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(Hypertension. 1998;31:21.)
© 1998 American Heart Association, Inc.

Scientific Contributions

Evolution of Chronic Nitric Oxide Inhibition Hypertension

Relationship to Renal Function

Changbin Qiu; Dianne Muchant; William H. Beierwaltes; Lorraine Racusen; Chris Baylis

From the Departments of Physiology (C.Q.) and Pediatrics, West Virginia University, Morgantown (D.M., C.B.); the Hypertension Research Division, Henry Ford Hospital, Detroit, Mich (W.H.B.); and the Department of Pathology, Johns Hopkins Medical School, Baltimore, Md (L.R.).

Correspondence to Chris Baylis, PhD, Department of Physiology, PO Box 9229, West Virginia University, Morgantown, WV 26506-9229. E-mail cbaylis{at}wvu.edu

Abstract—We conducted longitudinal measurements of blood pressure and renal function in the conscious, chronically catheterized rat before and during acute nitric oxide synthase inhibition (N-nitro-L-arginine methylester [L-NAME], 37 µmol/kg IV) and then chronic administration of oral L-NAME (37 µmol/kg per 24 hours). These studies specifically investigate the impact on plasma and renal renin as well as volume status during the evolution of this hypertension in rats not subjected to acute experimental stress. Blood pressure progressively increased with chronic administration of L-NAME and reached values greatly above those seen with acute administration of L-NAME. There were parallel increases in renal vascular resistance and development of proteinuria, and glomerular filtration rate began to decline at day 21, coincident with the appearance of renal damage. Twenty-four-hour urinary nitrite and nitrate excretion remained depressed, reflecting reduced nitric oxide synthesis. The plasma renin activity was variable and only increased transiently at 21 days, thus the angiotensin II dependence of this hypertension is not caused by stimulated plasma renin activity. Despite severe hypertension, sodium intake and excretion were unchanged over the 21 days of L-NAME administration. Plasma volume was significantly reduced at days 2 and 12 of L-NAME administration; thus the prolonged plasma volume contraction must result from the acute natriuretic response to the initial acute L-NAME administration.

Key Words: nitric oxide • renal vascular resistance • N-nitro-L-arginine methylester • natriuresis • plasma volume

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