Increase of ovarian progesterone secretion by β2-adrenergic stimulation in oestrous rats

1982 ◽  
Vol 101 (2) ◽  
pp. 268-272 ◽  
Author(s):  
Béla Zsolnai ◽  
Bertalan Varga ◽  
Edit Horváth
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Adrenergic Receptors ◽  
Hormone Secretion ◽  
Regulatory Role ◽  
Blood Levels ◽  
Ovarian Hormone ◽  
Adrenergic Stimulation ◽  
Venous Outflow ◽  
Progesterone Secretion

Abstract. Oestrous rats were anaesthetized with pentobarbital and one of the femoral arteries, femoral veins and utero-ovarian veins were cannulated. Five min blood fractions were collected from the ovary for 50 min. Following two control fractions fenoterol, noradrenaline, isoproterenol (0.5 μg/min) or 0.9% NaCl (0.02 ml/min) were infused iv for 40 min. In a group of oestrous animals fenoterol was given locally to the ovarian bursa. Blood pressure and the ovarian venous outflow were continuously recorded and blood levels of progesterone (P) and oestradiol-17β (E2) were determined by RIA. Fenoterol administered iv increased P secretion without altering ovarian blood flow, whereas noradrenaline and isoproterenol had no effect on P secretion. Fenoterol administered locally stimulated both P and E2 secretion, and this was prevented by iv infusion of propranolol. It is suggested that ovarian β2-adrenergic receptors have a regulatory role in ovarian hormone secretion.

The effect of ovarian arterial infusion of transforming growth factor α on ovarian follicle populations and ovarian hormone secretion in ewes with an autotransplanted ovary

1994 ◽  
Vol 143 (1) ◽  
pp. 13-24 ◽  
Author(s):  
B K Campbell ◽  
B M Gordon ◽  
R J Scaramuzzi
Keyword(s):  
Growth Factor ◽  
Luteal Phase ◽  
Transforming Growth Factor ◽  
Hormone Secretion ◽  
Follicular Phase ◽  
Ovarian Hormone ◽  
Arterial Infusion ◽  
Transforming Growth Factor Α ◽  
Progesterone Secretion ◽  
Factor Α

Abstract Transforming growth factor α (TGFα) inhibits hormone production by cultured follicular cells but evidence of an effect of TGFα on ovarian hormone secretion in vivo is still required. Eleven ewes with an autotransplanted ovary received, by ovarian arterial infusion, either 5 μg/h recombinant rat TGFα (n=6) or placebo (n=5) for 12 h on day 10 of the luteal phase. Two hours before the start and 1 hour before the end of the infusion each ewe received a single injection of gonadotrophin-releasing hormone (GnRH; 150 ng i.v.). Two hours after the end of the infusion luteal regression was induced with prostaglandin F2α (PGF2α; 125 μg i.m.). Ovarian and jugular venous blood samples were taken at 10-min, 15-min or 4-h intervals from 2 h before the start of the infusion until 96 h after PGF2α and the rates of secretion of ovarian oestradiol, inhibin, progesterone and androstenedione were determined. Jugular venous concentrations of LH and FSH were also measured and follicle populations monitored by real-time ultrasound scanning. Infusion of TGFα resulted in a significant (P<0.05) depression in the amplitude of the pulsatile response of oestradiol and androstenedione secretion to the GnRH-induced LH pulse at the end of the infusion. Ovarian inhibin secretion was acutely suppressed by TGFα infusion (P<0·001) and remained lower than controls for the period of the experiment. Luteal phase progesterone secretion was also acutely inhibited (P<0·001) by infusion of TGFα and in one treated ewe progesterone secretion was elevated 48–84 h after PGF2α. Jugular venous concentrations of FSH in TGFα-treated ewes were significantly (P<0·001) elevated over controls during the first 48 h of the follicular phase and the LH surge was delayed for about 10 h (P<0·05). Infusion of TGFα caused a marked decline (P<0·05) in the number of large follicles within 12 h of the end of the infusion. Two of the six treated ewes, including the one with high follicular phase progesterone, had unusually large (8·7 and 10 mm) follicles present from 48–96 h after PGF2α. We conclude that direct arterial infusion of TGFα results in acute inhibition of ovarian steroid and inhibin secretion that is associated with induction of atresia in the population of large follicles. The lack of feedback of ovarian hormones results in a rebound increase of FSH which stimulates the growth of more ovarian follicles and the eventual re-establishment of ovarian hormone secretion and normal cyclicity. Journal of Endocrinology (1994) 143, 13–24

PROGESTERONE SECRETION AND OVARIAN BLOOD FLOW IN THE PREGNANT RAT

1980 ◽  
Vol 85 (2) ◽  
pp. 327-330 ◽  
Author(s):  
N. W. BRUCE ◽  
G. T. MEYER ◽  
S. B. DIMMITT
Keyword(s):  
Blood Flow ◽  
Correlation Coefficient ◽  
Degrees Of Freedom ◽  
Venous Outflow ◽  
Pregnant Rat ◽  
Progesterone Secretion

A venous outflow technique was used to monitor the rates of ovarian blood flow and progesterone secretion simultaneously during periods of 2–3 h in nine rats pregnant for 16 days and anaesthetized with sodium pentobarbitone. The rate of ovarian blood flow was 0·460 ± 0·135 (s.d.) ml/min and that of progesterone secretion was 27·2 ± 7·0 μg/h per ovary. Within rats, progesterone secretion was unrelated to the rate of ovarian blood flow (common correlation coefficient, r = 0·136; degrees of freedom = 61; P, not significant) but the latter was inversely related to the arterio-venous difference in the concentration of progesterone (r = −0·731; P <0·01).

Effects of various sympathicomimetic drugs on renal hemodynamics in normotensive and hypotensive dogs

1960 ◽  
Vol 198 (6) ◽  
pp. 1279-1283 ◽  
Author(s):  
Lewis C. Mills ◽  
John H. Moyer ◽  
Carrol A. Handley
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Adrenergic Receptors ◽  
Filtration Rate ◽  
Renal Hemodynamics ◽  
Marked Activity ◽  
Renal Vascular

The effects of l-epinephrine, l-norepinephrine, phenylephrine, methoxamine, metaraminol and mephentermine on renal hemodynamics were studied in six groups of dogs. Although comparable rises in blood pressure were obtained, there were marked differences in the effects on renal hemodynamics. While infusion of mephentermine led to only slight reductions in glomerular filtration rate and renal blood flow, and only a slight increase in renal vascular resistance, methoxamine produced a marked fall in flow and a marked increase in resistance. The other agents tested had effects which were intermediate between these two. The effects of these same drugs on renal hemodynamics were also compared in dogs made hypotensive by bleeding. While blood pressure increased significantly in all groups, glomerular filtration rate and renal blood flow increased significantly only during infusion of mephentermine, metaraminol and phenylephrine. Since assays relative to the inherent vasodilator properties of these agents revealed epinephrine to be the only agent with marked activity, it seems unlikely that the observed effects were due to this factor. It is concluded that the observed changes were due to a greater reactivity of renal vascular vasoconstrictor adrenergic receptors with certain sympathicomimetic drugs than those of the vasculature in general.

scholarly journals Captopril-induced fall in glomerular filtration rate in cyclosporine-treated hypertensive patients.

1993 ◽  
Vol 3 (9) ◽  
pp. 1570-1574
Author(s):  
J J Curtis ◽  
D A Laskow ◽  
P A Jones ◽  
B A Julian ◽  
R S Gaston ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Renal Transplant ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Blood Levels ◽  
Hypertensive Patients ◽  
Transplant Patients ◽  
Renal Transplant Patients

It was found that two known renal vasodilators had different effects on RBF and GFR in the setting of therapeutic blood levels of cyclosporine in hypertensive renal transplant patients. Captopril lowered blood pressure in these patients but also lowered blood flow and GFR. Nifedipine lowered blood pressure to the same degree but without lowering either RBF or GFR.

scholarly journals Blood Pressure and Vascular Dysfunction Underlie Elevated Cerebral Blood Flow in Systemic Lupus Erythematosus

2012 ◽  
Vol 39 (4) ◽  
pp. 752-758 ◽  
Author(s):  
CHARLES GASPAROVIC ◽  
CLIFFORD QUALLS ◽  
ERNEST R. GREENE ◽  
WILMER L. SIBBITT ◽  
CARLOS A. ROLDAN
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Lupus Erythematosus ◽  
Control Group ◽  
Blood Levels ◽  
Dynamic Susceptibility ◽  
Systemic Lupus ◽  
Arterial Blood

Objective.In previous studies cerebral blood flow (CBF) was found to be altered in patients with systemic lupus erythematosus (SLE) compared to controls. We investigated the relationships between CBF and clinical data from subjects with SLE with the aim of determining the pathologic factors underlying altered CBF in SLE.Methods.A total of 42 SLE subjects and 19 age- and sex-matched healthy control subjects were studied. Dynamic susceptibility contrast (DSC) magnetic resonance imaging (MRI) was used to measure CBF. Patients and controls underwent complete clinical and laboratory evaluations in close proximity with their MRI studies.Results.A higher CBF was present in the SLE group and was independently associated in statistical models with higher systolic blood pressure (SBP; p < 0.01). The intensity of the relationships (slope of curve) between CBF and mean arterial blood pressure, diastolic blood pressure, or blood levels of tissue plasminogen activator in the SLE group was significantly blunted relative to the control group.Conclusion.These findings are consistent with an underlying cerebral hyperperfusion in SLE induced by elevated but nonhypertensive levels of SBP. The factors underlying this relationship may be functional and/or structural (atherosclerotic, thrombotic, thromboembolic, or vasculitic) cerebrovascular disease.

Baroreceptors, α1-adrenergic receptors, and regulation of mesenteric blood flow

1999 ◽  
Vol 78 (1) ◽  
pp. 54-57
Author(s):  
Isam Abu-Amarah ◽  
William A Cupples
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Adrenergic Receptors ◽  
Separate Experiment ◽  
Adrenergic Blockade ◽  
Arterial Baroreflex ◽  
Mesenteric Blood Flow ◽  
Dynamic Regulation ◽  
Mesenteric Circulation ◽  
Flow Transfer

In the mesenteric circulation of the rat a myogenic autoregulatory system operates at 0.1-0.15 Hz. Negative admittance phase in the region above 0.2 Hz suggested operation of an arterial baroreflex. The present study was designed to test this interpretation and to identify the neurotransmitter involved. In rats anesthetized with isoflurane, blood pressure and mesenteric blood flow (transit time ultrasound) were measured with central mechanisms intact, after sinoaortic denervation, and after denervation of the mesenteric bed. Sinoaortic denervation abrogated the negative phase in the band from 0.3 to 0.6 Hz and increased admittance gain in this region. Subsequent mesenteric denervation had no further effect on the pressure-flow transfer function. In a separate experiment, α1-adrenergic blockade reduced, but did not remove, the negative admittance phase in the 0.2- to 0.5-Hz band without altering admittance gain. It is concluded that the baroreflex acting on the mesenteric circulation can be identified by admittance phase, but that admittance gain is uninformative. Part of the response is mediated by α1-adrenergic transmission.Key words: mesenteric, α1-adrenergic receptors, dynamic regulation.

scholarly journals Moderate hyperbilirubinemia improves renal hemodynamics in ANG II-dependent hypertension

2010 ◽  
Vol 299 (4) ◽  
pp. R1044-R1049 ◽  
Author(s):  
Trinity Vera ◽  
David E. Stec
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Blood Pressure ◽  
Blood Flow ◽  
Antisense Oligonucleotides ◽  
Filtration Rate ◽  
Renal Hemodynamics ◽  
Blood Levels ◽  
Ang Ii ◽  
Osmotic Minipump

We have previously demonstrated that moderate hyperbilirubinemia decreases blood pressure in ANG II-dependent hypertension through mechanisms that decrease oxidative stress and increase nitric oxide levels. Since decreases in renal hemodynamics play an important role in mediating the hypertensive actions of ANG II, the goal of the present study was to examine the effect of moderate hyperbilirubinemia on glomerular filtration rate (GFR) and renal blood flow (RBF) in a mouse model of ANG II hypertension. Mice were made moderately hyperbilirubinemic by two methods: indinavir or specific morpholino antisense oligonucleotides against UGT1A1, which is the enzyme responsible for the conjugation of bilirubin in the liver. GFR and RBF were measured in mice after implantation of an osmotic minipump delivering ANG II at a rate of 1 μg·kg−1·min−1. GFR was measured by continuous infusion of I125-labeled iothalamate on days 5 and 6 of ANG II infusion in conscious mice. RBF was measured on day 7 of ANG II infusion in anesthetized mice. Blood levels of unconjugated bilirubin were significantly increased in mice treated with indinavir or anti-UGT1A1 ( P = 0.002). ANG II decreased GFR by 33% of control ( n = 9, P = 0.004), and this was normalized by moderate hyperbilirubinemia ( n = 6). Next, we examined the effect of moderate hyperbilirubinemia on RBF in ANG II-infused mice. ANG II infusion significantly decreased RBF by 22% ( P = 0.037) of control, and this decrease was normalized by moderate hyperbilirubinemia ( n = 6). These results indicate that improvement of renal hemodynamics may be one mechanism by which moderate hyperbilirubinemia lowers blood pressure in this model.

Catecholamines, Renin, Aldosterone and Arterial Pressure in Patients on Chronic Hemodialysis Treatment

1983 ◽  
Vol 6 (5) ◽  
pp. 255-260 ◽  
Author(s):  
D. Ratge ◽  
R. Augustin ◽  
H Wisser
Keyword(s):  
Blood Pressure ◽  
Plasma Catecholamines ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Chronic Hemodialysis ◽  
Blood Levels ◽  
Adrenergic Stimulation ◽  
Dialysis Patients ◽  
Arterial Blood

To assess the interaction between adrenergic activity and blood pressure regulation, plasma catecholamines (CA), plasma renin activity (PRA) and plasma aldosteron (PA) were measured in 66 normal subjects and 18 dialysis patients. Prior to dialysis, blood levels of free norepinephrine (NE), epinephrine (E) and PRA were normal, but total (free and conjugated) CA as well as PA were significantly elevated. There was a spectrum of response during hemodialysis. On an average mean arterial blood pressure (MAP) fell during the first two hours of treatment, concomitantly followed by an increase in mean NE level. Whereas PRA and PA were highest at the end of treatment, mean free NE returned promptly to predialysis values through the late dialysis period. Severe hypotensive episodes during dialysis were associated with a baroreceptor-mediated adrenergic stimulation. These results indicate a qualitatively normal reaction of dialysis patients to volume removal and the importance of the renin-angiotensin-system in maintaining blood pressure during dialysis.

Cerebral blood flow during hemorrhagic hypotension in the unanesthetized goat

1977 ◽  
Vol 232 (4) ◽  
pp. H368-H372
Author(s):  
B. Gomez ◽  
A. R. Vallejo ◽  
E. Alborch ◽  
G. Dieguez ◽  
S. Lluch
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Adrenergic Receptors ◽  
Blood Samples ◽  
Alpha Adrenergic Receptors ◽  
Arterial Blood ◽  
Flow Changes ◽  
Parallel Fashion

Changes in cerebral blood flow (CBF), arterial blood pressure (AP), and cardiac output (CO) were studied during stepwise blood losses in 12 unanesthetized goats. Bleeding was followed by a drop in CBF, AP and CO in a nearly parallel fashion. Control values (means +/- SE) for CBF, AP, and CO were 117 +/- 5.6 ml/min per 100 g, 105 +/- 3.1 mmHg, and 2,825 +/- 124 ml/min, respectively; and after bleeding, 66 +/- 3.9 ml/min per 100 g, 57 mmHg, and 1, 383 ml/min. Arterial blood samples obtained before bleeding, during the hypotensive state, and after reinfusion did not show any significant differences in pH, PCO2, and PO2 values. In phentolamine-treated animals, bleeding produced a drop in AP and CO similar to that observed in the nontreated animals; however, the decrease in CBF was less marked. These findings show that CBF follows pari passu the fall in AP, and they indicate that the alpha-adrenergic receptors of the cerebral vessels are involved in the cerebral blood flow changes in hemorrhage.

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