Journal
INTERNATIONAL JOURNAL OF IMPOTENCE RESEARCH
Volume 15, Issue 5, Pages 355-361Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.ijir.3901038
Keywords
nitric oxide; L-NAME; guanylate cyclase; arginase; female genital arousal; oximetry; laser Doppler flowmetry
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Funding
- NIDDK NIH HHS [K01-DK02696, R01-DK 56846] Funding Source: Medline
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The regulatory role of nitric oxide (NO) in vaginal perfusion remains unclear. We used specific inhibitors of enzymes in the NO-cyclic GMP (NO-cGMP) pathway and investigated their effects on vaginal blood flow in the rabbit. NO synthase (NOS) activity was similar in both the proximal and distal rabbit vagina; whereas, arginase activity was 3.4-fold higher in the distal vagina. Intravenous administration of the NOS inhibitor L-NAME resulted in a 66% reduction in genital tissue oxyhemoglobin and a 53% reduction in vaginal blood flow. This attenuation occurred despite a 20-30% increase in systemic arterial pressure. The arginase inhibitor ABH caused a 2.1-fold increase in genital tissue oxyhemoglobin and 34% increase in vaginal blood flow. The guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one and the phosphodiesterase type 5 inhibitor sildenafil caused in a 37% reduction and a 44% increase in vaginal blood flow, respectively. These observations suggest that the NO-cGMP pathway is an important regulator of vaginal hemodynamics.
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