Targeting vascular structure for the treatment of sexual dysfunction.
BACKGROUND
Erectile dysfunction (ED) and cardiovascular disease often coexist and have many common risk factors. In hypertension, the structure of blood vessels is modified such that there is an increase in medial wall thickness relative to lumen size. Certain antihypertensive agents have been found to induce a regression of vascular structure such that a "hypertensive" vessel appears phenotypically more like that from a normotensive.


OBJECTIVE
To provide an update on the findings to date on the impact of vascular remodeling on erectile function.


METHODS
Review of peer reviewed literature related to vascular remodeling induced by antihypertensive agents and the potential impact on sexual function.


METHODS
A literature review was performed on clinical and experimental evidence regarding the association between cardiovascular disease and ED, the impact of vascular remodeling on these conditions, the impact of antihypertensive therapy on ED, and the mechanisms of antihypertensive drug-induced remodeling.


RESULTS
There is increasing evidence that ED may be an early marker for progressing cardiovascular disease. Certain antihypertensive agents have beneficial effects on both vascular structure and erectile function. The major site of resistance in the penile vasculature occurs at the level of the pudendal artery. Although structural remodeling has not yet been investigated in this vessel specifically, antihypertensive drugs have been shown to induce remodeling of the pudendal-penile vasculature and cavernosal arteries. Antihypertensive drug-induced vascular remodeling can be characterized by a decrease in the ratio of wall thickness to lumen diameter, and may result from vascular smooth muscle cell apoptosis, rearrangement of cells around a smaller lumen, and/or changes in the extracellular matrix composition depending on the vessel type.


CONCLUSIONS
Determining the mechanisms involved in antihypertensive drug-induced vascular remodeling in the pudendal vasculature may provide novel targets for the treatment of ED.
Hale
Taben M
TM
Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, AZ 85004-2157, USA. taben.hale@arizona.edu
Hannan
Johanna L
JL
Carrier
Serge
S
deBlois
Denis
D
Adams
Michael A
MA
D000959:Antihypertensive Agents / Q000009:adverse effects* / Q000627:therapeutic use; D017209:Apoptosis / Q000502:physiology; D001158:Arteries / Q000502:physiology; D007172:Erectile Dysfunction / Q000139:chemically induced / Q000453:epidemiology* / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000453:epidemiology*; D007031:Hypothalamus / Q000502:physiology; D008297:Male; D009130:Muscle, Smooth / Q000098:blood supply / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D009434:Neural Pathways; D010413:Penis / Q000098:blood supply*; D015398:Signal Transduction; D017539:Tunica Intima / Q000473:pathology / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
D000959:Antihypertensive Agents