RESUMEN
Blood flow to the ovary varies dramatically in both magnitude and distribution throughout the estrous cycle to meet the hormonal and metabolic demands of the ovarian parenchyma as it cyclically develops and regresses. Several vascular components appear to be critical to vascular regulation of the ovary. As a first step in resolving the role of the resistance arteries and their paired veins in regulating ovarian blood flow and transvascular exchange, we characterized the architecture and intravascular pressure profile of the utero-ovarian resistance artery network in an in vivo preparation of the ovary of the anesthetized Golden hamster. We also investigated estrous cycle-dependent changes in resistance artery tone. The right ovary and the cranial aspect of the uterus in 26 female hamsters were exposed for microcirculatory observations. Estrous-cycle phase was determined in each animal before experimentation. The utero-ovarian vascular architecture was determined and resistance artery diameters were measured in each animal by video microscopy. Servo-null intravascular pressure measurements were made throughout the uteroovarian arterial network in 11 of the animals. Architectural data showed a complex anastomotic network jointly supplying the uterus and ovary. Resistance arteries showed a high degree of coiling and close apposition to veins, maximizing countercurrent-exchange capabilities. Arterial pressure dropped below 60% of systemic arterial pressure before the arteries entered the ovary. Both the ovarian artery and the uterine artery, which jointly feed the ovary, showed cycle day-dependent changes in diameter. Arterial diameters were smallest on the day following ovulation, during the brief luteal phase of the hamster. The data show that resistance arteries comprise a critical part of a complex network designed for intimate local communication and control and suggest that these arteries may play an important role in regulating ovarian blood flow in an estrous cycle-specific manner.
Asunto(s)
Presión Sanguínea/fisiología , Ciclo Estral/fisiología , Microcirculación/citología , Microcirculación/fisiología , Ovario/irrigación sanguínea , Útero/irrigación sanguínea , Vasoconstricción/fisiología , Animales , Cricetinae , Femenino , Mesocricetus , Tono Muscular , Ovario/citología , Útero/citología , Resistencia Vascular/fisiologíaRESUMEN
The transmembrane receptor-like protein tyrosine phosphatase-mu (RPTPmu) is thought to play an important role in cell-cell adhesion-mediated processes. We recently showed that RPTPmu is predominantly expressed in the endothelium of arteries and not in veins. Its involvement in the regulation of endothelial adherens junctions and its specific arterial expression suggest that RPTPmu plays a role in controlling arterial endothelial cell function and vascular tone. To test this hypothesis, we analyzed myogenic responsiveness, flow-induced dilation, and functional integrity of mesenteric resistance arteries from RPTPmu-deficient (RPTPmu(-/-)) mice and from wild-type littermates. Here, we show that cannulated mesenteric arteries from RPTPmu(-/-) mice display significantly decreased flow-induced dilation. In contrast, mechanical properties, myogenic responsiveness, responsiveness to the vasoconstrictors phenylephrine or U-46619, and responsiveness to the endothelium-dependent vasodilators methacholine or bradykinin were similar in both groups. Our results imply that RPTPmu is involved in the mechanotransduction or accessory signaling pathways that control shear stress responses in mesenteric resistance arteries.
Asunto(s)
Mecanotransducción Celular/fisiología , Arterias Mesentéricas/fisiología , Proteínas Tirosina Fosfatasas/genética , Vasodilatación/fisiología , Animales , Presión Sanguínea , Expresión Génica , Frecuencia Cardíaca , Operón Lac , Masculino , Ratones , Ratones Transgénicos , Proteínas Tirosina Fosfatasas Clase 2 Similares a Receptores , Vasoconstricción/fisiologíaRESUMEN
Coronary blood vessels are compressed by the contracting myocardium. This leads to oscillations in flow in especially the subendocardium. We examined the effects of steady and oscillating flow on isolated, cannulated subendocardial and subepicardial porcine arterioles. Steady flow-induced dilation in both vessel types, up to 12.9+/-0.8% of the passive diameter in subendocardials and 9.6+/-1.4% in subepicardials at 40 dyne/cm2. Dilation was completely abolished after treatment with 10 micromol/L L-NNA. Sinusoidal modulation of steady flow at 1.5 Hz and 50% to 200% amplitude did not affect dilation. Oscillating flow without a net forward component with peak-peak shear values up to 100 dyne/cm2 caused no dilation at all in these vessels. However, in the presence of 100 U/mL superoxide dismutase (SOD), oscillating flow induced dilation up to 19.5+/-2.3% in subendocardial vessels and 11.5+/-4.3% in subepicardials. LNNA (10 micromol/L) blocked this dilation by approximately 50%. SOD did not affect the magnitude of steady flow-induced dilation, but the response time after onset of steady flow shortened from 23.4+/-1.5 to 14.3+/-2.1 seconds. Diphenyleneiodinium, an inhibitor of NAD(P)H oxidase, uncovered dilation to oscillating flow in subendocardial vessels up to 9.5+/-1.6%. Flow causes production of both NO and O2-. During steady flow, the bioavailability of NO is sufficient to cause vasodilation. During oscillating flow, NO is quenched by the O2-, suppressing vasodilation. Considering the pulsatile nature of subendocardial flow and the vulnerability of this layer, pharmacological manipulation of the balance between NO and O2- may improve subendocardial perfusion.