BACKGROUND: Scarce information is available on stress-induced renal behavior in humans, especially in normotensives offspring of hypertensives (HP) and in hypertensives (HT). METHODS: Ten HP and 10 HT were compared to 10 normotensives with normotensive parents (NP). Systolic blood pressure (SBP) and renal functional parameters were determined during rest and stress periods. RESULTS: The stress SBP reactivity was significantly (P < .05) higher in HP than in NP and HT. At rest, HP were characterized by a significantly (P < .05) higher glomerular filtration rate. Stress significantly reduced glomerular filtration rate (-14 +/- 4 mL/min/1.73 m2, P < .05) only in HT. Renal plasma flow significantly (P < .05) decreased during stress in NP (-35 +/- 16 mL/min/1.73 m2) and in HT (-49 +/- 25 mL/min/1.73 m2), whereas it did not change in HP. The resulting filtration fraction increased significantly during stress only in NP (1.5% +/- 0.6%, P < .05). Despite the increase in BP, stress induced a similar decrease in sodium excretion rate in NP (-52 +/- 26 micromol/min) and in HT (-56 +/- 24 micromol/min). The stress-induced sodium reabsorption occurred only in the proximal part of the tubules (lithium clearance). In HP, stress did not alter either sodium excretion rate or plasma renin activity. CONCLUSIONS: The stress-induced renal modifications are characterized by an efferent vasoconstriction and a paradoxical increase in sodium reabsorption that occurred in the proximal part of the tubules in NP. In HP, genetically at risk of hypertension, basal renal alterations may explain a different stress-induced renal behavior. In HT, stress-induced increase in sodium reabsorption may be involved in the sustained BP level.
BACKGROUND: Scarce information is available on stress-induced renal behavior in humans, especially in normotensives offspring of hypertensives (HP) and in hypertensives (HT). METHODS: Ten HP and 10 HT were compared to 10 normotensives with normotensive parents (NP). Systolic blood pressure (SBP) and renal functional parameters were determined during rest and stress periods. RESULTS: The stress SBP reactivity was significantly (P < .05) higher in HP than in NP and HT. At rest, HP were characterized by a significantly (P < .05) higher glomerular filtration rate. Stress significantly reduced glomerular filtration rate (-14 +/- 4 mL/min/1.73 m2, P < .05) only in HT. Renal plasma flow significantly (P < .05) decreased during stress in NP (-35 +/- 16 mL/min/1.73 m2) and in HT (-49 +/- 25 mL/min/1.73 m2), whereas it did not change in HP. The resulting filtration fraction increased significantly during stress only in NP (1.5% +/- 0.6%, P < .05). Despite the increase in BP, stress induced a similar decrease in sodium excretion rate in NP (-52 +/- 26 micromol/min) and in HT (-56 +/- 24 micromol/min). The stress-induced sodium reabsorption occurred only in the proximal part of the tubules (lithium clearance). In HP, stress did not alter either sodium excretion rate or plasma renin activity. CONCLUSIONS: The stress-induced renal modifications are characterized by an efferent vasoconstriction and a paradoxical increase in sodium reabsorption that occurred in the proximal part of the tubules in NP. In HP, genetically at risk of hypertension, basal renal alterations may explain a different stress-induced renal behavior. In HT, stress-induced increase in sodium reabsorption may be involved in the sustained BP level.
Authors: John J Gildea; Dylan T Lahiff; Robert E Van Sciver; Ryan S Weiss; Neema Shah; Helen E McGrath; Cynthia D Schoeffel; Pedro A Jose; Robert M Carey; Robin A Felder Journal: Clin Chim Acta Date: 2013-02-27 Impact factor: 3.786