Renal sodium excretion in sons of hypertensive parents.

Abstract

The objective of this study was to evaluate whether renal excretion of sodium is impaired and whether tubular reabsorption of sodium is increased in normotensive white men with a familial predisposition to develop essential hypertension. We compared 11 normotensive sons of two hypertensive parents (SOHT) with 11 normotensive sons of two normotensive parents (SONT); renal sodium handling was assessed after 1 week of low-sodium diet ( A prevailing hypothesis to explain the familial predisposition to essential hypertension (hy-. pertension) is that inherited factors have effects that impair the kidneys' ability to excrete sodium chloride (sodium).1 Sodium excretion may be impaired either because less sodium is filtered by the kidneys or because more filtered sodium is reabsorbed by the renal tubules. Either alteration might result from an abnormality that is intrinsic to the kidneys or one that is secondary to extrarenal factors. Because plasma sodium concentration and glomerular filtration rate -the determinants of the filtered load of sodium-are not decreased early in the course of uncomplicated hypertension, 2 increased tubular reabsorption of sodium has been the renal alteration most often postulated to impair sodium excretion and contribute to the development of hypertension.Despite compelling arguments presented by Guyton and others that impairment of renal sodium excretion is Received February 15,1993; accepted in revised form April 28, 1993.From the Division of Hypertension, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minn (S.T.T.), and the Department of Human Genetics, University of Michigan, Ann Arbor (S.L.R.).Previously published in abstract form (Hypertension. 1989; 14:345).Correspondence to Stephen T. Turner, MD, Division of Hypertension, Mayo Foundation, Rochester, MN 55905. a sine qua non for hypertension to develop, 3 studies that have assessed renal excretion and tubular reabsorption of sodium in normotensive humans with a familial predisposition to develop hypertension have been inconsistent in their results. For example, the natriuretic response to intravenous saline infusion has been reported to be either decreased or increased in normotensive first-degree relatives of hypertensive patients, 4 " 6 and the fractional excretion of lithium -an inverse indicator of proximal tubular reabsorption of sodiumhas been reported to be either increased or no different in normotensive offspring of hypertensive patients. 7 -8 The reasons for these inconsistencies may include differences between studies in methods used to select subjects with contrasting predispositions to develop hypertension, differences in the level of dietary sodium intake before assessment of renal sodium handling, and differences in the measures used to assess renal sodium handling.We undertook the present study in search of evidence to support the hypothesis that renal excretion of sodium is impaired and that tubular reabsorption of sodium is increased in normotensive white men with a familial predisposit...

A hypertensive father, but not hypertensive mother, determines blood pressure in normotensive male offspring through body mass index

“…9,10,17,18 Considering these data from backcrossed SHR, Y chromosome from a male rat with hypertension is responsible in part for elevation of BP probably through enhanced adrenergic nerve system or androgen receptor mediated events. 11,19 If hypertensive Y chromosome influences adrenergic nerve activity in human as well, [12][13][14][15] this theory is able to explain the linkage between the genetic loading from a hypertensive father and BMI observed in the present study. In this context, we demonstrated in the present study that heart rate is one of the predictors of SBP in the male students having a hypertensive father.…”

“…More interestingly, higher levels of BP in the offspring of hypertensive parents are often associated with an increase in plasma insulin concentrations or a decrease in insulin sensitivity and increased response of adrenergic nervous system to mental stress. [9][10][11]14,15 In fact, Scherrer et al 16 have demonstrated the relationship between BMI and the rate of sympathetic nerve discharge to skeletal muscle vasculature in normotensive subjects. In this context, we have demonstrated in our previous study that BP levels are well correlated to BMI in non-obese, normotensive freshman students having both hypertensive parents, and that such offspring have relatively higher plasma insulin concentrations.…”

Prädiktive Untersuchungen bei phänotypisch gesunden Nachkommen von Patienten mit einem metabolischen Syndrom¹

“…Was die renale Natriumausscheidung anbetrifft, wurden in verschiedenen experimentellen Ansätzen keine relevanten Unterschiede zwischen gesunden Probanden mit und ohne hypertensiver Familienanamnese gefunden (9,51,27). Andererseits sind salzsensitive Nachkommen von Hypertonikern auch insulinresistent, was einen Zusammenhang von Natriumhaushalt und Insulinresistenz nahelegt (48).…”

Variability in Measures of Exhaled Breath Na+, Influence of pulmonary Blood Flow and salivary Na+

“…Previous studies have speculated on sources of variability based on collection methods, but have failed to investigate specific physiological sources as potential contributors to this variability. The transport of Na + , K + , and Cl − into the intracellular space across the basolateral membrane of epithelial cells is influenced by blood ion levels 14. Altering the driving force for ion transport by changing the electrochemical gradient could thereby affect the airway surface liquid ion composition and the reflection of its composition in the EBC collections by influencing apical ion and water movement.…”