, H(+) secretion was no longer restorable by CO(2). Unlike acetazolamide, ethoxzolamide caused progressive inhibition of H(+) secretion in the CO(2)-free system. The maximal extent of inhibition with ethoxzolamide and the behavior of inhibition in the presence of 2.5% CO(2) were the same as for acetazolamide. Evidence is presented that all surface epithelial cells secrete H(+) and generate OH(-) within the cell interior. The capacity of cells to dispose of OH(-) by CO(2) hydroxylation varies with the availability of cytoplasmic carbonic anhydrase. A small population of cells contains abundant carbonic anhydrase and secretes at high rates even when CO(2) is in short supply. On the basis of these results and histochemical data on the distribution of carbonic anhydrase within the mucosa, an analysis is presented of the epithelial organization of acidification by the turtle bladder.