Phase II of two-kidney, one
clip (2K1C)
Goldblatt hypertension in the rat is characterized by elevated blood pressure and near-normal plasma concentrations of
angiotensin II (Ang II) but is reversed by inhibition of the renin-angiotensin system. We hypothesized that this
angiotensin dependence is due to enhanced responsiveness to the slow pressor effect of Ang II caused by
renal artery stenosis. To test this idea, we submitted rats to either renal artery clipping or
sham operation. These groups were immediately subdivided; some animals received
enalapril in their
drinking water (508 mumol/L), and the rest drank distilled water only. After 10 to 14 days,
catheters were inserted into the aorta and vena cava, and the rats were housed in metabolism cages. After 3 control days of measurement of mean arterial pressure and other variables, the
enalapril-treated groups received an
intravenous infusion of Ang II at a dose of 3.8 pmol/min (4 ng/min) for 14 days. Rats not drinking
enalapril received only saline vehicle (2 mmol Na+ per day). After 3 days of Ang II infusion, the
enalapril-treated 2K1C rats had attained a significantly higher level of mean arterial pressure than the
enalapril-treated
sham rats. At the end of the Ang II infusion, mean arterial pressure in
enalapril-treated 2K1C rats was 151 +/- 6 mm Hg versus 107 +/- 7 mm Hg in
enalapril-treated
sham rats. Mean arterial pressure in the
enalapril-treated
sham rats after Ang II infusion was not significantly different from that of untreated
sham rats (109 +/- 2 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)