Long-term effect on hypertension of phlebotomy in posttransplant erythrocytosis.
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Adult↗
Biomedical subjects
W Zidek
Publications and source records attributed to W Zidek.
Erythropoietin increases cytosolic free calcium concentration and thrombin induced changes in cytosolic free calcium in platelets from spontaneously hypertensive rats.
Using fura-2 cytosolic free calcium concentrations were measured in intact washed platelets from 9 spontaneously hypertensive rats (SHR) and from 9 age-matched normotensive Wistar-Kyoto rats (WKY). In resting platelets cytosolic free calcium concentration was significantly higher in SHR than in WKY (171.8 +/- 64.4 nM vs 93.1 +/- 59.0 nM, p less than 0.05). After preincubation with erythropoietin cytosolic free calcium concentration was significantly higher in SHR than in WKY (197.5 +/- 83.2 vs 93.0 +/- 60.1, p less than 0.01). Using platelets from SHR erythropoietin increased mean resting cytosolic free calcium concentration by 14.9% (p less than 0.05) and mean thrombin induced changes of cytosolic free calcium by 58.3% (p less than 0.01). In contrast, erythropoietin caused no significant increase in the resting calcium concentration or in thrombin induced changes of cytosolic free calcium in platelets from WKY. It is concluded that erythropoietin is involved in the pathogenesis of hypertension by elevating cytosolic free calcium concentration.
Animals↗
Direct vasopressor effect of recombinant human erythropoietin on renal resistance vessels.
The contractile properties of recombinant human erythropoietin (rHuEPO) on isolated resistance vessels of renal and mesenteric vascular beds were studied in an in vitro model using a small vessel myograph. Under isometric conditions, rHuEPO caused a contraction of this vasculature in a concentration range between 10 U/ml and 200 U/ml. A maximal active wall tension of 1.52 +/- 0.19 mN/mm was obtained under a rHuEPO dose of 200 U/ml. In Ca2+ free solution, the pressor response to high rHuEPO-concentrations was attenuated, and the response to low rHuEPO concentrations was abolished. In the presence of verapamil, phentolamine and saralasin, rHuEPO-induced contractions were not affected significantly. A dose-dependent vasodilatation of mounted vasculature to acetylcholine (ACh) indicated that endothelium remained intact in our preparations. rHuEPO-induced vessel contraction was not abrogated after an enzymatical removal of endothelium by collagenase, confirming that the described contractile responses are endothelial independent. These findings suggest that a direct vasopressor effect of rHuEPO on proximal resistance vessels may contribute to development of hypertension seen in rHuEPO-treated hemodialysis patients.
Animals↗
Effect of plasma from patients with essential hypertension on vascular resistance in the isolated perfused rat kidney.
1. Isolated perfused rat kidneys were used to study the effects of plasma fractions obtained by gel filtration from essential hypertensive patients (n = 40) and from normotensive subjects (n = 36) on resistance vessels. Perfusion pressure was recorded at a constant flow. 2. Plasma fractions were obtained by gel filtration and contained substances with a molecular mass in the range 1000-1500 Da. The plasma fractions from hypertensive patients used in this study had been shown to increase blood pressure after intravenous injection in rats. 3. In the isolated rat kidneys, the hypertensive fractions increased perfusion pressure by 20 +/- 17 mmHg (mean +/- SD, range 5-58 mmHg, n = 40). The analogous fractions from normotensive subjects did not change perfusion pressure significantly. 4. In Ca2(+)-free medium containing 2 mmol/l ethyleneglycol bis-(aminoethyl ether)tetra-acetate, the change in perfusion pressure induced by active plasma fractions was reduced by 95.2 +/- 6.3%. Addition of nifedipine to the perfusion medium reduced, but did not abolish, the pressure response of the kidneys. 5. In solutions containing phentolamine or saralasin, vasoconstriction was not reduced. 6. Thus in the active fractions from hypertensive plasma, a vasopressor agent with direct action on resistance vessels can be demonstrated. This substance probably acts by increasing Ca2+ influx in vascular smooth muscle cells.
Adult↗
Event-related potentials in HIV-infected outpatients.
Event-related potentials (ERP) were determined in 138 human immunodeficiency virus (HIV)-infected outpatients and 92 healthy controls of a corresponding age. Of the HIV-infected patients, 31.8% showed an abnormal latency of the P3-component of ERPs (P3-ERP), exceeding the mean value + 2 SD of P3-ERP latencies from age-matched healthy subjects. From the untreated patients in stage Walter Reed (WR) = 6, 71.4% had abnormal P3-ERP latencies, whereas in WR = 2, only 19.6% of P3-ERPs were abnormal. Fourteen patients were observed over a period of 3-16 months. P3-ERP latencies were shortened in 7 patients under treatment with zidovudine. A marked increase in P3-ERP latencies was observed in 7 untreated HIV-infected patients. It is assumed that ERPs are a useful neurophysiological method to detect early cerebral dysfunction in HIV-infected patients.
Adult↗
Evaluation of the Ca2+ distribution in aortic tissue of spontaneously hypertensive and normotensive rats.
In the present study, particle-induced X-ray emission (PIXE) was used to get information on the spatial distribution of Ca2+ in aortas of spontaneously hypertensive rats (SHR) and normotensive controls aged 1 week, 4 weeks, and 12 weeks. To differentiate changes in Ca2+ metabolism in hypertensive arteries from secondary phenomena due to the arteriosclerosis, the animals were examined in the earliest stage of hypertension. It was found that the Ca2+ content was not elevated in the aortic smooth muscle of SHR aged 1 week (n = 11), as compared to normotensive controls (n = 10) (186.8 +/- 89.9 micrograms Ca2+/g tissue v 254.0 +/- 173.3 micrograms Ca2+/g). The Ca2+ content was raised (P less than .05) in the aortic smooth muscle of SHR aged 4 weeks (n = 13), as compared to 12 WKY rats (4 weeks) (726.0 +/- 130.4 micrograms Ca2+/g tissue v 440.3 +/- 214.4 micrograms Ca2+/g) and in 17 SHR (3 months), as compared to 13 WKY rats, respectively (3390.1 +/- 729.9 micrograms Ca2+/g tissue v 1632.1 +/- 569.5 micrograms Ca2+/g). The results confirm the age-related increase in the arterial Ca2+ content in normotensive rats and demonstrate additionally that this age-related rise in arterial Ca2+ content is accelerated in SHR.
Animals↗
Na+, K(+)-ATPase inhibition and intracellular electrolyte content in essential and secondary hypertension.
A crucial role of humoral factors in the pathogenesis of primary hypertension is discussed. In 1982 Hamlyn et al demonstrated the presence of a Na+, K(+)-ATPase inhibitor in the plasma of essential hypertensives and showed a significant correlation of the Na+, K(+)-ATPase inhibition with the blood pressure. In this study we examined whether an Na+, K(+)-ATPase inhibitor could be found in the blood of essential hypertensives as compared to patients with secondary hypertension (renal hypertension, renal artery stenosis, pheochromocytoma). Second, the possible correlation between an inhibition of Na+, K(+)-ATPase and the intracellular electrolyte composition was examined. The results demonstrate a similar reduction of Na+, K(+)-ATPase inhibition in both essential hypertensives and secondary hypertensives as compared to normotensive controls. Further, the intracellular electrolyte composition (Na+, Na; K+, Ca) does not show a significant correlation to the degree of Na+, K(+)-ATPase inhibition, whereas a significant correlation between the degree of Na+, K(+)-ATPase inhibition and intracellular Cl- concentration could be demonstrated. The present study shows that an endogenous Na+, K(+)-ATPase inhibitor is also present in secondary forms of hypertension, thus implying that a specific role in the pathogenesis of primary hypertension for an Na+, K(+)-inhibitor is unlikely.
Adult↗
Cardiovascular side effects after renal allograft rejection therapy with Orthoclone: prevention with nitrendipine.
Orthoclone (OKT-3), a monoclonal antibody, is an effective immunosuppressant in organ graft recipients. One of the reported side effects is serious pulmonary edema, heart failure, hyperdynamia, and elevation of blood pressure. It should be assessed whether patients treated with OKT-3 benefit from antihypertensive therapy with a calcium channel blocker before and during the allograft rejection therapy to prevent from cardiovascular side effects. To assess a preventive cardiovascular effect of therapy with nitrendipine before and during the OKT-3 rejection therapy, the patients studied (n = 28) were randomly allocated to two study groups. Group a without nitrendipine comprised 15 patients, and group b with 2 x 10 mg of nitrendipine daily comprised 13 patients. In study group a (without nitrendipine therapy), in 8 of 15 patients, there was a short-lasting increase in blood pressure during 3 h after the first injection of OKT-3 by 20.0 +/- 12.8 (systolic)/10.1 +/- 6.7 (diastolic) mm Hg. Whereas this initial rise of blood pressure on the first day was accompanied by an increase in heart rate by 24.1 +/- 10.8 beats/min, the longer-lasting increase in blood pressure at day 2 was not associated with significant changes in heart rate. In group b (patients receiving 2 x 10 mg of nitrendipine before OKT-3 therapy was started and during the whole treatment course), in 3 of 13 patients, a short increase in blood pressure (13.7 +/- 2.9/7.8 +/- 5.1 mm Hg) was recorded 5 h after the first dose of OKT-3.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Plasma membrane calcium content in essential hypertension.
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Adult↗
Twenty-four-hour blood pressure profile in elderly hypertensives: effects of heart failure.
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Aged↗
Effect of plasma from essential hypertensives on vascular tone of aortic strips, isolated perfused mesentery and isolated perfused kidney.
Different vascular models of normotensive Wistar rats, including aortic strips, isolated perfused mesentery and isolated perfused kidney, were used to study hemodynamic effects of plasma fractions obtained by gel filtration from the blood of essential hypertensive and normotensive subjects. Plasma fractions from essential hypertensives studied had been shown to increase blood pressure after intravenous injection in rats. In the aortic strips, 50 microliters of a hypertensive fraction (HF) elicited a calcium-dependent contraction of 0.14 +/- 0.035 mN (n = 20, p less than 0.05), which was inhibited by nifedipine, whereas tension of the strips was not significantly changed by normotensive fractions (NF) (n = 17). In the isolated perfused mesentery preparation, no significant change of perfusion pressure by HF or NF could be demonstrated (n = 10). In the isolated perfused kidney, a transient increase of perfusion pressure was induced by HF (19.5 +/- 16.6 mm Hg, n = 40, P less than 0.001) but not by NF. This increase was abolished in calcium-free, 2 mmol/l EGTA containing perfusion medium. The response was diminished, but not abolished by nifedipine. These data demonstrate vasopressor properties of plasma from essential hypertensives, which might be the consequence of a circulating vasoconstrictor substance in the blood of essential hypertensives.
Adult↗
Plasma and intracellular Mg2+ concentrations in pre-eclampsia.
Plasma and intra-erythrocytic magnesium concentrations were determined in 27 patients with pre-eclampsia and in 22 healthy pregnant women. In the pre-eclamptic women, the Mg2+ concentrations were measured before and after treatment with Mg2+ salts and after delivery. The plasma Mg2+ concentration was not significantly different in the pre-eclamptic and the healthy pregnant women. The intra-erythrocytic Mg2+ concentration before treatment with Mg2+ was significantly lower in the pre-eclamptic patients than in the healthy pregnant women [1.33 +/- 0.29 versus 1.01 +/- 0.16 mmol/l (means +/- s.d.); P less than 0.05] and increased after treatment with Mg2+ to 1.19 +/- 0.24 mmol/l. Lowered cellular Mg2+ concentrations in pre-eclampsia may contribute to the development of hypertension in this disorder.
Adult↗
Ca2+ release in permeabilized human neutrophils induced by ciclosporin.
In suspensions of permeabilized human neutrophils, the free Ca2+ concentration was measured to test the effects of ciclosporin. Free Ca2+ concentration was measured with a Ca2(+)-selective electrode. Ciclosporin (500 ng/ml) induced a transient increase in free Ca2+ concentration (maximum delta pCa, 0.41 +/- 0.17). Thereafter, the free Ca2+ concentration decreased again, but did not reach the baseline level in most experiments. Ruthenium red, but not orthovanadate, abolished the slow decline of free Ca2+ concentration after the initial increase. The experiments suggest that ciclosporin may induce a release of Ca2+ from cellular organelles, e.g. the endoplasmic reticulum, and a partial reuptake in mitochondria. A release of cellular Ca2+ may play a role in ciclosporin-induced hypertension.
Calcium↗
Effect of plasma from essential hypertensives on tension of aortic strips.
The effect of fractions of plasma from essential hypertensive (n = 27) and normotensive subjects (n = 26) on the tension of aortic strips (n = 27) from normotensive rats was examined. The fractions obtained from hypertensive patients had been shown to increase blood pressure, when injected intravenously in a normotensive rat. In aortic strips the hypertensive fractions elicited a transient relaxation of variable amplitude and subsequently a sustained contraction. The normotensive fractions did not alter tension of the strips significantly. In Ca2+ free medium and after addition of nifedipine hypertensive plasma fractions did not induce a contraction, whereas in Na+ free medium the contraction was not abolished. It is concluded that in the fraction of hypertensive plasma containing substances with a molecular weight in the range of 1000-1500 Da a vasopressor agent with direct actions on arterial smooth muscle is present. The substance probably acts by increasing Ca2+ influx in vascular smooth muscle.
Adult↗
[Action of trichlormethiazide and amiloride on cellular Na+, K+ and Mg+ concentrations].
While diuretic-induced changes of plasma electrolyte concentrations have often been described, comparatively few data exist on intracellular electrolyte concentrations under diuretic treatment. Therefore, we studied the effect on intracellular Mg2+, Na+ and K+ concentrations of a thiazide diuretic (trichlormethiazide 4 mg/d) in red blood cells of 14 patients with mild essential hypertension, and of a combination of a thiazide diuretic and a potassium-sparing diuretic (trichlormethiazide and amiloride 2 mg/d each) in red blood cells of 11 patients with mild essential hypertension. Measurements were performed by atomic absorption spectroscopy and flame photometry before starting treatment and after 4 and 8-12 weeks' diuretic treatment. There was no significant change in intracellular Na+ and K+ concentrations under either form of diuretic treatment. Intracellular Mg2+ concentrations decreased significantly under thiazide therapy, whereas there was a significant increase in intracellular Mg+ concentrations under thiazide and potassium-sparing combined diuretic therapy. The results show that the combination of a thiazide diuretic and a potassium-sparing diuretic is a useful means to avoid intracellular Mg2+ loss.
Amiloride↗
[Bing-Neel syndrome. Polyneuropathy within the scope of paraproteinemia].
A rare cause of polyneuropathy, first described in 1936, is the Bing-Neel syndrome. This polyneuropathy develops on the basis of a paraproteinemia. Five patients in whom the symptom constellation presented, were examined. All patients complained of motor or sensory deficiencies affecting the limbs, but had no evidence of malignant disease. Four patients had IgM paraprotein, one an IgG paraprotein in the serum. In two patients, the bone marrow revealed lymphocytic infiltration in the sense of an immunocytoma, in one other patient, a plasmacytoma was detected in the bone marrow. Three patients were treated in accordance with the Knospe regimen, the patient with the plasmocytoma with the Alexanian regimen. In one case satisfactory regression of the symptoms was observed, in the other two cases a moderate improvement occurred.
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Electron-probe X-ray microanalysis of sodium ion content in vascular smooth muscle cells from spontaneously hypertensive and normotensive rats.
In aortic smooth muscle cells from 12 spontaneously hypertensive rats (SHR) of the Münster strain and 11 normotensive Wistar-Kyoto rats (WKY), the intracellular Na+ content was measured by electron-probe microanalysis. Measurements were performed in aortic cryosections 3 microns thick; the Na+ content was 12.5 +/- 2.4 g/kg dry weight in SHR versus 6.96 +/- 1.1 g/kg dry weight in WKY (P less than 0.01). Thus, aortic smooth muscle cells from SHR are characterized by a markedly elevated intracellular Na+ content compared with normotensive cells. This may either be due to genetically determined disturbances in transmembrane Na+ transport or to a circulating factor affecting Na+ transport. Cellular Na+ handling may be disturbed in SHR aortic smooth muscle as it is in hypertensive blood cells.
Animals↗
Sodium reabsorption in the isolated perfused kidney of normotensive and spontaneously hypertensive rats.
Kidneys of 3-month-old spontaneously hypertensive rats (SHR) of the Münster strain and age- and weight-matched normotensive rats (Wistar-Kyoto; WKY) were isolated and perfused at a constant pressure of 100 mmHg with a modified, albumin-free Krebs-Henseleit solution. Fractional Na+ reabsorption, which is independent of the glomerular filtration rate under these conditions, was significantly elevated in SHR kidneys compared with WKY kidneys during 90 min of perfusion (P less than 0.01). Renal perfusion flow rates did not differ between SHR and WKY. These data support the concept of an intrinsic renal abnormality in Na+ excretion that may contribute to the maintenance of hypertension in SHR.
Absorption↗