Morphological and functional evidence for the contribution of the pudendal artery in aging-induced erectile dysfunction.
BACKGROUND
Aging increases the risk of both erectile dysfunction (ED) and cardiovascular disease. These conditions have similar etiologies and commonly coexist. One unifying concept is the role of arterial insufficiency which is a primary factor in the onset of age-related ED.


OBJECTIVE
Based on the novel finding that the pudendal arteries contribute 70% of the total penile vascular resistance, our objective was to morphometrically and functionally characterize this vessel in young and old normotensive rats.


METHODS
Erectile function was monitored in 15- and 77-week Sprague-Dawley rats using the apomorphine bioassay (80mg/kg, s.c.). Anesthetized animals were perfusion-fixed, aortic, renal, and internal pudendal arteries were excised, embedded, sectioned, stained, and morphometrically assessed using light microscopy. Hearts were excised, separated, and weighed prior to perfusion. Contractile and relaxation responses to acetylcholine (ACh) and phenylephrine (PE) were assessed by wire myograph.


METHODS
Erectile function, morphological measurements, concentration response curves to ACh and PE.


RESULTS
With age, there were marked decreases in erectile responses compared to younger rats (2.8±0.87 vs. 0.3±0.58). The pudendal arteries had a relatively small lumen (303±13.8µm) and a thick medial layer (47±2.2µm). In aged pudendal arteries, the lumen diameter did not change, and yet the medial layer, cross sectional area, and extracellular matrix were markedly increased. In contrast, the lumen diameter and wall thickness of the aorta and renal arteries in aged rats increased proportionally. An increase in small, round, smooth muscle cells was seen in aged pudendal arteries. Functionally, there were no differences in contractile responses to PE; however, ACh-induced relaxation decreased with age.


CONCLUSIONS
In aged rats, erectile function was severely diminished when pudendal arteries had undergone marked phenotypic changes. Specifically, there was endothelial dysfunction and pathological remodeling of this vessel with age, characterized by medial thickening, impaired vasodilation and significantly reduced capacity for penile blood flow.
Hannan
Johanna L
JL
Department of Pharmacology & Toxicology, Queen's University, Kingston, Ontario, Canada.
Blaser
Mark C
MC
Oldfield
Lauren
L
Pang
Judith J
JJ
Adams
Stephen M
SM
Pang
Stephen C
SC
Adams
Michael A
MA
D000109:Acetylcholine / Q000494:pharmacology; D000375:Aging / Q000473:pathology / Q000502:physiology; D000818:Animals; D001058:Apomorphine; D001158:Arteries / Q000473:pathology / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D007172:Erectile Dysfunction / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D010410:Penile Erection / Q000187:drug effects / Q000502:physiology; D010413:Penis / Q000098:blood supply* / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
D010656:Phenylephrine; D001058:Apomorphine; D000109:Acetylcholine