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Biomedical subjects

P Hannaert

Publications and source records attributed to P Hannaert.

44 records · Page 3Linked to original sources
PubMed1985

Atrial natriuretic factor inhibits Ca(2+)-dependent K+ fluxes in cultured vascular smooth muscle cells.

The interaction of the synthetic fragment Arg101-Tyr126 of atrial natriuretic factor (ANF) with Ca(2+)-dependent K+ efflux was studied in the following six different cell models: cultured vascular smooth muscle cells from rat aorta; isolated rat glomeruli; human platelets; cultured endothelial cells from bovine aorta; peritoneal mouse macrophages; human red cells. In human red cells and mouse macrophages, the dose-response curves of K+ efflux as a function of Ca2+ ionophore, A23187, concentration were not modified by addition of ANF. In endothelial cells and platelets, ANF slightly inhibited Ca(2+)-dependent K+ efflux. In renal glomeruli, ANF inhibits about one-third of this flux and in vascular smooth muscle cells ANF induced a five- to tenfold increase in the EC50 of A23187 effect. In experiments performed at constant concentrations of A23187, the IC50 of ANF was approximately 10(-9) mol/l. Similar results were obtained in mouse macrophages with cyclic GMP (cGMP). Our results suggest that ANF is able to counterbalance an increase in cytosolic free Ca2+ content in vascular smooth muscle and some glomerular cells. This effect may result from the ability of this hormone to stimulate cGMP synthesis.

Animals↗
PubMed1983

Abnormal Na+,K+ cotransport function in a group of patients with essential hypertension.

In 50 normotensive controls, the increase in erythrocyte Na+ concentration up to 12.4 +/- 2.0 mmol/l cells (mean +/- SD) ensures half-maximal stimulation of outward Na+,K+ cotransport fluxes. Forty-six out of sixty-five patients with essential hypertension required more than 16 mmol/l cells of internal Na+ concentration to obtain a similar effect, strongly suggesting an abnormal cotransport function. Seven out of fourteen hypertensive patients with normal Na,K cotransport function showed Na+,Li+ countertransport fluxes higher than the normal upper limit of 220 mumol (1 cells h)-1. Conversely, countertransport fluxes were normal in fourteen hypertensives with abnormal cotransport function. The above results indicate that the total population of patients with essential hypertension is heterogeneous and includes one subgroup of subjects with abnormal Na+,K+ cotransport function, and another with increased Na+,Li+ countertransport fluxes.

Adolescent↗
PubMed1983

The effect of cyclic nucleotides and icosanoids on Na+ and K+ transport in human red cells.

Cyclic AMP inhibits the bumetanide-sensitive Na+,K+ cotransport system in human red cells. The cotransport inhibition is enhanced by addition of phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine to the incubation medium. The cyclic AMP concentration giving half-maximal cotransport inhibition showed a wide variation among different individuals (from 0.1 to 5 mM external cyclic AMP concentration). In contrast to cyclic AMP, cyclic GMP showed little effect on the cotransport system. The ouabain-sensitive Na+,K+ pump was almost unaffected by cyclic nucleotides. Prostacyclin was the only tested prostaglandin showing an effect on Na+ and K+ transport in human red cells. In some individuals, this icosanoid stimulated the Na+,K+ cotransport system. Leukotriene B4 stimulated K+ fluxes.

1-Methyl-3-isobutylxanthine↗
PubMed1981

Abnormal erythrocyte Na+ K+ cotransport system, a proposed genetic marker of essential hypertension.

In erythrocytes, the extrusion of a cell sodium load is accomplished by the ouabain-sensitive sodium-potassium pump and by the furosemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. The precise characterization of these transport pathways requires the determination of the turnover rates of cation translocation and the affinities for substrates and effectors. The preliminary results of such kinetic study in essential hypertension is reported here. An abnormally low rate of net sodium extrusion by the sodium-potassium co-transport system was observed in essential hypertensive patients and in a high proportion of their young normotensive offspring. A normal cotransport system found in secondary hypertensive subjects devoid of familial history of hypertension confirmed that the abnormal cotransport system is not the consequence of high blood pressure per se. At the molecular level, the cotransport abnormality seems to be consecutive to a diminished apparent affinity for intracellular Na+. A 20-40% increase in the rate of net sodium extrusion by the sodium-potassium pump seems to compensate for the abnormal cotransport in erythrocytes from some young normotensive subjects born of essential hypertensive parents and from some benign essential hypertensive subjects. No difference could be detected between the passive sodium permeability of erythrocytes from hypertensive subjects and normotensive controls. In conclusion, essential hypertension seems to be associate with an inherited defect in the apparent affinity for intracellular Na+ of the sodium-potassium cotransport system. We propose therefore the laboratory study of this system for (i) the distinction between essential and secondary hypertension and (ii) the preventive investigation of young normotensive subjects in hypertensive families.

Biological Transport, Active↗
PubMedDate not supplied

Interaction of internal Na+ and external K+ with the erythrocyte Na+, K+ cotransport system in essential hypertension.

External K+ inhibits the maximal rate of outward Na+, K+ cotransport in human red cells with no effect on the apparent affinity for internal Na+. The K+ concentration giving half-maximal inhibition (KIK) varied from 16 to 30 mM in 24 normotensive control subjects. Six of the 38 hypertensive patients showed a KIK above the upper limit of this normal range. Only three hypertensive patients showed a KIK below normal range. The internal Na+ content giving half-maximal stimulation of outward Na+, K+ cotransport (KSNa) was measured in the hypertensive patients (a normal range of KSNa = 9 to 16 mmol/liter cells was previously established in 50 normotensive control subjects). Eighteen hypertensive patients showed an abnormally high KSNa, as previously described in hypertensive patients whose Na+, K+ cotransport system had a low affinity for internal Na+ (Co -). Comparison of KSNa with KIK showed that all six hypertensive patients with high KIK and all three hypertensive patients with low KIK were Co - hypertensive.

Adult↗
PubMedDate not supplied

Involvement of natriuretic hormones and Na+ transport in the antihypertensive action of canrenone.

Recent studies in essential hypertensive patients and rats with genetic hypertension strongly suggested that the development of primary hypertension takes place by a transient and chronic "cascade" of events (i) excess Na+ intake, (ii) secretion of natriuretic factors, (iii) abnormal cells Na+ homeostasis in the vascular wall, due to the presence of inherited abnormalities in different Na+ transport systems, and (iv) increase in cytosolic free Ca2+ content and catecholamines. Canrenone, an antihypertensive drug, behaves like a partial agonist at the digitalis-receptor site of the Na+, K+ pump. We observed here that (i) a 4 hr preincubation of human red cells with this compound increases its antagonistic properties against ouabain, (ii) in cultured smooth muscle cells, canrenone counterbalances the increase in cytosolic free Ca2+ induced by ouabain, and (iii) in a model of experimental hypertension with increased endogenous "ouabain-like" factors (rats with reduced renal mass), the administration of canrenone tends to normalize Na+, K+-pump activity and decrease blood pressure.

Animals↗