The influence of estrogen and progesterone on parasympathetic vasodilatation in the rat submandibular gland

Abstract

SUMMARYPrevious 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 17β-estradiol alone or a combination of 17β-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 + 17β-estradiol and OVX + 17β-estradiol + progesterone rats were indistinguishable from those observed in SHAM animals. Indomethacin had no effect on vasodilatation in SHAM and OVX + 17β-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 treatment, indomethatin caused a reduction in vasodilatation and L-NAME further diminished the remaining responses. Under these 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.

Endothelial and neuronal nitric oxide synthases variably modulate the oestrogen‐mediated control of blood pressure and cardiovascular autonomic control

“…In the latter study, selective NOS inhibition implicated nNOS, but not eNOS or iNOS, in the NO‐evoked increases in BP and renal sympathetic activity . In addition to its central role, peripheral NOS plays a fundamental role in cardiovascular and autonomic control, as well as in the E2‐dependent biological effects …”

“…15 Nitric oxide plays a contributory role in the E2-evoked parasympathetically mediated vasodilatation in the submandibular glands of female rats. 16 In OVX rats, the reduced NO release from the skeletal muscle, caused by E2 deficiency, contributes to augmented sympathetically mediated vasoconstriction during muscle contraction. 17 Apart from its interaction with E2, NO derived from the myocardial phosphatidylinositol 3-kinase/Akt/endothelial (e) NOS and inducible (i) NOS pathway also facilitates the increased cardiac parasympathetic dominance and hypotension caused by ethanol in female rats.…”

Gender differences in the effects of streptozotocin-induced diabetes on parasympathetic vasodilatation in the rat submandibular gland

“…Further, both NO-dependent and NO-independent mechanisms play a role in endothelial regulation of vascular tone in the submandibular gland9. Previous studies demonstrate that submandibular vascular responses to parasympathetic stimulation are gender-dependent and that both estrogen and progesterone influence the relative contributions of specific endothelium-derived vasodilators8,12. Nitric oxide, PGI 2 and EDHF all contribute to the parasympathetic vascular responses in the rat submandibular gland, but NO and EDHF are the predominant endothelium-derived vasodilators irrespective of gender8.…”

“…Under those conditions the remaining vasodilatory responses, presumed to be EDHF-dependent , were significantly lower in males than in females. Furthermore, in females the loss of estrogen (ovariectomy) diminishes submandibular vascular responses to parasympathetic stimulation, and all three pathways are affected12.…”

Histological effect of ovariectomy and estrogen replacement on parotid gland of adult albino rat

“…Estrogen regulates the balance between endothelial dependent vasoconstrictor and vasodilator influences, possibly via estrogen-specific actions on nitric oxide and prostaglandin (PG2)-dependent pathways. This leads to vasodiltataion of blood vessels and edema [28]. Edema manifested by cellular infilteration within thickened CT septa and blood vessels congestion [27].…”