Morphological changes in cavernous tissue in spontaneously hypertensive rats.
Erectile dysfunction has an increased prevalence in hypertensive patients and is associated with cardiovascular diseases. For many years the discussion has been polarized on whether in hypertensive patients, it is the arterial hypertension or the antihypertensive therapy that is the cause of male erectile dysfunction. The aim of our study was to determine the morphologic changes in cavernous tissue (CT) in an animal model of arterial hypertension. Male spontaneously hypertensive rats (SHR) (n = 15) and normotensive Wistar-Kyoto (WKY) rats (n = 15) were studied for 8 months. Animals were allowed to drink tap water and fed a standard rat chow ad libitum. Systolic blood pressure (SBP) was measured monthly by the tail/cuff method. At the end of the experiment all the animals were sacrificed for microscopic studies. Cavernous tissue was processed by hematoxylin and eosin, Masson's trichrome, and monoclonal anti-alpha smooth muscle actin. Cavernous smooth muscle (CSM) and vascular smooth muscle (VSM) proliferation and CT fibrosis were evaluated by a semiquantitative score. SHR showed a higher proliferative score in CSM (2.7 +/- 0.28 v 1.1 +/- 0.07; P < .001), as well as in VSM (2.7 +/- 0.25 v 1 +/- 0.05; P < .001), and higher CT fibrosis score (2.8 +/- 0.28 v 0.1 +/- 0.07; P < .001), when compared to WKY rats. Furthermore, SHR showed a positive correlation between SBP and CSM proliferative score (r2 = 0.9277), SBP and VSM proliferative score (r2 = 0.8828), and SBP and CT fibrosis score (r2 = 0.7775). In addition, an increase in the surrounding connective tissue at the perineurium and endoneurium of the amielinic nerves in CT was observed in the SHR group. According to these results we conclude that SHR present morphologic changes in vessels as well as in cavernous spaces of the erectile tissue that have a high positive correlation with high blood pressure. Moreover, the increase in extracellular matrix expansion seems to affect not only the interstitium but also the neural structures of the penis.
Toblli
J E
JE
Laboratory of Experimental Medicine, Hospital Alemán, and Instituto de Investigaciones Cardiológicas, Buenos Aires, Argentina. jtoblli@hospitalaleman.com
Stella
I
I
Inserra
F
F
Ferder
L
L
Zeller
F
F
Mazza
O N
ON
D000199:Actins / Q000276:immunology / Q000378:metabolism; D000818:Animals; D000911:Antibodies, Monoclonal; D001794:Blood Pressure / Q000502:physiology; D002455:Cell Division; D005355:Fibrosis / Q000473:pathology; D006973:Hypertension / Q000150:complications / Q000473:pathology* / Q000503:physiopathology; D018783:Impotence, Vasculogenic / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D010413:Penis / Q000473:pathology*; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY
D000199:Actins; D000911:Antibodies, Monoclonal