Intravascular pressure and diameter profile of the utero-ovarian resistance artery network: estrous cycle-dependent modulation of resistance artery tone

2007 ◽  
Vol 293 (5) ◽  
pp. H2937-H2944 ◽  
Author(s):  
Terrence E. Sweeney ◽  
Pooneh Bagher ◽  
Jocelyn Bailey ◽  
Salvatore J. Cherra ◽  
Frank N. Grisafi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Estrous Cycle ◽  
Cycle Phase ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Vascular Regulation ◽  
Cycle Dependent ◽  
Intravascular Pressure

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.

Enhanced resistance artery sensitivity to agonists under isobaric compared with isometric conditions

1994 ◽  
Vol 266 (1) ◽  
pp. H147-H155 ◽  
Author(s):  
W. R. Dunn ◽  
G. C. Wellman ◽  
J. A. Bevan
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Myogenic Tone ◽  
Isometric Contractions ◽  
Fundamental Interaction ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Enhanced Resistance ◽  
Increased Sensitivity

We have compared the responsiveness of rabbit mesenteric resistance arteries with agonists under isometric and isobaric conditions. When pressurized (60 mmHg), arteries spontaneously reduced their diameter by 18.1%. An equivalent isometric stress did not generate force in a “wire” myograph. Subsequently, much higher concentrations of norepinephrine (NE) and histamine were required to cause isometric contractions than were needed to reduce vascular diameter of pressurized vessels, whereas angiotensin II produced a maintained response only in pressurized arteries. Reducing transmural pressure to 20 mmHg abolished pressure-induced myogenic tone and decreased arterial sensitivity to NE. Under isometric conditions, partial depolarization with KCl increased sensitivity to NE and histamine to within the concentration range effective in pressurized vessels and also "revealed" responses to angiotensin II. The membrane potential of the vascular smooth muscle cells under partially depolarized conditions was similar to that found in vivo and in vessels studied isobarically. These observations demonstrate a fundamental interaction between pressure-induced myogenic tone and the sensitivity of resistance arteries to vasoactive stimuli. This influence was mimicked in isometrically mounted vessels by partial depolarization, indicating a possible pivotal role for membrane potential in determining the reactivity of the resistance vasculature.

Site of recruitment in the pulmonary microcirculation

1989 ◽  
Vol 66 (5) ◽  
pp. 2079-2083 ◽  
Author(s):  
W. L. Hanson ◽  
J. D. Emhardt ◽  
J. P. Bartek ◽  
L. P. Latham ◽  
L. L. Checkley ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Total Surface Area ◽  
Capillary Recruitment ◽  
Fluid Load ◽  
Pulmonary Arterial ◽  
Pulmonary Microcirculation ◽  
Adequate Oxygenation ◽  
Made In

Increasing the total surface area of the pulmonary blood-gas interface by capillary recruitment is an important factor in maintaining adequate oxygenation when metabolic demands increase. Capillaries are known to be recruited during conditions that raise pulmonary blood flow and pressure. To determine whether pulmonary arterioles and venules are part of the recruitment process, we made in vivo microscopic observations of the subpleural microcirculation (all vessels less than 100 microns) in the upper lung where blood flow is low (zone 2). To evoke recruitment, pulmonary arterial pressure was elevated either by an intravascular fluid load or by airway hypoxia. Of 209 arteriolar segments compared during low and high pulmonary arterial pressures, none recruited or derecruited. Elevated arterial pressure, however, did increase the number of perfused capillary segments by 96% with hypoxia and 165% with fluid load. Recruitment was essentially absent in venules (4 cases of recruitment in 289 segments as pressure was raised). These data support the concept that recruitment in the pulmonary circulation is exclusively a capillary event.

Role of estrogens and age in flow-mediated outward remodeling of rat mesenteric resistance arteries

2014 ◽  
Vol 307 (4) ◽  
pp. H504-H514 ◽  
Author(s):  
K. Tarhouni ◽  
M. L. Freidja ◽  
A. L. Guihot ◽  
E. Vessieres ◽  
L. Grimaud ◽  
...  
Keyword(s):  
Blood Flow ◽  
Female Rats ◽  
Male Rats ◽  
Resistance Arteries ◽  
Cross Sectional ◽  
Male And Female ◽  
Male And Female Rats ◽  
Arterial Contractility

In resistance arteries, a chronic increase in blood flow induces hypertrophic outward remodeling. This flow-mediated remodeling (FMR) is absent in male rats aged 10 mo and more. As FMR depends on estrogens in 3-mo-old female rats, we hypothesized that it might be preserved in 12-mo-old female rats. Blood flow was increased in vivo in mesenteric resistance arteries after ligation of the side arteries in 3- and 12-mo-old male and female rats. After 2 wk, high-flow (HF) and normal-flow (NF) arteries were isolated for in vitro analysis. Arterial diameter and cross-sectional area increased in HF arteries compared with NF arteries in 3-mo-old male and female rats. In 12-mo-old rats, diameter increased only in female rats. Endothelial nitric oxide synthase expression and endothelium-mediated relaxation were higher in HF arteries than in NF arteries in all groups. ERK1/2 phosphorylation, NADPH oxidase subunit expression levels, and arterial contractility to KCl and to phenylephrine were greater in HF vessels than in NF vessels in 12-mo-old male rats only. Ovariectomy in 12-mo-old female rats induced a similar pattern with an increased contractility without diameter increase in HF arteries. Treatment of 12-mo-old male rats and ovariectomized female rats with hydralazine, the antioxidant tempol, or the angiotensin II type 1 receptor blocker candesartan restored HF remodeling and normalized arterial contractility in HF vessels. Thus, we found that FMR of resistance arteries remains efficient in 12-mo-old female rats compared with age-matched male rats. A balance between estrogens and vascular contractility might preserve FMR in mature female rats.

Effect of Propofol on Norepinephrine-induced Increases in [Ca2+](i) and Force in Smooth Muscle of the Rabbit Mesenteric Resistance Artery 

1998 ◽  
Vol 88 (6) ◽  
pp. 1566-1578 ◽  
Author(s):  
Nami Imura ◽  
Yoshihisa Shiraishi ◽  
Hirotada Katsuya ◽  
Takeo Itoh
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
High K ◽  
Small Resistance ◽  
Vasodilating Activity ◽  
Mesenteric Resistance Artery

Background Propofol (2,6-diisopropylphenol) possesses vasodilating activity in vivo and in vitro. The propofol-induced relaxation of agonist-induced contractions in small resistance arteries has not been clarified. Methods The effect of propofol was examined on the contractions induced by norepinephrine and high K+ in endothelium-denuded rabbit mesenteric resistance artery in vitro. The effects of propofol on the [Ca2+]i mobilization induced by norepinephrine and high K+ were studied by simultaneous measurement of [Ca2+]i using Fura 2 and isometric force in ryanodine-treated strips. Results Propofol attenuated the contractions induced by high K+ and norepinephrine, the effect being greater on the high K+-induced contraction than on the norepinephrine-induced contraction. In Ca2+-free solution, norepinephrine produced a transient contraction resulting from the release of Ca2+ from storage sites that propofol attenuated. In ryanodine-treated strips, propofol increased the resting [Ca2+]i but attenuated the increases in [Ca2+]i and force induced by both high K+ and norepinephrine. In the presence of nicardipine, propofol had no inhibitory action on the residual norepinephrine-induced [Ca2+]i increase, whereas it still modestly increased resting [Ca2+]i, as in the absence of nicardipine. Conclusions In smooth muscle of the rabbit mesenteric resistance artery, propofol attenuates norepinephrine-induced contractions due to an inhibition both of Ca2+ release and of Ca2+ influx through L-type Ca2+ channels. Propofol also increased resting [Ca2+]i, possibly as a result of an inhibition of [Ca2+]i removal mechanisms. These results may explain in part the variety of actions seen with propofol in various types of vascular smooth muscle.

scholarly journals Myogenic Tone in Peripheral Resistance Arteries and Arterioles: The Pressure Is On!

2021 ◽  
Vol 12 ◽  
Author(s):  
William F. Jackson
Keyword(s):  
Blood Flow ◽  
Smooth Muscle ◽  
Steady State ◽  
Vascular Smooth Muscle ◽  
Signaling Pathways ◽  
Vascular Resistance ◽  
Myogenic Tone ◽  
Resistance Artery ◽  
Resistance Arteries ◽  
Fluid Exchange

Resistance arteries and downstream arterioles in the peripheral microcirculation contribute substantially to peripheral vascular resistance, control of blood pressure, the distribution of blood flow to and within tissues, capillary pressure, and microvascular fluid exchange. A hall-mark feature of these vessels is myogenic tone. This pressure-induced, steady-state level of vascular smooth muscle activity maintains arteriolar and resistance artery internal diameter at 50–80% of their maximum passive diameter providing these vessels with the ability to dilate, reducing vascular resistance, and increasing blood flow, or constrict to produce the opposite effect. Despite the central importance of resistance artery and arteriolar myogenic tone in cardiovascular physiology and pathophysiology, our understanding of signaling pathways underlying this key microvascular property remains incomplete. This brief review will present our current understanding of the multiple mechanisms that appear to underlie myogenic tone, including the roles played by G-protein-coupled receptors, a variety of ion channels, and several kinases that have been linked to pressure-induced, steady-state activity of vascular smooth muscle cells (VSMCs) in the wall of resistance arteries and arterioles. Emphasis will be placed on the portions of the signaling pathways underlying myogenic tone for which there is lack of consensus in the literature and areas where our understanding is clearly incomplete.

Feasibility of transabdominal Doppler ultrasonography for studying ovarian blood flow characteristics in cycling gilts

2019 ◽  
Vol 47 (02) ◽  
pp. 77-85 ◽  
Author(s):  
Rosa Stark ◽  
Catherine Herlt ◽  
Haukur L. Sigmarsson ◽  
Johannes Kauffold
Keyword(s):  
Blood Flow ◽  
Estrous Cycle ◽  
Doppler Ultrasonography ◽  
Ovarian Tissue ◽  
Color Doppler ◽  
Flow Characteristics ◽  
Color Doppler Ultrasonography ◽  
Seasonal Effects ◽  
Ovary Function ◽  
Cycle Dependent

Abstract Objective The aim of this study was to assess ovarian blood flow characteristics by applying transabdominal color Doppler ultrasonography during the course of the estrous cycle in gilts. Materials and methods Estrus and ovulation were synchronized in 15 pubertal gilts. During their consecutive spontaneous estrous cycle the gilts were sonographically scanned daily and ovarian blood flow was determined by imaging perfused areas of the ovarian hilus and the ovarian tissue. Recorded video clips were then analyzed for the parameters perfused area (Amix), blood flow velocity (vmix) as well as resistance (RIvmix) and pulsatility index (PIvmix) using the software PixelFlux®. Results All blood flow parameters showed an estrous cycle dependent course, with Amix and vmix being highest in diestrus, followed by proestrus, while RIvmix and PIvmix patterns were inversely proportional. Conclusion and clinical relevance Transabdominal color Doppler ultrasonography proved feasible to study ovarian perfusion characteristics in pubertal gilts. The ovarian blood flow was dependent on the stage of estrous cycle and highest in diestrus. The results of this study encourage the use of color Doppler ultrasonography to also investigate reasons of ovary-caused infertility including corpus luteum insufficiency or seasonal effects on ovary function.

scholarly journals Estrous cycle-dependent modulation of in vivo microvascular dysfunction after nanomaterial inhalation

2018 ◽  
Vol 78 ◽  
pp. 20-28 ◽  
Author(s):  
P.A. Stapleton ◽  
C.R. McBride ◽  
J. Yi ◽  
A.B. Abukabda ◽  
T.R. Nurkiewicz
Keyword(s):  
Estrous Cycle ◽  
Microvascular Dysfunction ◽  
Cycle Dependent

Acute and chronic head-down tail suspension diminishes cerebral perfusion in rats

2002 ◽  
Vol 282 (1) ◽  
pp. H328-H334 ◽  
Author(s):  
M. Keith Wilkerson ◽  
Patrick N. Colleran ◽  
Michael D. Delp
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Brain Regions ◽  
Brain Blood Flow ◽  
Tail Suspension ◽  
Resistance Arteries ◽  
Total Brain ◽  
Regional Blood Flows

10.1152/ajpheart.00727.2001.—The purpose of this study was to test the hypothesis that regional brain blood flow and vascular resistance are altered by acute and chronic head-down tail suspension (HDT). Regional cerebral blood flow, arterial pressure, heart rate, and vascular resistance were measured in a group of control rats during normal standing and following 10 min of HDT and in two other groups of rats after 7 and 28 days of HDT. Heart rate was not different among conditions, whereas mean arterial pressure was elevated at 10 min of HDT relative to the other conditions. Total brain blood flow was reduced from that during standing by 48, 24, and 27% following 10 min and 7 and 28 days of HDT, respectively. Regional blood flows to all cerebral tissues and the eyes were reduced with 10 min of HDT and remained lower in the eye, olfactory bulbs, left and right cerebrum, thalamic region, and the midbrain with 7 and 28 days of HDT. Total brain vascular resistance was 116, 44, and 38% greater following 10 min and 7 and 28 days of HDT, respectively, relative to that during control standing. Vascular resistance was elevated in all cerebral regions with 10 min of HDT and remained higher than control levels in most brain regions. These results demonstrate that HDT results in chronic elevations in total and regional cerebral vascular resistance, and this may be the underlying stimulus for the HDT-induced smooth muscle hypertrophy of cerebral resistance arteries.

Receptor-activating peptides distinguish thrombin receptor (PAR-1) and protease activated receptor 2 (PAR-2) mediated hemodynamic responses in vivo

1998 ◽  
Vol 76 (1) ◽  
pp. 16-25 ◽  
Author(s):  
Wai-man Cheung ◽  
Patricia Andrade-Gordon ◽  
Claudia K Derian ◽  
Bruce P Damiano
Keyword(s):  
Arterial Pressure ◽  
Thrombin Receptor ◽  
Cellular Functions ◽  
Hemodynamic Responses ◽  
Induced Hypotension ◽  
Vascular Regulation ◽  
Rebound Hypertension ◽  
Prolonged Hypotension ◽  
Protease Activated Receptor 2

Vascular expression and cellular functions of the thrombin receptor (PAR-1) and protease activated receptor 2 (PAR-2) suggest similar but distinct vascular regulatory roles. The vascular actions of PAR-1 and PAR-2 in vivo were differentiated by monitoring mean arterial pressure (MAP) and heart rate (HR) of anesthetized mice in response to intravenous SFLLRN (0.1, 0.3, and 1 µmol/kg) and SLIGRL (0.1, 0.3, and 1 µmol/kg), the respective receptor-activating sequences for PAR-1 and PAR-2, and TFLLRNPNDK (0.3, 1, and 3 µmol/kg), a synthetic peptide selective for PAR-1. All peptides dose dependently decreased MAP (order of potency: SLIGRL >> SFLLRN >> TFLLRNPNDK). SLIGRL induced a more prolonged hypotension with a slow return to baseline, whereas SFLLRN- and TFLLRNPNDK-induced hypotension was followed by a rapid return towards baseline and a sustained moderate hypotension. SFLLRN and TFLLRNPNDK, but not SLIGRL, decreased HR. N omega -Nitro-L-arginine methyl ester HCl (L-NAME), an inhibitor of nitric oxide synthesis, attenuated the cumulative hypotensive response to SLIGRL but had no effect on the SFLLRN and TFLLRNPNDK hypotension. However, L-NAME revealed a rebound hypertension in response to SFLLRN and TFLLRNPNDK but not SLIGRL. In conclusion, activation of either PAR-1 or PAR-2 in vivo results in hypotension. In addition, only PAR-1 activation induced hypertension following L-NAME, reflecting concurrent PAR-1-mediated vasoconstriction. Thus, these different hemodynamic responses in vivo suggest distinct physiological or pathophysiological roles for PAR-1 and PAR-2 in local vascular regulation. Key words: protease activated receptor, thrombin receptor, protease activated receptor 2 (PAR-2), arterial pressure.

Diameter and blood flow of skeletal muscle venules during local flow regulation

1986 ◽  
Vol 250 (5) ◽  
pp. H828-H837 ◽  
Author(s):  
S. D. House ◽  
P. C. Johnson
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Blood Viscosity ◽  
Vessel Diameter ◽  
Sartorius Muscle ◽  
Viscosity Data ◽  
Pressure Reduction ◽  
Local Flow

Whole organ studies suggest that venous resistance increases as blood flow falls and decreases when blood flow increases. In experiments on skeletal muscle we tested the hypotheses that these resistance changes may be due to changes in venous diameter, changes in the number of venules with blood flow, and/or changes in the shear rate of blood in venules. The hypotheses were tested by measuring diameter and red cell velocity in cat sartorius muscle venules (7–200 microns diam) during arterial pressure reduction and muscle contraction. There was no observable change in venular diameter and an insignificant change in the number of venules with blood flow during these perturbations. There was a significant decrease in the normalized velocity (bulk velocity/vessel diameter) of blood from a mean of 13 s-1 under control conditions to 5 s-1 during arterial pressure reduction to 20 mmHg. Combining these blood velocity data with published in vivo viscosity data, it is deduced that apparent blood viscosity in venules would increase 100% when blood flow was reduced 60%. During postcontraction hyperemia the normalized velocity of blood in venules increased from 16 to 38 s-1, suggesting that apparent blood viscosity in venules would fall 54%.

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