ORCID Profile
0000-0002-8365-3618
Current Organisation
Università Vita Salute San Raffaele
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Publisher: Elsevier BV
Date: 1990
DOI: 10.1016/0005-2736(90)90377-Z
Abstract: This paper describes experiments to examine Rb+ fluxes via the Na+/K+/Cl- cotransporter in membrane vesicles from renal outer medulla of three strains of rat: (A) Wistar (B) Milan hypertensive (MHS) and normotensive (MNS), and (C) Sabra salt-sensitive hypertensive (SBH) and salt-resistant (SBN). Initially, Na(+)-dependent furosemide- or bumetanide-inhibited 86Rb+ fluxes were characterised using Wistar rat microsomes. The latter were partially purified on a metrizamide cushion, and assay conditions were optimized for use with microsomes from the other rats. The major result is that in microsomes from adult Milan hypertensive (MHS) rats the rate of the Na+/K+/Cl(-)-cotransporter mediated 86Rb flux at sub-saturating concentrations of Rb, appears to be significantly greater than in the normotensive (MNS) controls. The effect reflects an increased apparent Rb affinity of the cotransporter in MHS microsomes. There is no difference in maximal rate or in the apparent Na+ activation affinity of the 86Rb+ flux. In addition bumetanide appears to be a somewhat more effective inhibitor in MHS compared to MNS microsomes. The 86Rb+ flux result is compatible with a previous finding that in red cells, Na+/K+ -cotransporter mediated fluxes are increased in MHS compared to MNS. It supports the notion that the Na+/K+/Cl(-)-cotransporter in in both red cells and kidney is a genetic marker for hypertension. It is of interest that apparently more than one Na+ transport system is affected in MHS hypertensive kidneys (a) the Na+/K+/Cl- cotransporter in the thick ascending limb of Henle and (b) the Na+/H+ exchanger and/o a conductive Na(+)-pathway in brush-border membranes from proximal tubule. It is conceivable that in the hypertensive animals a common regulatory pathway (e.g., phosphorylation) or protein (e.g., cytoskeleton) is affected along the length of the nephron. In Sabra SBH and SBN rat microsomes, no difference was found for the 86Rb+ flux via the Na+/K+/Cl- cotransporter (or via a K+ channel).
Publisher: Oxford University Press (OUP)
Date: 02-1989
DOI: 10.1093/AJH/2.2.2S
Abstract: The role of the kidney in "essential" or "genetic" types of hypertension has been evaluated both in a rat model such as the Milan hypertensive strain (MHS) or in humans. In both species, abnormalities of renal function have been demonstrated before the development of hypertension. Moreover hypertension could be "transplanted" with the kidney when kidney cross-transplantation was carried out between MHS and the Milan normotensive strain (MNS). Also in humans, the familiality for hypertension of the donor affected the requirement of antihypertensive therapy of the recipient. Further studies furnished results that were consistent with the hypothesis that a primary increase in Na transport across the tubular cell could be responsible for the pressor effect of the kidney in MHS or in humans. Because many similarities were found between the function of the tubular cell and the red blood cell in MHS, red blood cells were used to gain information about the molecular genetic mechanisms underlying these cellular changes. The results so far obtained showed that red blood cell abnormalities in MHS were genetically determined within the stem cells and genetically associated with the development of hypertension in F2 hybrids obtained by crossing the F1 (MHS X MNS). Moreover, the abnormal Na transport across the cell membrane may be due to an abnormal function of the membrane skeleton proteins. Studies are in progress to evaluate a possible cause-effect relationship between: membrane skeleton protein-ion transport across the cell membrane and the development of hypertension.
Publisher: Wiley
Date: 23-09-1991
DOI: 10.1016/0014-5793(91)81259-B
Abstract: The (Na+,K+)-ATPase activity from the kidney cortex of the Milan hypertensive rat strain (MHS) and the corresponding normotensive control (MNS) was measured both in active solubilized enzyme preparations and in isolated basolateral membrane vesicles. Kinetic analysis of the purified enzyme showed that the Vmax value was significantly higher in MHS rats. The difference between MHS and MNS was not linked to a different number of sodium pumps, but was related to the molecular activity of the enzyme. Using basolateral membrane vesicles, an increased ATP-dependent ouabain-sensitive sodium transport was also demonstrated in MHS rats. These results support the hypothesis that a higher tubular sodium reabsorption may be involved in the pathogenesis of hypertension in this rat strain.
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United States of America
No related grants have been discovered for Giuseppe Bianchi.