PubMed Health⌕ Search

Biomedical subjects

A Botey

Publications and source records attributed to A Botey.

At least 37 records · Page 2Linked to original sources
PubMed1994

Intracellular calcium concentration and activation of the Na+/H+ exchanger in essential hypertension.

To investigate the relationship between changes in intracellular calcium concentration ([Ca2+]i) and agonist-induced activation of the Na+/H+ exchanger in essential hypertension (EH), platelet [Ca2+]i and pHi were measured in 24 patients with EH (14 males) aged 48 +/- 2 years and 23 matched normotensive controls (NT) (12 males) aged 45 +/- 3 years. Measurements were done with spectrofluorimetry using the dyes Fura-2 for [Ca2+]i and BCECF for pHi. [Ca2+]i and pHi were measured in the resting condition and after stimulation in vitro with 0.1 U/ml human thrombin. The thrombin-induced rise in pHi was Na+ dependent and amiloride sensitive, indicating that it was mediated by the Na+/H+ exchanger. Unstimulated [Ca2+]i was higher in patients with EH than in NT (60 +/- 3 vs. 48 +/- 1 nmol/liter, P < 0.005), but there were no differences in resting pHi between both groups (7.16 +/- 0.01 vs. 7.16 +/- 0.008). In the presence of 1 mmol/liter external calcium (Ca2+o), thrombin-induced increment in [Ca2+]i was significantly greater in patients with EH than in NT (281 +/- 21 vs. 206 +/- 19; P < 0.05) as was the pHi increment (EH: 0.137 +/- 0.01; NT: 0.095 +/- 0.01; P < 0.05). Both agonist-induced increments in [Ca2+]i and in pHi were correlated with mean arterial pressure (MAP) only in the EH group (r = 0.58, P < 0.005 and r = 0.59, P < 0.005, respectively). The agonist-induced rise in pHi was positively correlated with the rise in [Ca2+]i both in the EH group (r = 0.65, P < 0.001) and in the NT (r = 0.55, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Platelets↗
PubMed1994

Effect of antihypertensive treatment on intracellular calcium concentration and intracellular pH in essential hypertension.

The platelet intracellular calcium concentration ([Ca2+]i) and intracellular pH (pHi) were measured by spectrofluorimetry with the dyes Fura-2 and BCECF, respectively, in 19 patients with essential hypertension (10 males), aged 48 +/- 2 years, before and after 12 weeks of antihypertensive treatment and in 19 normotensive controls (11 males), aged 46 +/- 3 years. [Ca2+]i and pHi were measured in the resting state and after stimulation in vitro with 0.1 U/ml human thrombin. In patients with essential hypertension, both resting [Ca2+]i (61 +/- 4 nmol/l) and thrombin-induced maximal increase in [Ca2]i (291 +/- 26 nmol/l) were significantly (P < 0.01) greater than in the normotensive controls (resting 49 +/- 2 nmol/l and thrombin-induced 199 +/- 21 nmol/l). With respect to pHi, no difference in resting pHi between both groups was found (7.16 +/- 0.01 vs. 7.16 +/- 0.01). However, pHi increment at 300 seconds in response to thrombin was higher in the patients with essential hypertension than in the controls (0.131 +/- 0.02 vs. 0.083 +/- 0.01 pH units, P < 0.05). The increment in pHi was blunted by the amiloride derivative EIPA, indicating that it was mediated by the Na+/H+ exchanger. After antihypertensive therapy in the essential hypertensive patients, basal [Ca2+]i was significantly reduced (52 +/- 2 nmol/l, P < 0.01) and was not statistically different to the value found in the normotensive controls. Resting pHi suffered no significant modification after treatment (7.17 +/- 0.01, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Intracellular calcium mobilization and activation of the Na+/H+ exchanger in platelets.

The aim of the present study was to evaluate the regulatory relationship between the cytosolic free calcium concentration ([Ca2+]i and cytosolic pH (pHi). [Ca2+]i and pHi were measured using the fluorescent dyes fura-2 and BCECF [2',7'-bis-(carboxyethyl)-5,6-carboxyfluorescein] respectively. In a medium with 1 mmol/l extracellular calcium, thrombin (2.5 units/ml) induced an increment in [Ca2+]i of 638 +/- 31 nmol/l (n = 5) and an intracellular alkalinization of 0.14 +/- 0.01 pH units (n = 8). Both responses were dependent on the concentration of thrombin, displaying a sigmoidal dose-response pattern. The intracellular alkalinization was dependent upon extracellular Na+ and was amiloride-sensitive, indicating that it was mediated by activation of the Na+/H+ exchanger. When extracellular calcium was chelated with EGTA prior to the addition of thrombin, the intracellular alkalinization was not affected (0.15 +/- 0.02 at 2.5 units/ml thrombin, n = 8). Under these circumstances, the [Ca2+]i increment represents mobilization from internal stores, reaching 157 +/- 42 nmol/l at 2.5 units/ml thrombin. When platelets were preloaded with the intracellular calcium chelator MAPTAM (1,2-bis-5-methylaminophenoxylethane-NNN'-tetraacetoxymethyl acetate) to block the increase in [Ca2+]i induced by thrombin, no increment in pHi was observed. Moreover, MAPTAM-loaded calcium-depleted platelets had a basal pHi that was more acidic than in the presence of 1 mmol/l extracellular calcium (6.93 +/- 0.09 versus 7.14 +/- 0.01, n = 26, P < 0.001). Ionomycin induced an elevation of [Ca2+]i that was accompanied by a concomitant increase in pHi, which was Na(+)-dependent and amiloride-sensitive. [Ca2+]i and pHi increases induced by ionomycin were both dependent on the concentration of ionomycin. In conclusion, an increase in [Ca2+]i is necessary for the agonist-induced activation of the Na+/H+ exchanger in platelets. Non-agonist-induced increases in [Ca2+]i seems to prompt activation of the exchanger. In addition, Ca(2+)-depleted platelets have a more acidic basal pHi, indicating that the basal level of [Ca2+]i is also important for maintaining the basal pHi.

Blood Platelets↗
PubMed1993

Penicillamine-induced rapidly progressive glomerulonephritis in a patient with rheumatoid arthritis.

A 67-year-old woman with rheumatoid arthritis presented rapidly progressive glomerulonephritis (RPGN) after 5 months of D-penicillamine (250 mg/day) treatment. Light microscopy study showed severe glomerulonephritis with crescent formation in 60% of the glomeruli and infiltration of inflammatory cells in the wall of an arteriole. Immunofluorescence revealed scanty granular IgG, IgA and C3 deposits along the capillary walls and mesangium. The patient was treated with steroid pulse, plasmapheresis, cyclophosphamide and antiplatelet agents. A complete recovery of renal function was achieved in a few weeks. This new case of RPGN in the course of D-penicillamine treatment emphasizes the need for frequent monitoring of renal function and evaluation of urinary sediment and proteinuria in these patients. The prompt discontinuation of D-penicillamine and vigorous treatment measures could allow for a good prognosis as in this case.

Aged↗
PubMed1991

[Late recurrence in pheochromocytoma: need for a long term follow up].

Pheochromocytoma is a catecholamine secreting tumor which has been traditionally considered as a potentially curable cause of hypertension. However, the existence of malignant pheochromocytomas as well as the problem which the recurrence of benign pheochromocytomas present, make the eradication of this tumor more complicated. It is note worthy the difficulty in localizing recurrent pheochromocytomas as well as the prognostic interest that presents the possibility of differentiating between recurrence and metastasis. We refer the case of a female patient suffering benign adrenal pheochromocytoma, who, 10 years it was surgically removed, presented a relapse of symptoms, and was diagnosed of extra-adrenal pheochromocytoma, in Zuckerkandl organ. The importance of performing a long term post-surgical follow-up in these patients is stressed.

Adrenal Gland Neoplasms↗
PubMed1990

[Lymphocyte beta 2-adrenergic receptors in pheochromocytoma].

To assess the effect of chronic exposure to high circulating catecholamine concentrations on the beta 2-adrenergic receptors, the density and affinity of lymphocyte beta 2-adrenergic receptors were measured in 5 patients with pheochromocytoma (2 males and 3 females, with a mean age of 39 +/- 12 years). In 4 patients the studies were repeated 15 days after tumor removal. Before surgery, all patients had high plasma catecholamine concentration. The density of beta 2-adrenergic receptors was reduced, although their affinity was within the reference range. There was an inverse correlation between plasma epinephrine concentration and beta 2-adrenergic receptor density (r = -0.959, p = 0.01). After surgical resection, plasma catecholamine concentrations and receptor density became normal. The dissociation constant decreased in the four patients. In conclusion, in the presence of chronically high levels of circulating catecholamines the density of lymphocyte beta 2-adrenergic receptors is reduced. However, it becomes normal when plasma catecholamine concentration returns to the reference values, the dynamic character of this regulation being thus shown. The measurement of these receptors in the lymphocyte could be useful for the diagnosis and follow up of patients with pheochromocytoma.

Adrenal Gland Neoplasms↗
PubMed1990

[Subacute kidney insufficiency in exclusively vascular kidney amyloidosis].

Two patients are reported with secondary amyloidosis in whom renal biopsy disclosed massive amyloid deposition with exclusively extravascular localization. In one case, autopsy showed selective amyloid deposition in the vessel walls of most examined organs. In both patients, the clinical presentation consisted of subacute renal failure without proteinuria. A possible reduction of renal perfusion, secondary to a depleted blood volume in one case and to pharmacological inhibition of prostaglandin synthesis in the other, could enhance renal dysfunction in both patients, who, on the other hand, previously had mild renal failure. The clinical presentation of renal amyloidosis basically depends on the distribution and severity of amyloid deposits. Vascular localization represents an uncommon pattern of renal amyloidosis, generally associated with chronic renal failure with minimal or no proteinuria.

Acute Kidney Injury↗
PubMed1990

Silent renal microangiography after mitomycin C therapy.

Mitomycin C (MMC) is an alkylating agent which has been associated with microangiopathic hemolytic anemia and acute renal failure, with an overall incidence between 2 and 10%. This complication can develop several months after the initiation of chemotherapy. Isolated renal impairment without overt microangiopathic hemolytic anemia, although reported, is less frequently documented. We describe a 63-year-old man who developed progressive renal failure without any evidence of hemolysis or thrombopenia 10 months after beginning chemotherapy with MMC and Ftorafur. A renal biopsy displayed features of microangiopathy. The patient required the institution of chronic hemodialysis. In conclusion, it is important to be aware of this indolent but severe renal complication in patients treated with MMC. Urinary parameters and renal function should be monitored over a long period for an early diagnosis.

Adenocarcinoma↗
PubMed1989

Acute aluminum encephalopathy in an uremic patient.

A patient on maintenance hemodialysis developed an acute encephalopathy closely related to a rapid increase in serum aluminum levels. Aluminum hydroxide and sucralfate had been given in large amounts for the treatment of a gastrointestinal bleeding episode. The breach of the gastrointestinal barrier to aluminum absorption, the increase in gastric pH caused by cimetidine, and the presence of gastric telangiectasia acting together in a uremic patient could have precipitated the acute aluminum encephalopathy.

Acute Disease↗
PubMed1989

Lymphocyte beta 2-adrenergic receptors in essential hypertension: studies in basal conditions and after dynamic exercise.

In order to study the density and response to dynamic exercise of lymphocyte beta 2-adrenoceptors in essential hypertension, 30 moderate essential hypertensives (12 men: 18 women, mean age 50.3 +/- 9.2 years) and 14 normotensive controls (8 men: 7 women, mean age 47 +/- 15 years) were studied. Beta 2-adrenoceptors density in basal conditions was higher in essential hypertensives than in controls (1950 +/- 625 vs 1278 +/- 356 binding sites per cell [bs/c], respectively, p less than 0.01) (mean +/- SD). After dynamic exercise beta 2-adrenoceptors density increased both in controls (to 1491 +/- 342 bs/c, p less than 0.01) and in hypertensives (to 2632 +/- 715 bs/c, p less than 0.001). However, the percentage of increase after the exercise was significantly higher in hypertensives than in controls (40.5 +/- 6.1 vs 20.2 +/- 6.5%, p less than 0.05). In summary, the higher density in basal conditions, as well as the exaggerated increase in the number of beta 2-adrenoceptors after dynamic exercise observed in essential hypertension, suggest an impaired regulation of these receptors in essential hypertension.

Adult↗
PubMed1988

Improvement of renal function in azotaemic hypertensive patients after surgical revascularization.

Between 1974 and 1986, 17 patients (16 men and 1 woman) with renal insufficiency (serum creatinine greater than 1.5 mg/dl, mean 3.75 mg/dl), with a mean age of 51.3 years, underwent surgical renal revascularization. Two of them were on maintenance haemodialysis. All were severely hypertensive in spite of antihypertensive drugs. Atherosclerosis was the cause of renal stenosis in 14 cases and fibromuscular dysplasia in 3. Operative procedures included splenorenal shunt (5), autotransplantation (3), aortorenal bypass (3), hepatorenal bypass (1), bilateral renal endarterectomy (1), renal ostial closure (1) and nephrectomy (3). Mean serum creatinine showed a decrease from 3.76 to 1.65 mg/dl (P less than 0.005). Mean arterial pressure dropped from 161 mmHg to 103 mmHg (P less than 0.001). Systolic and diastolic pressures also showed significant decreases. Two patients died. Four patients required a second operation and the renal function and blood pressure then improved. Renovascular disease must be ruled out in patients with renal insufficiency associated with hypertension, including those patients on haemodialysis. We conclude that renal revascularization surgery is a reliable and efficient form of treatment in selected cases of renal failure of renovascular origin.

Blood Pressure↗