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pubmed:abstractText |
Previous studies suggest that NO- and PGI(2)-independent pathways play a greater role in parasympathetic vasodilatation in the submandibular glands (SMG) of female than of male rats. Thus, the purpose of this study was to determine whether estrogen and progesterone influence the relative contributions of NO and PGI(2) to parasympathetic vasodilatation in the SMG. Vascular responses to chorda-lingual nerve stimulation were examined in sham-operated (SHAM) and ovariectomized (OVX) female rats and in OVX rats treated with either 17beta-estradiol alone or a combination of 17beta-estradiol and progesterone. Compared with SHAM animals, increases in vascular conductance in OVX rats were reduced at 1, 2 and 5 Hz (p<0.05). Blood flow responses in OVX+17beta-estradiol and OVX+17beta-estradiol+progesterone rats were indistinguishable from those observed in SHAM animals. Indomethacin had no effect on vasodilatation in SHAM and OVX+17beta-estradiol rats, but increased vascular responses in OVX animals (p<0.02). The addition of L-NAME resulted in a significant reduction in vasodilatation at all frequencies. In OVX rats treated with both estrogen and progesterone, indomethacin caused a reduction in vasodilatation and L-NAME further diminished the remaining responses. Under all conditions, vasodilatation was due largely, if not exclusively, to direct parasympathetic rather than antidromic sensory nerve activation. Finally, both neuronally-derived and endothelium-derived NO appeared to be responsible for the NO-dependent vasodilatation, but endothelium-derived NO became increasingly important as the frequency of stimulation increased. We conclude that estrogen and progesterone influence parasympathetic vasodilatation through combined effects on NO-, PGI(2)- and non-NO/PGI(2)-mediated pathways.
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