GLOMERULAR HYPERFILTRATION DURING SYMPATHETIC NERVOUS-SYSTEM ACTIVATION IN EARLY ESSENTIAL-HYPERTENSION

Citation
Re. Schmieder et al., GLOMERULAR HYPERFILTRATION DURING SYMPATHETIC NERVOUS-SYSTEM ACTIVATION IN EARLY ESSENTIAL-HYPERTENSION, Journal of the American Society of Nephrology, 8(6), 1997, pp. 893-900
Citations number
52
Categorie Soggetti
Urology & Nephrology
ISSN journal
10466673
Volume
8
Issue
6
Year of publication
1997
Pages
893 - 900
Database
ISI
SICI code
1046-6673(1997)8:6<893:GHDSNA>2.0.ZU;2-O
Abstract
Glomerular hyperfiltration may be important for the development of ess ential hypertension. Both the renin-angiotensin system and the sympath etic nervous system influence renal hemodynamic regulation. To test th e hypothesis that glomerular hyperfiltration can be unmasked by sympat hetic nervous system activation, renal hemodynamics and humoral compon ents of the renin-angiotensin system were examined at rest and during mental stress in 45 young normotensive healthy subjects and 37 young p eople with mild essential hypertension. GFR and renal plasma flow (RPF ) were determined with inulin and para-aminohippuric acid clearance at rest and during stress, At rest, RPF, GFR, filtration fraction, plasm a renin activity, angiotensin (Ang) II concentrations, and serum aldos terone values were similar in normotensive and hypertensive subjects, After stress, blood pressure increased (P < 0.01), but this was nearly identical in normotensive and hypertensive subjects (7.05 +/- 6.9 ver sus 7.03 +/- 4.6 mmHg, NS). The decrease in RPF (-27 +/- 54 versus -22 +/- 25 ml/min per 1.73 m(2), NS) was also similar in the two groups. In contrast, the increase in GFR (+10.5 +/- 7.2 versus 6.08 +/- 5.7 ml /min per 1.73 m(2), P < 0.001) and filtration fraction (+2.48 +/- 1.38 versus 1.82 +/- 1.49%, P < 0.05) was more marked in hypertensive than in normotensive subjects, The concomitant increase in Ang II concentr ations was greater in hypertensive than in normotensive subjects (+4.6 +/- 1.0 versus -1.0 +/- 0.45 pg/ml, P < 0.001). The increase in GFR d uring mental stress was correlated with the increment in Ang II concen trations (r = 0.39, P < 0.001). Compared with the placebo control phas e, blockade of the renin-angiotensin system with an angiotensin-conver ting enzyme inhibitor attenuated the increase in GFR during stress in hypertensive (8.04 +/- 5.01 versus 10.1 +/- 5.7 ml/min per 1.73 m(2), P < 0.05), but not in normotensive, subjects. Even in early essential hypertension, glomerular hyperfiltration is evident during sympathetic nervous system activation, which is mediated by postglomerular vasoco nstriction, This early stress-induced glomerular hyperfiltration may c ontribute to, or trigger, the development of essential hypertension.