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Biomedical subjects

D B Farley

Publications and source records attributed to D B Farley.

10 recordsLinked to original sources
PubMed1992

Evidence for declining extracellular calcium uptake and protein kinase C activity in uterine arterial smooth muscle during gestation in gilts.

Uterine arterial blood flow and uterine arterial diameter are known to increase dramatically and progressively throughout gestation. Previous data from our laboratory have demonstrated that the KCl-induced membrane depolarization of uterine arterial smooth muscle specifically induces Ca2+ uptake through the potentially sensitive channels (PSC). Evidence from other laboratories suggests that calcium uptake through the PSC mediates long-term changes in uterine arterial diameter and flow (tone), possibly through activation of protein kinase C (PKC). In study 1 we evaluated uterine arteries removed from gilts on Days 20, 50, 80, and 110 of gestation for their ability to take up extracellular Ca2+ and to contract in response to a depolarizing dose of KCl. The ability of KCl to induce contraction of uterine arteries as well as its ability to stimulate extracellular 45Ca2+ uptake by these same arteries declines (p less than 0.01) progressively from Day 20 through Day 110 of gestation. Estrogen concentrations in systemic blood were negatively correlated with the contractile response (r = -0.57; p less than 0.01) and extracellular 45Ca2+ uptake (r = -0.93; p less than 0.0001) of uterine arteries during gestation. In study 2 we evaluated changes in uterine arterial PKC and protein kinase M (PKM) throughout the estrous cycle and gestation. It was determined that cytosolic PKC declined with the advancement of gestation whereas PKM progressively increased (r = -0.63; p less than 0.01). These data suggest a decreasing ability of the uterine artery to take up extracellular Ca2+ through the PSC as gestation advances, in association with decreasing cytosolic PKC.

Animals↗
PubMed1992

Increase in uterine peroxidase activity in the rat uterus during oestrogen hyperaemia.

The administration of oestrogen results in increased arterial blood flow in all mammalian species studied to date, but its mechanism of action has not been elucidated. Because an interval of 30-60 min is observed between oestrogen injection and uterine hyperaemia, it has been suggested that a vasoactive intermediate is involved and recent evidence suggests that catechol oestrogens are the vasoactive oestrogen intermediates. Uterine peroxidase catalyses the conversion of oestrogens to their catechol forms and thus may play an important role in oestrogen-induced uterine hyperaemia. The present studies evaluated the time course and dose-response effects of oestrogen on uterine peroxidase activity and related these to changes in uterine blood volume, an index of uterine hyperaemia in immature rats. These data demonstrated that the minimal effective hyperaemic dose of oestradiol also increased (P less than 0.05) uterine peroxidase activity. The oestradiol-induced increase in uterine peroxidase activity preceded significant increases in uterine blood volume (1 h versus 2 h, respectively). These data are consistent with a role for peroxidase-mediated conversion of oestradiol to catechol oestradiol in facilitating uterine hyperaemia in rats.

Animals↗
PubMed1978

Phenylbutazone-induced decrease in renal blood flow.

Phenylbutazone (Butazolidin), and anti-inflammatory agent, has been reported to decrease renal excretion of sodium and water. Whether or not an alteration in renal hemodynamics could be involved in producing these effects was tested in anesthetized dogs. Renal blood flow (RBF) was monitored with electromagnetic flow probes. After i.v. administration of phenylbutazone, 2 mg/kg, RBF fell by 20%. Glomerular filtration rate, sodium and water excretion were also decreased and blood pressure increased slightly. The reduction of RBF and glomerular filtration rate by phenylbutazone indicates that a hemodynamic mechanism could be involved in the retention of sodium and water induced by this agent. The decreased blood flow was correlated with a depressed renal secretion of prostaglandin E. Also, in animals pretreated with indomethacin, another inhibitor of prostaglandin synthesis, administration of phenylbutazone did not result in any additional changes in renal hemodynamics or excretion of sodium and water. In addition, phenylbutazone antagonized the ability of furosemide to increase RBF, an inhibition which has previously been shown to occur with indomethacin. Thus, phenylbutazone appears to alter renal mechanisms in a manner similar to indomethacin.

Animals↗
PubMed1978

Plasma prostaglandins in pregnancy.

Plasma prostaglandins were determined by radioimmunoassay in 92 pregnant and 14 nonpregnant women. There was significant elevation of PGA-like material in the first trimester of pregnancy (1744 pg/ml) over that seen in nonpregnant women (576 pg/ml) with continuation of that elevation in the second and third trimesters. No significant difference existed among PGE levels of the nonpregnant group (251 pg/ml) and the first two trimesters of pregnancy (384 pg/ml and 294 pg/ml); the PGE level of the third trimester group (443 pg/ml) was significantly elevated over that of the nonpregnant group. PGF levels remained constant during all trimesters (135 pg/ml, 144 pg/ml, and 130 pg/ml) but exhibited plasma concentrations significantly higher than the nonpregnant group (78 pg/ml). Potential role (s) of prostaglandins as mediators of cardiovascular and renal changes of pregnancy are discussed.

Cardiovascular Physiological Phenomena↗
PubMed1977

Role of endogenous prostaglandins in regulation of uterine blood flow and adrenergic neurotransmission.

Earlier studies from these laboratories have demonstrated that prostaglandins (PG's) of the A and E series are potent uterine vasodilators whereas PGF's do not significantly alter uterine vascular resistance. In addition, PGE's and PGF's are also able to modify adrenergic vasoconstrictor responses in the canine uterus. In the present study the role of endogenous prostaglandins in regulating uterine vascular resistance and adrenergic neurotransmission was evaluated. Intra-arterial infusion of the prostaglandin synthesis inhibitor meclofenamate resulted in a significant reduction in PGE levels in uterine venous plasma and increased vascular resistance. Uterine vasoconstrictor responses produced by sympathetic nerve stimulation and norepinephrine were enhanced when endogenous PG synthesis was inhibited. During sympathetic nerve stimulation, uterine venous plasma levels of radioimmunoassayable prostaglandins of the E of F series did not change, suggesting that the adrenergic activation of PG synthesis is not detectable in uterine venous efferent. These data suggest that endogenous prostaglandins of the E series appear to play an important role in regulating uterine blood flow (I) by relaxing uterine vascular smooth muscle and (2) by depressing adrenergic vasoconstrictor responses.

Animals↗
PubMed1977

Radioimmunoassay of PGE and an approach to the specific measurement of PGE1.

A specific radioimmunoassay for prostaglandins of the E series is presented. Several refinements of the conventional procedures used for unknown sample preparation prior to assay are described. Validation of the method through recovery of labeled and unlabeled prostaglandin E from plasma indicates: 74% extraction efficiency, 80% chromatographic separation efficiency, and a 67% overall recovery figure for the complete assay. The development of an "absorbed system" approach for measuring one E prostaglandin (PGE1) without interference from the other E prostaglandin (PGE2) is also described. A preliminary study of rat tissue and male plasma samples measured by these assay systems is included. Alternate approaches to the development of a specific PGE1 assay, although less feasible in these authors' hands, are discussed.

Animals↗
PubMed1977

Plasma prostaglandins in the normal menstrual cycle.

Plasma prostaglandins were studied by radioimmunoassay on alternate days during the menstrual cycle in fourteen normal women. No cyclic patterns were found for A-like prostaglandins using an assay which measured 13,14-dihydro-PGA. Mean subject values of PGA-like prostaglandin ranged from 367 to 904 pg/ml and varied significantly among women. Prostaglandin E determinations showed an upward trend beginning 8 days before the LH peak. PGE subject means varied significantly and ranged from 182 to 362 pg/ml. Prostaglandin F did not exhibit a cyclic pattern. The average concentration of PGF for individual women ranged from 58 to 153 pg/ml, showing significant variance. The physiologic implications of the results are discussed as well as recommendations for the design of future studies.

Adult↗
PubMed1976

Ethacrynic acid induced release of prostaglandin E to increase renal blood flow.

Ethacrynic acid administered to anesthetized dogs was found to increase the level of prostaglandin E as determined by radioimmunoassay in renal venous blood at the time when renal blood flow was increased by this agent. No change was found in the renal venous level of prostaglandin F. When ethacrynic acid was administered after treatment with indomethacin, which blocks the increase in renal blood flow induced by the natriuretic agent, no increase in the renal venous level of prostaglandin E was seen. Thus, the dilation of the renal vasculature would appear to be caused by a stimulation of synthesis and release of prostaglandin E by ethacrynic acid.

Animals↗
PubMed1975

Furosemide induced release of prostaglandin E to increase renal blood flow.

Levels of PGE in renal venous blood were found to be significantly elevated at the time RBF was increased by furosemide. Following indomethacin, a second dose of furosemide failed to increase RBF and levels of PGE in renal venous blood were not elevated. Levels of PGF and PGA were not affected by furosemide. The increase of PGE in renal venous blood at the time of renal dilation supports the hypothesis that furosemide increases RBF by releasing PGE. An intrarenal action of the released PGE is implied by this mechanism.

Animals↗