Purpose: There is a strong association between hypertension and erectile dy
sfunction. Studies of the treatment of hypertension have shown that some ph
armacological agents are capable of inducing regression of the vascular str
ucture during treatment. We determined whether penile vascular structure is
as susceptible as other vascular beds to regression during antihypertensiv
e drug treatment.
Materials and Methods: Adult spontaneously hypertensive rats were treated f
or 1 or 2 weeks with 30 mg./kg. enalapril daily, or for 2 weeks with 45 mg.
/kg. hydralazine daily. Structurally based vascular resistance was determin
ed in isolated penile and skeletal muscle vascular beds perfused with Tyrod
e-dextran. A cumulative alpha1-adrenoceptor concentration constrictor respo
nse curve to 1 to 100 mug./ml. methoxamine was constructed and the maximum
constrictor response (vasopressin, methoxamine and angiotensin II) indicati
ng the tissue yield point (that is the average medial bulk of vascular smoo
th muscle) was determined. The hearts were excised and the ventricles were
separated and weighed.
Results: Enalapril treatment progressively regressed cardiac and vascular s
tructure during the 1 and 2-week treatment periods with a mean tissue yield
point plus or minus standard deviation of -5.91% +/- 5.1% (p <0.05) and -1
2.1% +/- 6.0% (p <0.05), and a mean left ventricle mass of -11.8% +/- 2.2%
(p <0.05) and -13.6% +/- 3.2% (p <0.05), respectively. Hydralazine treatmen
t for 2 weeks was less effective on vascular regression with a mean yield o
f -7.3% +/- 2.9% (p <0.05) and it did not alter left ventricle hypertrophy
compared with controls (3.7% +/- 5.0%).
Conclusions: The data suggest that renin-angiotensin system inhibition may
at least partially normalize penile vascular structure. The impact of these
changes on erectile function must be determined.