Contraction and endothelium-dependent relaxation in mesenteric microvessels from pregnant rats

Pascoal, I.; Lindheimer, M. D.; Nalbantian-Brandt, C.; Umans, Jason G.

doi:10.1152/ajpheart.1995.269.6.h1899

Cited by 25 publications

(28 citation statements)

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“…We observed no differences in SNP-induced relaxation, which agrees with previous studies showing no changes in the sensitivity to NO donors between arteries from pregnant and nonpregnant rats. 9,10 Our results are consistent with other reports describing that EDHF may be increased in vascular segments during pregnancy. 8 -10 Because ACh-induced maximum relaxation was greater in KCl-constricted arteries from the pregnant rats, it seems that enhanced synthesis/efficacy of EDHF per se does not explain the increased ACh vasodilation and that NO or other factors may also play a role in this response.…”

Section: Discussionsupporting

confidence: 92%

Increased Acetylcholine-Induced Vasodilation in Pregnant Rats

et al. 1999

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Abstract-We have tested the hypothesis that increased gap junctional communication contributes to the augmented endothelium-dependent vasodilation in pregnancy. Contractile force and connexin43 expression were measured in aortic rings from nonpregnant and pregnant rats. Norepinephrine-constricted aortas from pregnant rats were more sensitive to acetylcholine, but not to sodium nitroprusside, compared with those from nonpregnant rats. Vessels from pregnant rats, constricted either with 45 mmol/L KCl or with norepinephrineϩ10 Ϫ4 mol/L N G -monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide synthase, also exhibited greater relaxation to acetylcholine. Heptanol, an uncoupler of gap junctional communication, inhibited acetylcholine responses in norepinephrine-constricted aortas from nonpregnant rats but greatly impaired acetylcholine relaxation in aortas from pregnant rats. Heptanol also inhibited in both groups acetylcholine responses in vessels constricted with KCl, only minimally affected acetylcholine relaxation in arteries constricted with norepinephrineϩL-NMMA, and did not change sodium nitroprusside-induced relaxation. Tetraethylammonium chloride induced greater contractions in control aortas compared with aortas from pregnant rats. Increased connexin43 mRNA levels were found in the uterus and in the mesenteric, uterine, and thoracic aortic arteries, but not in the heart and brain, from pregnant rats. These results suggest that increased gap junctional communication, possibly due to increased gap junction protein expression, may facilitate the effects of endothelium-derived relaxing factors, contributing to the augmented endothelium-dependent relaxation in arteries from pregnant rats. Key Words: preeclampsia Ⅲ rats Ⅲ gap junctions Ⅲ nitric oxide Ⅲ endothelium-derived factor P regnancy is associated with a decrease in systemic vascular resistance, which maintains or reduces maternal blood pressure despite the increase in plasma volume and cardiac output. 1 Pregnancy in women and in other mammals, such as the rat, is also characterized by a blunted pressor response 2,3 and decreased vascular reactivity 4,5 to a series of vasoconstrictors. The mechanism(s) responsible for these cardiovascular changes in pregnancy is not fully understood but has been under intense investigation, particularly because its malfunction may have a role in preeclampsia. 6 Because blunted constrictor responses in arteries from pregnant animals are observed in vitro 4,5 and no changes in receptor number or affinity seem to occur, 2,7 it has been suggested that a general mechanism, occurring within the blood vessel wall, is involved. Enhanced endothelium-dependent vasodilation, which may contribute to the attenuated vasoconstriction during pregnancy, has been systematically shown in vessels from pregnant animals, including the uterine, mesenteric, thoracic, and abdominal aortic arteries. 8 -11 Nitric oxide (NO), but not prostaglandins, is considered to contribute substantially to the increased endothelium-dependent relaxation in...

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Section: Discussionsupporting

confidence: 92%

Increased Acetylcholine-Induced Vasodilation in Pregnant Rats

et al. 1999

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“…In the rat, NO is likely to play a major role [18,19] ; for example, the increased sensitivity of the mesenteric arteries to ACh in pregnancy is due to changes in the vascular responses to both NO [15,20,21] and EDHF [15]. The importance of NO in the physiological mechanisms securing the cardiovascular adaptations to pregnancy in rats has been emphasized by a study showing that inhibition of NO causes a dose-dependent reduction in the normal increase in plasma volume [22].…”

Section: Discussionmentioning

confidence: 99%

Low-protein diet impairs vascular relaxation in virgin and pregnant rats

et al. 2002

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Pregnancy is associated with increases in maternal cardiac output and plasma volume and a reduction in peripheral vascular resistance. Cardiac output and plasma volume are substantially reduced in pregnant rats fed a low-protein diet, but it is not known whether vascular function is also compromised. We have investigated vascular function in virgin and pregnant Wistar rats subjected to dietary protein restriction [9% (w/v) casein, compared with 18% (w/v) casein for controls]. The diets were fed to the groups for 18 days; in the pregnant rats, the diets were given from day 1 of pregnancy. Branches of the mesenteric arteries were studied on day 18 of the dietary period using myography. Significant reductions in sensitivity to acetylcholine occurred in vessels from virgin (P=0.04) and pregnant (P=0.01) rats that had consumed the 9% casein diet. In arteries from the virgin rats on the restricted diet there was also a significant reduction in sensitivity (P=0.0003) and maximum relaxation (P=0.009) to the NO donor spermine NONOate. Mean placental and fetal weights were significantly lower in the rats fed on 9% casein (P<0.0001 and P=0.005 respectively). Thus low-protein diets impair vasodilator responses in female rats. These effects may contribute to the poor cardiovascular adaptation to pregnancy and lower fetal weights associated with restricted protein intake.

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“…Pregnancy is a physiological state where vasodilation is necessary to accommodate a 40-50% increase in blood volume required to meet the oxygen and nutritional requirements of the growing uterus and developing fetuses (18,43). This is accompanied by an attenuated responsiveness of maternal vessels to pressor agents (17,29,30,39,40,45) and an enhanced response to vasodilators (28,31). The mechanisms underlying these vascular changes are not clearly understood.…”

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confidence: 99%

Oxytocin does not directly affect vascular tone in vessels from nonpregnant and pregnant rats

Miller

Davidge

Mitchell

2002

American Journal of Physiology-Heart and Circulatory Physiology

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Recent evidence suggests oxytocin (OT) may regulate vascular tone. OT and its receptor (OTR) have been identified in the rat heart and great vessels. Expression of OT and OTR is increased in some tissues during pregnancy. We hypothesized that the OT/OTR system may be a physiological regulator of vascular tone and mediate the decreased vascular resistance noted during pregnancy. Using a wire myograph system, we measured changes in vascular tone in response to OT in small mesenteric arteries, uterine arcuate arteries, and thoracic aorta from nonpregnant and pregnant rats. Additionally, we used reverse transcriptase-polymerase chain reaction (RT-PCR) to measure mRNA for OTR in these vascular tissues. Although OTR mRNA was identified by RT-PCR, OT did not elicit a vasodilatory effect in any of the vessels studied. High concentrations of OT (>10−8 M) caused vasoconstriction that was eliminated by a specific vasopressin V1a receptor antagonist. Although it may have an indirect effect in regulation of peripheral resistance, we conclude that OT is unlikely to play a direct role in the physiological regulation of vascular tone.

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Contraction and endothelium-dependent relaxation in mesenteric microvessels from pregnant rats

Cited by 25 publications

References 0 publications

Increased Acetylcholine-Induced Vasodilation in Pregnant Rats

Increased Acetylcholine-Induced Vasodilation in Pregnant Rats

Low-protein diet impairs vascular relaxation in virgin and pregnant rats

Oxytocin does not directly affect vascular tone in vessels from nonpregnant and pregnant rats

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