Effect of acute NaCl depletion on NaCl-sensitive hypertension in borderline hypertensive rats.

Abstract

The borderline hypertensive rat (BHR) is the first generation offspring of a mating between a female spontaneously hypertensive rat and a male normotensive Wistar-Kyoto rat. With increased dietary NaCl intake, the BHR develops hypertension and augmented cardiovascular and renal responses to acute environmental stress. This investigation sought to examine the role of extracellular fluid volume (ECFV) in these changes. Three groups of 16-week-old BHR were studied: (1) rats on a 1% NaCl diet for 12 weeks; (2) rats on an 8% NaCl diet for 12 weeks; and (3) rats on an 8% NaCl diet for 12 weeks plus furosemide (50 mg/kg, i.p., twice daily) for the preceding 2 days. Rats were chronically instrumented for the measurement of mean arterial pressure (MAP), heart rate and renal hemodynamic, excretory and sympathetic nerve activity responses to acute environmental stress (acute air jet stress). ECFV was measured as inulin space. BHR fed an 8% NaCl diet had increased MAP, urinary sodium excretion and ECFV compared with those fed a 1% NaCl diet; they also exhibited augmented pressor, tachycardic, renal sympathetic nerve excitatory and antinatriuretic responses to acute environmental stress. When 8% NaCl-diet BHR were treated with furosemide for 2 days, arterial pressure, urinary sodium excretion, ECFV and cardiovascular and renal responses to acute environmental stress returned to values seen in 1% NaCl-diet BHR. The hypertension and increased cardiovascular and renal responses to acute environmental stress produced by increased dietary NaCl intake in BHR derive from a central nervous system site of action via a mechanism(s) related to ECFV and/or sodium.