The importance of the loss of ovarian function to the progression of hypert
ension and heart disease in women is controversial. We investigated whether
ovariectomy would accelerate development of hypertension, congestive heart
failure, and neurohumoral activation in adult spontaneous hypertension hea
rt failure (SHHF) rats, a genetic model of heart failure. Six months after
ovariectomy, no significant differences between central and ovariectomized
rats were seen in systolic or diastolic blood pressure, left ventricular fr
actional shortening by echocardiography, or heart weight. Percent V-1 myosi
n isozyme was significantly lower in ovariectomized rats. Northern blot ana
lysis failed to show significant differences between groups in expression o
f hepatic angiotensinogen, renal renin, or left ventricular atrial or brain
natriuretic peptide mRNA. In a second experiment, serial measures of systo
lic pressure and left ventricular shortening fractions failed to document a
significant difference between control and ovariectomized rats as they dev
eloped heart failure, although there was a significant decline in shortenin
g fraction in both groups at the age when regular estrous cycling naturally
ceases. Survival time was similar between groups. In summary, ovariectomy
of adult SHHF rats does not appear to affect the progression of genetically
programmed hypertension and heart failure in this model.