To determine whether the increase in baroreflex sensitivity previously reported in lifetime
captopril-treated spontaneously hypertensive rats (SHR) was due to an inhibition of brain
angiotensin II mechanisms, we tested the effect of intracerebroventricular administration of an
angiotensin II receptor antagonist on baroreflex control of heart rate in lifetime
captopril-treated and untreated male and female SHR. Baroreceptor reflex control of heart rate was assessed by the slope of the relationship between changes in mean arterial pressure (delta MAP, mmHg) and changes in pulse interval (delta PI, ms). MAP was raised and lowered with infusions of
phenylephrine and
nitroprusside, respectively. Following basal assessment of baroreflex control of heart rate, rats received an intracerebroventricular injection (100 pmol) of Sar1Thr8
angiotensin II (
sarthran) and reflex control of heart rate was reassessed. Adequacy of blockade was tested with central and peripheral administration of
angiotensin II.
Captopril-treated male (130 +/- 7 mmHg) and female (123 +/- 4 mmHg) rats had significantly lower MAP than untreated rats (174 +/- 4 and 173 +/- 8 mmHg, respectively) and enhanced
bradycardia in response to increases in MAP. Intracerebroventricular administration of
sarthran had no effect on basal blood pressure or heart rate but enhanced the
bradycardia in response to increases in MAP in both untreated and
captopril-treated rats. The increase in the slope of the line relating delta MAP to delta PT was greater for untreated than
captopril-treated SHR (male untreated 2.7-fold versus
captopril-treated 1.5-fold; female untreated 1.6-fold versus
captopril-treated 1.5-fold).(ABSTRACT TRUNCATED AT 250 WORDS)