PubMed Health⌕ Search

Biomedical subjects

J A Sandler

Publications and source records attributed to J A Sandler.

10 recordsLinked to original sources
PubMed1984

Beta-endorphin stimulates the secretion of insulin and glucagon in diabetes mellitus.

Administration of human beta-endorphin (2.5 mg IV bolus) to three subjects with non-insulin-dependent diabetes mellitus (type II) induced prompt and simultaneous increments in the plasma concentrations of insulin and glucagon lasting up to 90 minutes. In contrast to the hyperglycemic response previously observed in normal subjects following beta-endorphin, these diabetics showed a progressive decline in plasma glucose throughout the study period. This disparity may be related to a relatively greater release of insulin and lesser rise in glucagon observed in diabetic subjects than in nondiabetic subjects. These preliminary findings suggest that further studies to elucidate the role of pancreatic beta-endorphin on glucoregulation may be rewarding.

Aged↗
PubMed1980

Postpartum glycosylated hemoglobin levels in mothers of large--for--gestational age infants.

Glycosylated hemoglobin levels were determined in 19 women who were delivered of large--for--gestational age (greater than 4,082 grams) infants and compared to control values. Although the mean level for each group did not differ significantly (6.7% +/- 1.5% versus 6.5% +/- 0.2%) three women had increased hemoglobin glycosylation. In this series the birth of a large infant correlated with prepregnancy obesity and greater weight gain during pregnancy.

Birth Weight↗
PubMed1977

Histamine modulation of eosinophil migration.

Preincubation of eosinophils with 10(-5) M or higher concentrations of histamine inhibited the eosinophil chemotactic response to endotoxin-activated serum whether by using the nucleopore filter assay and counting the cells migrating through the filter, or by using the Zigmond-Hirsch assay and counting the cells at each 10-mum interval. When the H2-receptor sites on the eosinophils were blocked by metiamide, the inhibitory capacity of histamine was prevented. Preincubation of eosinophils with 10(-6) M histamine increased the number of responding eosinophils to endotoxin-activated serum and this enhancement was blocked by an H1-receptor antagonist. Isoproteronol and aminophylline inhibited eosinophil movement and increasing concentrations of dibutryl cyclic AMP inhibited eosinophil migration. Concentrations of histamine that consistently resulted in inhibition of eosinophil movement stimulated an increase in cyclic AMP that was prevented by blocking the H2-receptor but not the H1-receptor. Thus, histamine-dependent inhibition of the eosinophil chemotactic response to other agents is mediated through the H2-receptor and is associated with an increase in the intracellular level of cyclic AMP whereas histamine dependent enhancement of eosinophil migration to other agents appears to be mediated through the H1-receptor. Eosinophils behave as a heterogeneous population as assessed by the ability of histamine to augment or inhibit cell migration. This may reflect differences in H1 to H2 receptor density or cell responsiveness to receptor stimulation. The chemoattractant activity of histamine itself is not influenced by H1 or H2 receptor antagonists, thus it is possible that an eosinophil has a third type of histamine receptor.

Bucladesine↗
PubMed1975

The role of calcium in regulation of cyclic nucleotide content in human umbilical artery.

In term gestational human umbilical artery segments incubated in room air at 37 degrees, histamine, acetylcholine, bradykinin, K+, and serotonin (agonists that cause contraction) cause accumulation of guanosine 3':5'-monophosphate (cGMP) without altering the content of adenosine 3':5'-monosphophate (cAMP); prostaglandin E1 (PGE1), which relaxes the artery, causes cAMP accumulation without affecting the cGMP content (Clyman, R. I., Sandler, J.A., Manganiello, V.C., and Vaughan, M. (1975) J. Clin. Invest., in press). It has been postulated that Ca-2+ is important in the regulation of cyclic nucleotides in other tissues. In the umbilical artery the control of cAMP content by PGE1 was independent of Ca-2+. After incubation in Ca-2+-free medium, the c GMP contentof the artery segments was decreased by 50% and was unaffected by histamine, acetylcholine, bradykinin, and K+. Readdition of Ca-2+ (2.7 mM) or Sr-2+ (3.6 mM) to the medium partially restored the basal cGMP content and the agonist effects on the cGMP content. However, Sr-2+ was not as effective as Ca-2+ in this regard. Ionophores A23187 and X537A (agents that facilitate Ca-2+ movement through membranes) mimicked the effects of these Ca-2+-dependent agonists on cGMP content. Incubation with the phosphodiesterase inhibitor 3-isobutyl-1-methyl xanthine (0.1 mM) increased both the basal content of cGMP and the histamine-induced accumulation 3-fold. This effect was dependent on the presence of Ca-2+ also. Accumulation of cGMP induced by serotonin, on the other hand, was not diminished in Ca-2+-depleted arteries and, in fact, seemed to be inhibited by 2.7 mM Ca-2+. These observations are consistent with the existence in the umbilical artery of two separate mechanisms for control of cGMP synthesis that are influenced differently by Ca-2+.

Anti-Bacterial Agents↗
PubMed1975

The effect of serotonin (5-hydroxytryptamine) and derivatives on guanosine 3',5'-monophosphate in human monocytes.

The effects of several putative mediators of inflammatory responses on the cyclic nucleotide content of mononuclear leukocytes from human peripheral blood were investigated. Incubation of mononuclear cells with 100 muM serotonin (a maximally effective concentration) for 5 min caused a five- to eightfold increase in their content of guanosine 3',5'-monophosphate (cAMP)...

Bradykinin↗
PubMed1975

Guanosine 3',5'-monophosphate and adenosine 3',5'-monophosphate content of human umbilical artery.

Human umbilical arteries are unique vessels in that they close quickly and completely at birth. It has been suggested that cyclic uanosine 3',5'-monophosphate (cAMP) in relaxation. This hypothesis has been evaluated in term gestational human umbilical artery segments incubated at 37 degrees C and in room air. (a) The basal cGMP content (1 pmol/mg protein) of artery segments incubated in room air was almost twice that of cAMP. (b) Bradykinin, histamine, serotonin, acetylcholine, and K+ ion, which cause umbilical artery constriction, can increase the cGMP content of the artery segments within 30 s of exposure without altering the cAMP content. (c) Prostaglandin E1, but not isoproterenol, caused accumulation of cAMP which is consistent with reports that umbilical arteries lack functional beta-receptors and that only prostaglandin E1 can bring about relaxation of umbilical arteries. (d) 1 muM atropine blocked the effect of 100 muM acetylcholine on cGMP content without altering the responses to histamine, bradykinin, serotonin, or K+ ion. (e) Pyrilamine (an H1 antagonist), but not metiamide (an H2 antagonist), blocked the effect of histamine on cGMP from which it is inferred that histamine causes accumulation of cGMP in umbilical artery via its interaction with H1 receptors. The results are consistent with the view that metabolism of the two cyclic nucleotides is independently controlled in the human umbilical artery and that cGMP is involved in contraction of the artery at birth.

Acetylcholine↗
PubMed1975

Stimulation of monocyte cGMP by leukocyte dialysates. An antigen-independent property of dialyzable transfer factor.

We studied the effects of dialysates from leukocyte lysates containing dialyzable transfer factor activity and other leukocyte dialysates devoid of transfer factor activity on accumulation of cyclic nucleotides in human leukocytes. Dialysates from normal leukocytes produced 4- to 11-fold increases in leukocyte cGMP, and experiments with purified cell populations revealed that the increases were predominantly, if not entirely, in blood monocytes. Substances that increased monocyte cGMP could be obtained from several cell populations including mononuclear cells from Hypaque-Ficoll gradients, plastic-adherent monocytes, nonadherent lymphocytes, and neutrophils, but were not present in dialysates of leukemic lymphocytes from patients with the Sezary syndrome. Moreover, dialysates that increased leukocyte cGMP had essentially no effect on intracellular cAMP. Dialysates of lysed mononuclear cells contained serotonin, ascorbate, and an unidentified cholinergic activity, agents known to increase leukocyte cGMP. After passage of dialyzable transfer factor from mononuclear cells through a gel-filtration column, four fractions were obtained that increased leukocyte cGMP. Two of these fractions contained ascorbate; two other active fractions, including one that also caused conversion of delayed skin tests, did not contain detectable ascorbate or serotonin. The dialysate of lysed neutrophils also increased cGMP, but this activity was limited to the column fractions which contained ascorbic acid. These observations raise the possibility that alterations in monocyte cGMP content could modulate either the specific antigen-dependent, or, more likely, the antigen-independent activities in preparations of transfer factor.

Ascorbic Acid↗