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Biomedical subjects

J Quilley

Publications and source records attributed to J Quilley.

48 records · Page 3Linked to original sources
PubMed1986

Hypotensive effects of eicosapentaenoic acid (EPA) and its influence on eicosanoid metabolism in spontaneously hypertensive rats.

Oral administration of pure eicosapentaenoic acid (EPA) ethyl ester caused a reversible hypotensive effect in spontaneously hypertensive rats. Treatment with EPA also lowered the platelet response to ADP and inhibited the conversion of leucotrienes (LTs) A4 and LTB4 and other sulphidopeptide leucotrienes. Therefore, diet supplemented with EPA may lower blood pressure in hypertensive rats and affect cardiovascular functions which may be mediated through eicosanoid metabolism.

Animals↗
PubMed1986

Influence of insulin on urinary eicosanoid excretion in rats with experimental diabetes mellitus.

Urinary prostaglandin (PG) and thromboxane (Tx) excretion, measured by radioimmunoassay, were examined in two groups of male Wistar rats made diabetic with streptozotocin, 70 mg/kg, one of which received daily insulin beginning on the 7th day after administration of streptozotocin. In addition, urinary kallikrein excretion and blood pressure were monitored. After the induction of diabetes the profile of urinary eicosanoid excretion was altered. 6-keto-PGF1 alpha and TxB2 excretion increased markedly within 24 to 48 hr and remained elevated for the duration of the study, up to 58 days. PGF2 alpha excretion also increased, the change being apparent after 6 days whereas PGE2 excretion was reduced at this time. Urinary kallikrein excretion was unchanged but blood pressure became elevated above control levels 2 weeks after the induction of diabetes. Insulin treatment, to maintain mean blood glucose levels below 200 mg/dl, resulted in decreased excretion of TxB2, PGF2 alpha and 6-keto-PGF1 alpha. However, excretion of PGE2 and kallikrein were increased after insulin treatment which also prevented the elevation in blood pressure. These studies indicate that insulin treatment of experimental diabetes corrects alterations in renal arachidonic acid metabolism and prevents the associated increase in blood pressure.

Animals↗
PubMed1985

Arachidonic acid metabolism and urinary excretion of prostaglandins and thromboxane in rats with experimental diabetes mellitus.

Urinary prostaglandins (PGs) and thromboxane excretion, measured by radioimmunoassay, were examined in male Wistar rats made diabetic with streptozotocin, 70 mg/kg. In addition, immunoreactive (i) 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) production by aortic rings was studied as well as conversion of [14C] arachidonic acid (AA) by aortic rings, polymorphonuclear leukocytes, and macrophages isolated from diabetic and age-matched control rats. The profile of urinary eicosanoid excretion changed after induction of diabetes. iPGF2 alpha excretion transiently increased, reaching a peak at 7 days and declining to control values by 48 days. iPGE2 excretion declined with time after induction of diabetes while marked increases in i thromboxane B2 and i6-keto-PGF1 alpha excretion occurred within 48 h and were maintained for the duration of the study, up to 176 days. However, serum i thromboxane B2 levels were similar in control and diabetic rats. Formation of i6-keto-PGF1 alpha by aortic rings obtained from diabetic rats was approximately one-half that of aortic rings from control rats. Similarly, conversion of [14C]AA revealed a diminished capacity of aortic rings from diabetic rats to synthesize prostacyclin (PGI2) measured as 6-keto-PGF1 alpha. Conversion of [14C]AA by polymorphonuclear leukocytes and macrophages obtained from diabetic rats did not differ from those obtained from control rats. In conclusion, experimental diabetes mellitus is accompanied by temporal alterations in AA metabolism, the functional significance of which is unknown at this time.

Animals↗
PubMed1982

Captopril decreases vascular reactivity independently of changes in converting enzyme activity and prostaglandin release in the rat isolated kidney.

The relationship of the vascular effect of captopril to angiotensin converting enzyme activity and prostaglandin-dependent mechanism was studied in rat isolated kidneys, perfused with Krebs-Henseleit at 20 ml/min per 2 kidneys, with basal perfusion pressures of 78 +/- 1 mm Hg (Mean +/- S.E.M.). Two doses of captopril were used; both low (0.05 microgram/ml) and high doses (5 microgram/ml) inhibited maximally the vasoconstrictor responses to 100 and 200 ng of angiotensin I. Captopril at the low dose did not affect the renal vasoconstrictor responses to norepinephrine (NE) (25-400 ng), whereas high-dose reduced the vasoconstriction to all doses of NE. Treatment with captopril tended to diminish dose-related release of prostaglandins in response to NE. Indomethacin (1 microgram/ml) prevented NE-induced release of bioassayable and radioimmunoassayable prostaglandins but did not affect the ability of captopril to reduce NE-induced vasoconstriction. High-dose captopril also decreased the vascular reactivity to angiotensin II (5 ng) and lysine vasopressin (10 mU); however, the renal vasoconstriction caused by PGE2 (80 ng) was unaffected by captopril. We conclude that high-dose captopril decreased vascular reactivity by a mechanism independent of converting enzyme inhibition and unrelated to a prostaglandin-dependent vascular mechanism.

Animals↗
PubMed1980

Prostaglandins, kinins and the regulation of blood pressure.

Prostaglandins participate in the regulation of vascular reactivity and blood pressure by opposing the vasoconstrictor and antinatriuretic actions of pressor hormones, and by moderating the release of norepinephrine from vasoconstrictor nerves. Blood vessels synthesize prostaglandins intramurally, where their local release influences vascular reactivity. PGI2, unlike PGE2, may be a circulating hormone and may influence vascular resistance of organs remote from its site of synthesis. Prostaglandins not only attenuate the effects of vasoconstrictor hormones but also amplify the effects of the kallikrein-kinin system intrarenally and within the vasculature.

Angiotensins↗
PubMed1979

Immunological features of juvenile onset diabetic patients correlated to HLA type.

Ninety-six juvenile onset type diabetics showed an increase in the frequency of HLA B8 and B15 and a decrease in frequency of HLA B7 antigens. Sixty-four maturity onset diabetics showed no disturbance in the frequency of these antigens. Fifty-four of the juvenile onset type diabetics, with an average duration of disease of 3.2 years were tested for the presence of islet cell antibodies (ICAs). Thirty-two per cent were positive, the incidence decreasing from 70% in those patients tested within 1 year of diagnosis to zero in those patients tested within 1 year of diagnosis to zero in those patients tested more than 5 years after diagnosis. No correlation was found between the incidence of ICAs and either cell-mediated immune reactions or HLA type. B15 positive patients were associated with cell-mediated immune reactions to pancreatic antigens and with the presence of other tissue autoantibodies. HLA phenotypes were not associated with environmental data. Diabetic siblings had identical HLA A-B haplotypes more often than could be expected to occur by chance.

Adolescent↗
PubMedDate not supplied

Studies on the frequency and associations of islet-cell antibodies in juvenile diabetes mellitus.

Ninety-six juvenile onset type diabetics showed an increase in the frequency of HLA B8 and B15 and a decrease in frequency of HLA B7 antigens. Sixty-four maturity onset diabetics showed no disturbance in the frequency of these antigens. Fifty-four of the juvenile onset type diabetics, with an average duration of disease of 3.2 years were tested for the presence of islet cell antibodies (ICAs). Thirty-two percent were positive, the frequency decreasing from 70% in those patients tested within one year of diagnosis to 0.5% in those patients tested more than 5 years after diagnosis. No correlation was found between HLA type and the frequency of ICAs, but there was an increase in other autoantibodies in B15 positive patients. Preliminary absorption studies suggest a cross reactivity of ICAs and Coxsackie B4 virus.

Adolescent↗
PubMedDate not supplied

An investigation into cytotoxic mechanisms in type I diabetes mellitus.

T- and K-cell cytotoxic activity has been measured in groups of type I diabetic patients and comparable groups of healthy control subjects. The mean cytotoxic indices for T-cell activity were 0.72 for 13 type I diabetics and -2.38 for a control group. These values are not significantly different. K-cell cytotoxic activity was measured using both chicken red blood cells and Chang liver cells coated with appropriate xenogenic antibodies. Using the chicken red blood cell system the percentage specific chromium release was 55.3 for 17 type I diabetics and 50.0 for a control group. These values are not significantly different. Using the chicken red blood cell system the percentage specific chromium release was 55.3 for 17 type I diabetics and 50.0 for a control group. These values are not significantly different. Using the Chang liver cell system the percentage specific chromium release was 13.9 for 37 type I diabetics and 9.7 for a control group. This difference is statistically significant (p less than 0.05).

Antibody-Dependent Cell Cytotoxicity↗
PubMedDate not supplied

Endothelial mechanism in the vascular action of hydralazine.

Relaxation of precontracted isolated chains of aortic rings with intact endothelium and in those with the endothelium removed was studied in response to various antihypertensive vasodilator drugs. Of the drugs tested--nitroprusside, nitroglycerin, prazosin, minoxidil, diazoxide and hydralazine--only the vascular relaxant effects of hydralazine were found to be dependent, in part, on the presence of intact endothelium. The endothelial component of the hydralazine response represented a major contribution to the net relaxant effect on the vascular smooth muscle, particularly at lower concentrations, 90 nM to 1 microM, which are also clinically relevant.

Acetylcholine↗
PubMedDate not supplied

Apamin/charybdotoxin-sensitive endothelial K+ channels contribute to acetylcholine-induced, NO-dependent vasorelaxation of rat aorta.

BACKGROUND: Activation of endothelial K+ channels and the subsequent increase in intracellular Ca2+, may be an important step in the release of relaxant factors in response to endothelium-dependent vasodilator agents. However, the type of K+ channel involved in hyperpolarization of the endothelium and the subsequent release of relaxing factors remains to be defined. MATERIAL AND METHODS: Rat aortic rings precontracted with U46619 were used to address the effects of inhibitors of K+ channels on the vasorelaxant response to acetylcholine (Ach). As responses to Ach were mediated solely by endothelium-derived NO and responses to NO derived from nitroprusside were unaffected by inhibition K+ channels, any effect of K+ channel inhibitors could be attributed to actions on endothelial K+ channels to modify NO release. RESULTS: Tetraethylammonium (TEA) and elevated K+ attenuated the relaxant effect of Ach, indicating a role for K+ channels in NO release. The Ca2+-activated K+ channel inhibitors, apamin, charybdotoxin and iberiotoxin as well as glibenclamide and BaCl2, inhibitors of ATP-sensitive K+ channels and inwardly rectifying K+ channels, respectively, did not affect the response to Ach. However, a combination of apamin and charybdotoxin, but not apamin and iberiotoxin, attenuated the vasorelaxant response to Ach. CONCLUSIONS: The results of this study indicate that NO release in response to Ach involves activation of an endothelial K+ channel that is inhibited by a combination of apamin and charybdotoxin.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMedDate not supplied

The position of NO among endogenous vasodilators.

Bradykinin stimulates phospholipases to release arachidonic acid (AA) which can be metabolized by cyclooxygenase, lipoxygenase and cytochrome P450 (P450) to yield vasoactive products that may contribute to the effect of the peptide. In the rat kidney, pharmacological evidence suggests that a substantial component of the vasodilator response is dependent on P450-AA metabolism. In the heart, the vasodilator response to bradykinin is independent of NO and prostaglandins but reduced by inhibitors of P450, including 17-ODYA, an inhibitor of fatty acid metabolism, also suggesting a role of P450-AA. Moreover, the renal and coronary vasodilator responses to bradykinin are associated with release of P450-AA products measured by gas chromatography-mass spectrometry (GC-MS). The coronary vasodilator response to bradykinin is also dependent on activation of K+ channels linking P450-AA and hyperpolarization. Formation of vasodilator eicosanoids derived via the P450 pathway may make important contributions to the control of vascular tone, local blood flow and, thereby, blood pressure.

Acetylcholine↗