Sustained influence of the renal nerves to attenuate sodium retention in angiotensin hypertension

Citation
Te. Lohmeier et al., Sustained influence of the renal nerves to attenuate sodium retention in angiotensin hypertension, AM J P-REG, 281(2), 2001, pp. R434-R443
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Physiology
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
ISSN journal
0363-6119 → ACNP
Volume
281
Issue
2
Year of publication
2001
Pages
R434 - R443
Database
ISI
SICI code
0363-6119(200108)281:2<R434:SIOTRN>2.0.ZU;2-B
Abstract
Recent studies indicate that baroreflex suppression of renal sympathetic ne rve activity is sustained for up to 5 days of ANG II infusion; however, ste ady-state conditions are not associated with ANG II hypertension of this sh ort duration. Thus the major goal of this study was to determine whether ne urally induced increments in renal excretory function during chronic intrav enous infusion of ANG II are sustained under more chronic conditions when h ypertension is stable and sodium balance is achieved. Experiments were cond ucted in five conscious dogs subjected to unilateral renal denervation and surgical division of the urinary bladder into hemibladders to allow separat e 24-h urine collection from denervated (Den) and innervated (Inn) kidneys. ANG II was infused after control measurements for 10 days at a rate of 5 n g . kg(-1) . min(-1). Twenty-four-hour control values for mean arterial pre ssure (MAP) and the ratio for urinary sodium excretion from Den and Inn kid neys (Den/Inn) were 92 +/- 4 mmHg and 0.99 +/- 0.05, respectively. On days 8-10 of ANG II infusion, MAP was stable (+30 +/- 3 mmHg) and sodium balance was achieved. Whereas equal amounts of sodium were excreted from the kidne ys during the control period, throughout ANG II infusion there was a greate r rate of sodium excretion from Inn vs. Den kidneys (day 10 Den/Inn sodium = 0.56 +/- 0.05), indicating chronic suppression of renal sympathetic nerve activity. The greater rate of sodium excretion in Inn vs. Den kidneys duri ng renal sympathoinhibition also revealed a latent impairment in sodium exc retion from Den kidneys. Although the Den/Inn for sodium and the major meta bolites of nitric oxide (NO) decreased in parallel during ANG II hypertensi on, the Den/Inn for cGMP, a second messenger of NO, remained at control lev els throughout this study. This disparity fails to support the notion that a deficiency in NO production and action in Den kidneys accounts for the im paired sodium excretion. Most importantly, these results support the conten tion that baroreflex suppression of renal sympathetic nerve activity is sus tained during chronic ANG II hypertension, a response that may play an impo rtant role in attenuating the rise in arterial pressure.