PMID- 2695468 OWN - NLM STAT- MEDLINE DCOM- 19900323 LR - 20190816 IS - 0167-5273 (Print) IS - 0167-5273 (Linking) VI - 25 Suppl 1 DP - 1989 TI - Pathogenetic mechanisms in essential hypertension. Analogies between a rat model and the human disease. PG - S29-36 AB - Essential hypertension is a genetic disease. Its phenotypic expression depends on the interaction between genetic and environmental factors. In prehypertensive rats of the Milan hypertensive strain (MHS) a genetically inherited increase of tubular reabsorption was found, which causes the increase of blood pressure. Studies of ion transport systems in these rats have shown that the Na-K cotransport activity is increased both in erythrocytes and in tubular cells of MHS rats compared with their normotensive controls (MNS) and that this alteration is genetically linked to the transmission of high blood pressure levels. Also, in young human normotensives prone to develop essential hypertension there is an abnormal pattern of renal function which could be in agreement with a primitive increase in tubular reabsorption. Studies of erythrocyte ion transport systems in these subjects suggest that at least in a subgroup of humans predisposed to develop essential hypertension a pathogenetic mechanism similar to the one proposed for the MHS rat can be at work. FAU - Cusi, D AU - Cusi D AD - Institute of Medical Sciences, Postgraduate School of Nephrology, University of Milano, Italy. FAU - Alberghini, E AU - Alberghini E FAU - Pati, P AU - Pati P FAU - Tripodi, G AU - Tripodi G FAU - Barlassina, C AU - Barlassina C FAU - Colombo, R AU - Colombo R FAU - Cova, T AU - Cova T FAU - Niutta, E AU - Niutta E FAU - Vezzoli, G AU - Vezzoli G FAU - Bianchi, G AU - Bianchi G LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Review PL - Netherlands TA - Int J Cardiol JT - International journal of cardiology JID - 8200291 SB - IM MH - Animals MH - Disease Models, Animal MH - Humans MH - Hypertension/*physiopathology MH - Rats MH - Species Specificity RF - 29 EDAT- 1989/01/01 00:00 MHDA- 1989/01/01 00:01 CRDT- 1989/01/01 00:00 PHST- 1989/01/01 00:00 [pubmed] PHST- 1989/01/01 00:01 [medline] PHST- 1989/01/01 00:00 [entrez] AID - 0167-5273(89)90090-9 [pii] AID - 10.1016/0167-5273(89)90090-9 [doi] PST - ppublish SO - Int J Cardiol. 1989;25 Suppl 1:S29-36. doi: 10.1016/0167-5273(89)90090-9.