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Biomedical subjects

J Endo

Publications and source records attributed to J Endo.

At least 91 records · Page 5Linked to original sources
PubMed1985

Effects of long-chain cis-unsaturated fatty acids and their alcohol analogs on aggregation of bovine platelets and their relation with membrane fluidity change.

The effects of long-chain cis-unsaturated fatty acids with different alkyl chain lengths and different numbers of double bonds on aggregation of bovine platelets and membrane fluidity were investigated. All the cis-unsaturated fatty acids tested inhibited aggregation and at the same time increased membrane fluidity in accordance with their inhibitory effects. The saturated fatty acids and trans-unsaturated fatty acid tested for comparison had much lower or no effects on aggregation and membrane fluidity. The inhibitory effects of mono cis-unsaturated fatty acids increased with increase of their alkyl chain length. cis-Unsaturated fatty acids with two or more double bonds had more inhibitory effects than mono-unsaturated fatty acids. The position of the double bonds had less influence than the number of double bonds. We also examined the effects of cis-unsaturated fatty acids on membrane fluidity with diphenylhexatriene and anthroyloxy derivatives of fatty acids as probes and observed increased fluidity to be considerable in the membrane. The alcohol analogs of cis-unsaturated fatty acids also inhibited aggregation and increased membrane perturbation. These results suggest that the inhibition of platelet aggregation by cis-unsaturated compounds is due to perturbation of the lipid layer.

Adenosine Diphosphate↗
PubMed1985

Angiotensin II and phorbol ester enhance isoproterenol- and vasoactive intestinal peptide (VIP)-induced cyclic AMP accumulation in vascular smooth muscle cells.

The importance of Ca2+ and cAMP in the regulation of cellular functions has been well demonstrated. We studied the effect of angiotensin II (AII), a potent Ca2+-mobilizing hormone, on cAMP accumulation induced by isoproterenol (ISO) and vasoactive intestinal peptide (VIP) in cultured vascular smooth muscle cells (VSMC). Although the addition of AII alone caused little increase of cAMP, it enhanced ISO- and VIP-induced cAMP accumulations in a dose-dependent manner. This enhancement was mimicked by tumor-promoting phorbol ester but not by Ca2+ ionophore. This observation suggested that AII enhanced agonist-induced cAMP accumulation through the activation of protein kinase C in VSMC.

Angiotensin II↗
PubMed1985

Vasopressin-induced calcium increases in smooth muscle cells from spontaneously hypertensive rats.

Cytosolic free Ca2+ concentrations [( Ca2+]i) were measured in smooth muscle cells (SMC) from spontaneously hypertensive rats (SHR) and age and sex matched Wistar-Kyoto rats (WKY). Resting levels of [Ca2+]i were 114 +/- 6 nM and 116 +/- 5 nM in SMC from WKY and SHR, respectively. Angiotensin II (AII) induced a dose-dependent large increases in [Ca2+]i in SMC. There were no significant differences in resting or AII-stimulated levels of [Ca2+]i when SMC from WKY and SHR were compared. Arg-vasopressin (AVP) caused a similar but smaller [Ca2+]i increase than AII in SMC. AVP caused larger [Ca2+]i increases in SMC from SHR than in SMC from WKY. Although concentrations of AVP higher than those ordinarily detected in plasma were necessary to obtain different responses between SHR and WKY, these differences may be related to the pathogenesis of hypertension.

Aminoquinolines↗
PubMed1985

Influence of chronic hyperprolactinemia induced by sulpiride on the hypothalamo-pituitary-testicular axis in normal men.

For elucidation of the effects of hyperprolactinemia on the hypothalamic-pituitary-testicular axis, five healthy men were exposed to sulpiride (300 mg/day by mouth); four among the five maintained hyperprolactinemia (71.6 to 95.3 ng/ml) for 78 days. Clomiphene citrate (CC), luteinizing hormone (LH)-releasing hormone, and human chorionic gonadotropin tests were performed before and after sulpiride treatment. The CC test, given as a measure of hypothalamic function, was carried out in each of the five volunteers before sulpiride treatment (control) and on days 14 (2 weeks) and 60 (2 months) of sulpiride administration. Each value of plasma LH stimulated by CC was integrated and expressed as a ratio of the integrated value obtained after administering CC at 2 weeks and 2 months to that from each control experiment. The mean ratio in the four subjects at 2 months (mean +/- standard deviation, 0.769 +/- 0.121) was significantly lower than that at 2 weeks (0.942 +/- 0.073; P less than 0.05) and before sulpiride treatment (1.000; P less than 0.01). Impairment of LH responses to CC by 2-month long sulpiride-induced hyperprolactinemia suggests that chronic hyperprolactinemia in men partly suppresses LH secretion by its inhibitory action on the hypothalamus.

Adult↗
PubMed1985

Transmural conduction velosity index in healthy schoolchildren.

Transmural conduction velosity index (TCVI) was obtained in 174 healthy children. TCVI was defined as the echocardiographically determined interventricular septal thickness (IVST) divided by the ventricular activation time (VAT) measured by body surface potential mapping. TCVI ranged from 14 to 49 cm/sec and was highly correlated with IVST (r = 0.75, TCVI = 3.25 X IVST + 0.56). It was concluded that the left ventricular hypertrophy with muscular thickness does cause the greater conduction velosity in healthy children.

Adolescent↗
PubMed1984

Activation of bovine platelets induced by long-chain unsaturated fatty acids at just below their lytic concentrations, and its mechanism.

The effects of long-chain unsaturated fatty acids such as linoleic acid on bovine platelets were examined. Not only linoleic acid, but also oleic and linolenic acid, at just below the concentrations causing marked cell lysis, induced an absorbance decrease of the platelet suspension in the presence of Ca2+. Since this absorbance decrease was reversed by the addition of EDTA and moreover aggregate formation was found by macroscopic and microscopic observation, it was concluded that unsaturated fatty acids at just below their lytic concentrations caused platelet aggregation. Unsaturated fatty acids also caused release of adenine nucleotides, but there was a lag time between the release and the aggregation, just as with ADP-induced release, suggesting that the aggregation was independent of the release of ADP. It was revealed that this activation of platelets by unsaturated fatty acids was caused by marked Ca2+ uptake into the cytoplasm, resulting from significant membrane perturbation.

Adenosine Triphosphate↗
PubMed1984

Effects of four types of reagents on ADP-induced aggregation and Ca2+ mobilization of bovine blood platelets.

The effects of four types of reagents--a stimulant analog (ATP), reagents increasing cAMP (theophylline and (-)-isoproterenol), Ca2+ blockers (chlorpromazine, procaine, dibucaine and tetracaine) and nonspecific membrane-reactive reagents (n-butanol, n-hexanol and linoleate) - on ADP-induced Ca2+ mobilization and aggregation of platelets were investigated. All the reagents tested inhibited the aggregation. Of these reagents, those increasing cAMP and the stimulant analog inhibited the aggregation at least partly by inhibiting Ca2+ mobilization, whereas Ca2+ blockers and nonspecific membrane-reactive reagents must have inhibited the aggregation by different mechanisms, because they had: (1) no effect on ADP-induced Ca2+ mobilization, (2) accelerated it, or (3) themselves stimulated Ca2+ mobilization. The results showed that the inhibitory effects of Ca2+ blockers were at least partly due to competition with Ca2+ for binding sites on the outside of the membrane, whereas the effects of the nonspecific membrane-reactive reagents tested were due to membrane perturbation.

Adenosine Diphosphate↗
PubMed1984

Anorexia nervosa precipitated by a prepubertal pyometra.

A severe pyometra was found in a typical case of anorexia nervosa, with the latter illness apparently precipitated by the former. Compulsory alimentation before and after operation brought some weight gain as well as reversal of dilated cerebral sulci and hypothyroidism, though hypothalamo-pituitary dysfunction persisted.

Anorexia Nervosa↗
PubMed1983

Inhibitory effects of 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) on the ADP-stimulated aggregation of gel-filtered bovine blood platelets.

The effect of DIDS, a specific inhibitor of anion transport in the erythrocyte membrane, on the ADP-stimulated aggregation of gel-filtered bovine blood platelets was examined. Marked inhibition of aggregation was observed at concentrations of more than 5 x 10(-5)M DIDS. On preincubation with platelets for 30 min, DIDS was more potent and significant inhibition was observed at concentrations of over 2 x 10(-7)M. Since ADP-stimulated aggregation of bovine gel-filtered platelets precedes the release reaction, these results suggest that an anion transport system in the plasma membrane is involved in platelet aggregation.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1982

Potentiation of isoproterenol-induced salivation by labetalol.

The authors previously reported that low doses of labetalol potentiated isoproterenol (ISO)-induced salivation in mice. The present study was carried out to ascertain the potentiating effect of labetalol in in vitro experiments using rat parotid tissue slices and their isolated cells. ISO-induced amylase release was enhanced by low concentrations of labetalol (less than 10(-6) M), while it was inhibited by high doses (more than 10(-5) M). This potentiating effect of labetalol did not occur in the Ca-free medium used for incubation or in experiments using the dispersed parotid cells or the parotid tissues which were obtained from 6-hydroxy-dopamine- or reserpine-treated rats. The effect of ISO on cyclic AMP accumulation in parotid tissue was completely blocked by the addition of labetalol in concentrations which were sufficient to increase the ISO-induced amylase release. Labetalol also inhibited the ISO-induced reduction of potassium release in parotid tissue. From these results, it is concluded that increases in the secretion of amylase and potassium from salivary glands due to the stimulation of glandular alpha-adrenoceptors by endogenous norepinephrine may play an important role in the potentiating effect of labetalol on ISO-induced salivation in mice.

Amylases↗
PubMed1982

Effects of a new angiotensin-converting enzyme inhibitor, MK 421, in normal men and patients.

Effects of MK 421, a new angiotensin-converting enzyme inhibitor, were studied in normal men and patients. MK 421 was given at 0900 h as a single oral dose of 20 mg, to 5 normal men and 2 patients with essential hypertension and 10 mg to a patient with Bartter's syndrome, in the recumbent position. In all of them blood pressure (BP) fell, plasma angiotensin I (Pl AI) and plasma renin activity (PRA) increased, and plasma aldosterone (PA) decreased from 2 h to 6 h. Maximum effects were observed at 4 or 6 h. Then the effects attenuated gradually but still remained at 24 h. In the same 5 normal men angiotensin I (AI) was infused iv at a rate of 20 ng/kg . min from 0900 h to 1500 h, from 2030 h to 2100 h, and the next morning from 0830 to 0900 h. At first the BP rose and PA increased. The onset of the BP fall was at 35, 55, 60, 70 and 85 min in each subject, respectively. Then the BP and PA began to decrease and the Pl AI and PRA began to increase. The maximum effects were observed at 4 or 6 h. Then these inhibitory effects on the AI were attenuated but still remained at 24 h. The 2 patients with essential hypertension and a patient with malignant hypertension was treated with MK 421 at a daily doses of 5 to 40 mg for 2 to 6 months. They all showed a fall in BP and no side-effects were noted. From these results it is concluded that MK 421 is a strong and long-acting antihypertensive drug and its clinical application seems very useful for the treatment of hypertension.

Adult↗
PubMed1981

Suppression of captopril-induced increase in plasma renin activity by des-Asp1-,Ileu8-angiotensin II in man.

One hundred milligrams of oral captopril (SQ 14225) caused a significant increase in PRA and a significant decrease in plasma aldosterone (PA) in five normal men and five hypertensive patients. Blood pressure (BP) showed no change in the normal men, but it fell significantly in the patients. An iv infusion of 200 ng/kg.min des-Asp1-,Ileu8-angiotensin II (AIIIA) for 2 h caused a significant decrease in PRA and a slight but significant increase in PA, but caused no change in BP in the normal men. When 100 mg captopril were given orally immediately before the start of the AIIIA infusion, BP showed no change in the normal men, but fell in the patients. However, PRA showed a significant decrease and PA showed a slight but significant increase in both the normal men and the patients, except for one patient with renovascular hypertension who showed a decrease in PA. Thus, this suppression of captopril-induced PRA increase by AIIIA, a derivative of angiotensin II, is not related to BP change, and it suggests that the principal cause of the PRA increase after captopril is a disappearance of endogenous angiotensin II.

Adult↗