title: Antihypertensive drugs induce structural remodeling of the penile vasculature.
abstract: OBJECTIVE
  There is a strong association between hypertension and erectile dysfunction. Studies of the treatment of hypertension have shown that some pharmacological agents are capable of inducing regression of the vascular structure during treatment. We determined whether penile vascular structure is as susceptible as other vascular beds to regression during antihypertensive drug treatment.
  
  
  METHODS
  Adult spontaneously hypertensive rats were treated for 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 determined in isolated penile and skeletal muscle vascular beds perfused with Tyrode-dextran. A cumulative alpha1-adrenoceptor concentration constrictor response curve to 1 to 100 microg./ml. methoxamine was constructed and the maximum constrictor response (vasopressin, methoxamine and angiotensin II) indicating the tissue yield point (that is the average medial bulk of vascular smooth muscle) was determined. The hearts were excised and the ventricles were separated and weighed.
  
  
  RESULTS
  Enalapril treatment progressively regressed cardiac and vascular structure 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 -12.1% +/- 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 treatment for 2 weeks was less effective on vascular regression with a mean yield of -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.
authors.affiliation: Departments of Pharmacology and Toxicology and Urology, Queen's University, Kingston, Ontario, Canada.
authors.forename: T M
authors.initials: TM
authors.lastname: Hale
authors.forename: H
authors.initials: H
authors.lastname: Okabe
authors.forename: J P
authors.initials: JP
authors.lastname: Heaton
authors.forename: M A
authors.initials: MA
authors.lastname: Adams
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D004656:Enalapril / Q000494:pharmacology; D006830:Hydralazine / Q000494:pharmacology; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D010413:Penis / Q000098:blood supply* / Q000187:drug effects; D051381:Rats; D011918:Rats, Inbred SHR; D012084:Renin-Angiotensin System / Q000187:drug effects; D014655:Vascular Resistance / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology; D020257:Ventricular Remodeling
chemical_list: D000959:Antihypertensive Agents; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D014667:Vasopressins; D000804:Angiotensin II; D006830:Hydralazine; D004656:Enalapril; D008729:Methoxamine