title: Salt sensitivity in normotensives with family history of hypertension: studies of membrane transport, intracellular electrolytes and alpha 2-adrenergic receptors.
abstract: Using long-term automatic blood pressure recording it has previously been shown that subjects with family history of hypertension show a minute fall of blood pressure during sodium restriction, which is reversible by high sodium intake. Thus normotensives with hypertensive antecedents as a group are salt-sensitive, whereas normotensives without heredity of hypertension as a group are salt-resistant. The present study compares intracellular sodium, potassium and calcium, sodium pump activity, NaK-cotransport of red blood cells and density and affinity of alpha 2-adrenergic receptors of platelets in normotensive subjects classified according to family history of hypertension and according to 'salt sensitivity' and 'salt resistance'. Neither the family history of hypertension nor salt sensitivity correlated with intracellular sodium, potassium, calcium, Na-pump activity and NaK-cotransport. Alpha 2-adrenergic density was higher in salt-sensitive than in salt-resistant subjects (P < 0.05) but similar in subjects with a positive and negative family history of hypertension. However, alpha 2-adrenergic receptor density decreased significantly during 2 weeks of moderate salt restriction from 169.6 +/- 34.2 to 142.6 +/- 30.8 (P < 0.01, paired t-test), which may explain the decreased pressor response to infused noradrenaline observed in a previous study during moderate salt restriction. It is concluded that in humans there is no association of genetic predisposition of hypertension or of salt sensitivity to an alteration of sodium pump activity, NaK-cotransport, intracellular sodium and calcium. Alpha 2-receptor density of platelets deserves further study as a possible predictor of salt sensitivity in normotensives.
authors.affiliation: Department of Internal Medicine, University Hospital, Innsbruck, Austria.
authors.forename: F
authors.initials: F
authors.lastname: Skrabal
authors.forename: G
authors.initials: G
authors.lastname: Gruber
authors.forename: B
authors.initials: B
authors.lastname: Meister
authors.forename: M
authors.initials: M
authors.lastname: Ledochowski
authors.forename: P
authors.initials: P
authors.lastname: Doll
authors.forename: F
authors.initials: F
authors.lastname: Lang
authors.forename: E
authors.initials: E
authors.lastname: Cerny
mesh_terms: D000328:Adult; D001794:Blood Pressure / Q000187:drug effects*; D002462:Cell Membrane / Q000378:metabolism; D004573:Electrolytes / Q000378:metabolism; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D012982:Sodium, Dietary / Q000494:pharmacology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects
chemical_list: D004573:Electrolytes; D011942:Receptors, Adrenergic, alpha; D012982:Sodium, Dietary; D000254:Sodium-Potassium-Exchanging ATPase; D009638:Norepinephrine