Role of nitric oxide and cyclooxygenase products in controlling vascular tone in uterine microvessels of rats

Abstract

The importance of nitric oxide (NO) and dilator prostaglandins in uterine resistance arterioles was investigated. In pentobarbital anaesthetized rats at dioestrus-2, the uterine microcirculation in vivo was transilluminated by a fibreoptic probe and microvessels (circumferential arterioles) viewed by video microscopy. Arteriolar diameters were measured while increasing concentrations of acetylcholine (ACh), serotonin (5-HT), phenylephrine (PE), or angiotensin II (AII) were applied topically (suffused) over the uterus. Agonists were applied alone or with ibuprofen (IBU; cyclooxygenase inhibitor), N\g=w\-nitro-L-arginine (L-NA; nitric oxide synthase inhibitor) or both. Circumferential arterioles were dilated by ACh and 5-HT (10\m=-\8\p=n-\10\m=-\4mol l \ m=-\ 1) and constricted by PE (10\ m=-\ 8\ p=n-\ 10\ m=-\ 5 mol l \m=-\1) and AII (10\ m=-\ 11\ p=n-\ 10\ m=-\ 7 mol l \ m=-\ 1).

Therapeutic efficacy of early photobiomodulation therapy on the zones of stasis in burns: An experimental rat model study

“…To further explore how photobiomodulation therapy improved blood flow in the zone of stasis, we evaluated the ability of the photobiomodulation therapy photochemical reaction to promote the production and secretion of NO, which inhibits necrosis by relaxing microvessels and protecting vascular endothelial cells to improve blood flow. We found that the NO levels were significantly higher in the zones of stasis of wounds subjected to photobiomodulation therapy after 96 hours, which was accompanied by significant reductions in the expression of TM, a marker of vascular endothelial cell necrosis.…”

Uterine microvascular sensitivity to nanomaterial inhalation: An in vivo assessment

“…Uterine vascular anatomy of interest at this level includes arteriolar-venular pairing (Saha et al, 1998), which allows for significant vascular crosstalk, matching of capillary blood in-flow and out-flow, and exchange of vasoactive factors (Hester and Hammer, 2002). These communications are frequently targeted during pathology.…”

“…Analysis of individual spiral arterioles is notoriously difficult, due to their tortuous anatomy, spacing, and possible ischemia-reperfusion (Gannon et al, 1997). Due to these unique anatomical differences within the endometrial vasculature, general vascular agonist delivery (dissolved in the superfusate) (Leonard et al, 2013; Sweeney et al, 1999, 2007; Saha et al, 1998), may not lead to a distinct evaluation of specific local mechanisms, but rather, complex reactivity in tandem or conducted in series. Whereas, iontophoresis locally applies agonists more discretely to assess microvascular reactivity within the immediate environment, with all systemic controls intact (Hungerford et al, 2000).…”

Interaction of Endothelial Nitric Oxide and Angiotensin in the Circulation

“…In anesthetized rats, suffusion of ACh over the uterus dilated circumferential arterioles, the effect being inhibited by L-NA or ibuprofen alone and abolished by L-NA with ibuprofen; ANG II-induced vasoconstriction was enhanced by ibuprofen or L-NA and further enhanced by their combination, suggesting that ACh can release either NO or cyclooxygenase products to cause uterine arteriolar dilatation and that constrictor responses evoked by ANG II are attenuated by both NO and vasodilator PG release (Saha et al, 1998). Lambers et al (2000) found that in nonpregnant, estrogenized ewes, ANG II injected into the uterine artery produced decreases in uterine blood flow, which were potentiated by PD123319; uterine vasodilatation noted under treatment with the AT 1 antagonist L-158809 was reversed by the AT 2 antagonist or by L-NAME.…”