Effect of Progesterone on Peripheral Blood Flow in Prepubertal Female Anesthetized Pigs

Molinari, Claudio; Battaglia, A; Grossini, Elena; Mary, D. A. S. G.; Surico, N; Vacca, Giovanni

doi:10.1159/000051093

Cited by 21 publications

(17 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In that regard, we observed two increasing phases of uterine blood flow: the first increasing phase (days 0 to 5) was accompanied by increasing concentrations of progesterone and increasing NOS mRNA expression; the second increasing phase (days 11 to estrus) was accompanied by increasing concentrations of estradiol and increasing NOS mRNA expression. Both estrogens and progesterone can cause systemic and uterine vascular relaxation and increased blood flow, which are mediated primarily by NO [16,30,35,36], as reported in sheep [16,19,30,37], pigs [36] and rats [12,35]. Also, we assume that both hormones can cause NO-mediated vasorelaxation in the uterine vascular bed during the estrus cycle in the mare; progesterone seems to stimulate uterine blood flow during early diestrus, and estradiol seems to stimulate it towards estrus.…”

Section: Regulation Of Uterine Blood Flow Cyclic Maressupporting

confidence: 61%

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Honnens¹,

Weisser²,

Welter

et al. 2011

J. Reprod. Dev.

View full text Add to dashboard Cite

Abstract. The objective of this study was to investigate the relationships between uterine perfusion and estrogen, progesterone and the uterine nitric oxide synthase (NOS) system in five trotter mares during the estrous cycle. Color Doppler sonography for measurement of uterine blood flow and collection of blood for determination of plasma estrogen and progesterone concentrations were performed on days 0 (= ovulation), 1, 5, 11 and 15 and daily during estrus (days -1 to -4) of one estrous cycle; endometrial biopsy collection for mRNA expression analysis of NOS and estrogen receptors was performed on days 0, 1, 5, 11, 15 and -3. Blood flow in each uterine artery was assessed by calculating the mean time-averaged maximum velocity (TAMV) and the pulsatility index (PI). Plasma concentrations of estrogen and progesterone were determined using specific enzyme immunoassays. The mRNA expressions of endothelial NOS (eNOS), inducible NOS (iNOS) as well as estrogen receptors α (ERα) and β (ERβ) were quantified using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. The TAMV and PI had a biphasic pattern during the estrous cycle (P<0.05), with maximum and minimum, respectively, values on days 5 and -4. Estrogen receptor mRNA concentrations increased significantly during days 15 (ERα) and -3 (ERβ). Transcript expression of eNOS, but not iNOS, had a biphasic pattern during the cycle (P<0.05) with maximum levels on days 5 and -3 and correlated positively with TAMV (r=0.81, P=0.05). We infer that the uterine NOS system, especially eNOS, plays an important role in the regulation of uterine blood flow during the estrous cycle in mares. Key words: Endometrial messenger RNA expression, Estrous cycle, Nitric oxide synthases, Steroid hormones, Uterine perfusion (J. Reprod. Dev. 57: [43][44][45][46][47][48] 2011) haracteristic uterine blood flow patterns have been reported during the estrous cycle in mares based on color Doppler sonography [1,2]. Uterine perfusion had a wave-shaped profile throughout the cycle, showing maximal blood flow during estrus and the early luteal phase [1][2][3][4]. Variations in uterine blood flow in cycling mares have been attributed to changes in circulating estrogen concentrations. However, due to a weak correlation between the resistance to uterine blood flow and plasma estrogen concentrations, other factors may also regulate uterine blood flow [2].Changes in uterine blood flow during the estrous cycle in many species are mediated mainly by estrogens [5]; although flow was enhanced by high plasma estradiol concentrations [6,7] and decreased during the luteal phase [8,9], the mechanisms involved have not been elucidated. Estrogens appear to act via two pathways: the genomic and non-genomic pathways [10]. Briefly, in the classical genomic pathway, estrogens bind to their nuclear receptors, subsequently regulating the transcription of target genes. For example, administration of estradiol increased estrogen receptors within 48 h in cyclic ewes [11]. Furthermore, a non-genomic pathway wit...

show abstract

Section: Regulation Of Uterine Blood Flow Cyclic Maressupporting

confidence: 61%

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Honnens¹,

Weisser²,

Welter

et al. 2011

J. Reprod. Dev.

View full text Add to dashboard Cite

show abstract

“…Because both estrogen (28) and progesterone (29) have been shown to relax renal arteries and increase renal blood flow in animal models, probably mediated by increased NO activity, we cannot implicate a direct genomic or nongenomic effect of either hormone in this phenomenon. Rather, both Hollenberg and colleagues (27) and Kang and colleagues (1) suggest RAS activation as a cause of these renal hemodynamic effects.…”

Section: Discussionmentioning

confidence: 94%

Effects of Oral Contraceptive Use on the Renal and Systemic Vascular Response to Angiotensin II Infusion

Ahmed¹,

Kang²,

Burns³

et al. 2004

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract.We have previously shown that users of oral contraceptive (OC) medications exhibit increased plasma levels of angiotensin II (Ang II) with only modest hemodynamic consequences, suggesting estrogen-mediated Ang II type 1 (AT 1 ) receptor downregulation. Accordingly, in 10 women who were OC users and 10 women who, as OC nonusers, served as controls, all mean age 26 Ϯ 1 yr, we examined the renal and peripheral hemodynamic response to graded Ang II infusion, plasma and urine cyclic guanosine monophosphate (cGMP) levels as a surrogate marker for AT 1 and/or AT 2 receptormediated activation of the nitric oxide pathway, and AT 1 receptor expression in skin biopsies. The OC nonusers were studied during the follicular and luteal phases of the menstrual cycle, whereas OC users were studied once during the 21-d medication phase. Subjects ingested a controlled sodium diet for 7 d before each study. Renal hemodynamic function was assessed using standard inulin and p-aminohippurate clearance techniques. AT 1 receptor mRNA levels in skin biopsy samples were assessed using a real-time PCR protocol. In response to graded Ang II infusion, OC users exhibited renal and peripheral hemodynamic responses that were augmented compared with those of OC nonusers, in conjunction with evidence of increased tissue AT 1 receptor expression. Plasma cGMP levels and 24-h urinary cGMP excretion did not differ. These data suggest that, contrary to our original hypothesis, OC use does not appear to be associated with AT 1 receptor downregulation. The factor protecting OC users from the hemodynamic impact of increased Ang II levels remains elusive.Gender and estrogen status are important determinants of renin angiotensin system (RAS) function and the renal and systemic response to angiotensin II (Ang II) (1-3). This laboratory has previously shown that ethinyl estradiol use in the form of the oral contraceptive (OC) pill results in dramatic increases of circulating RAS components, including Ang II; yet, in normal women, the hemodynamic consequences are modest, consisting of a small increase in BP and filtration fraction (1). Ang II, the primary effector of the RAS, is a multifunctional peptide hormone, the actions of which are primarily mediated by two receptors, Ang II type 1 (AT 1 ) and type 2 (AT 2 ). The majority of the physiological and pathophysiological effects of Ang II occur via the AT 1 receptor. The function of the AT 2 receptor is controversial, but it may act in opposition to AT 1 receptors (4). It has been reported in some (5-8) but not all (1-3) studies that high estrogen decreases circulating renin and Ang II levels, downregulates AT 1 receptor expression in vascular smooth muscle cells, adrenal cortex, and hypothalamus (9 -11), and upregulates renal AT 2 receptor expression (4). It has also been demonstrated that the hemodynamic response to Ang II infusion is blunted in high-estrogen states, such as the luteal phase of the normal menstrual cycle (3), and in normal pregnancy (12)(13)(14). Therefore, we hypothesized that wome...

show abstract

“…The dose of 1 mg kg –1 of phentolamine has been shown in the same experimental model to abolish the reflex coronary vasoconstriction caused by distension of the gallbladder [27] and the reflex renal and iliac vasoconstriction caused by distension of the stomach [28] and has previously been used to block coronary, renal and iliac α-adrenergic receptors [see, for example, ref. [21, 22,29,30,31]. Similar doses of the blocking agents have been used in anesthetized pigs by other authors [32].…”

Section: Discussionmentioning

confidence: 98%

Human Placental Lactogen Decreases Regional Blood Flow in Anesthetized Pigs

Grossini

Molinari²,

Battaglia³

et al. 2006

J Vasc Res

Self Cite

View full text Add to dashboard Cite

In 22 pigs anesthetized with sodium pentobarbitone, changes in blood flow caused by infusion of human placental lactogen into the left renal, external iliac, and anterior descending coronary arteries were assessed using electromagnetic flowmeters. In 17 pigs, infusion of human placental lactogen whilst keeping the heart rate and arterial pressure constant decreased coronary, renal and iliac flow. In 5 additional pigs, increasing the dose of human placental lactogen produced a dose-related decrease in regional blood flow. The mechanisms of the above response were studied in 15 of the 17 pigs by repeating the experiment of infusion. The human placental lactogen-induced decrease in regional blood flow was not affected by blockade of cholinergic receptors (5 pigs) or of α-adrenergic receptors (5 pigs), but it was abolished by blockade of β₂-adrenergic receptors (5 pigs). The present study showed that intra-arterial infusion of human placental lactogen primarily decreased coronary, renal and iliac blood flow. The mechanism of this response was shown to be due to the inhibition of a vasodilatory β₂-adrenergic receptor-mediated effect.

show abstract

Effect of Progesterone on Peripheral Blood Flow in Prepubertal Female Anesthetized Pigs

Cited by 21 publications

References 15 publications

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Relationships Between Uterine Blood Flow, Peripheral Sex Steroids, Expression of Endometrial Estrogen Receptors and Nitric Oxide Synthases During the Estrous Cycle in Mares

Effects of Oral Contraceptive Use on the Renal and Systemic Vascular Response to Angiotensin II Infusion

Human Placental Lactogen Decreases Regional Blood Flow in Anesthetized Pigs

Contact Info

Product

Resources

About