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Biomedical subjects

H A Bern

Publications and source records attributed to H A Bern.

At least 127 records · Page 7Linked to original sources

Effects of somatostatin and urotensin II on tilapia pituitary prolactin release and interactions between somatostatin, osmotic pressure Ca++, and adenosine 3',5'-monophosphate in prolactin release in vitro.

Both somatostatin (SRIF) and urotensin II, a dodecapeptide from the teleost caudal neurosecretory system, inhibit PRL release from the organ-cultured rostral pars distalis of the tilapia, Sarotherodon mossambicus, in a dose-related manner. The inhibitory action of SRIF on PRL release was completely prevented by the presence of the calcium ionophore A23187. PRL release was also blocked when Ca++ was excluded from the incubation medium, even in the presence of the ionophore. Both dibutyryl cAMP (dbcAMP) and the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine, alone or in combination, stimulated PRL release during incubation in high osmotic pressure medium. The effect of dbcAMP appeared to be dose related. Together, dbcAMP and 3-isobutyl-1-methylxanthine were also effective in preventing the inhibition of PRL release by SRIF. These results are consistent with the notion that Ca++, and possibly cAMP, may be important mediators of PRL secretion, and it is likely that SRIF may inhibit PRL release by blocking a Ca++- or cAMP-mediated mechanism.

1-Methyl-3-isobutylxanthine↗

Growth of mouse mammary glands after neonatal sex hormone treatment.

Mammary gland growth was examined in female mice immediately and during 1 month after neonatal treatment with sex hormones. BALB/c mice were given daily injections of hormones for the first 5 days after birth. As a criterion of growth, the number of ductal branchings was counted in stained wholemounts of the fourth (inguinal) pair of glands. At day 6, the growth of the glands was significantly inhibited in animals treated with 17 beta-estradiol (E) or diethylstilbestrol (DES); after treatment with progesterone (P) or androgens, no immediate effect was evident. At day 33, neonatal treatment with E stimulated growth, as did neonatal treatment with testosterone (T) or 5 alpha-dihydrotestosterone (5 alpha-DHT); treatment with a high dose of DES inhibited growth. Treatment with P or 5 beta-dihydrotestosterone had no effect. In conclusion, neonatal treatment with sex hormones has two distinct effects on the growth of mouse mammary gland: 1) inhibition by estrogens, observed immediately after treatment, and 2) stimulation by E, T, and 5 alpha-DHT, observed 4 weeks after treatment.

Animals↗

Urotensin II: a somatostatin-like peptide in the caudal neurosecretory system of fishes.

Urotensin II, a peptide hormone from the caudal neurosecretory system of the teleost, Gillichthys mirabilis, was isolated by using classical chromatographic techniques and high-performance liquid chromatography (HPLC). Direct microtechniques for sequence determination were used to establish its structure. Urotensin II from Gillichthys is a 1363-dalton dodecapeptide with the amino acid sequence Ala-Gly-Thr-Ala-Asp-Cys-Phe-Trp-Lys-Tyr-Cys-Val. This sequence is homologous with somatostatin in positions 1 and 2 and 7-9. The sequence has been verified by the production of a bioactive synthetic urotensin II. The possible chemical and physiological significance of its homology to somatostatin is discussed.

Amino Acid Sequence↗

Ion transport by the urinary bladder of the gobiid teleost, Gillichthys mirabilis.

Transport characteristics of the two epithelial cell types lining the urinary bladder of the goby can be studied in Ussing-type chambers. Cuboidal cell regions from seawater- and 5% seawater-acclimated fish exhibit little mucosal-to-serosal Na or Cl transport. In contrast, columnar cell regions from both seawater- and 5% seawater-acclimated fish transport substantial amounts of Na and Cl. Whereas all electrolyte transport in 5% seawater-acclimated fish is electrically silent (neutral), columnar cell regions from seawater-acclimated fish possess an electrogenic Na transport component in addition to the neutral transport. Columnar cell regions also possess a Cl/Cl exchange diffusion mechanism. Neutral Na and Cl transport are not altered in response to external salinity; electrogenic transport varies both with acclimation to salinity and season. Reabsorption of Na and Cl from urine reduces excretory losses of these ions from 5% seawater-acclimated fish and drives urinary bladder water reabsorption in seawater-acclimated fish.

Animals↗

Teleostean urophysis: urotensin II and ion transport across the isolated skin of a marine teleost.

The caudal neurosecretory peptide urotensin II rapidly inhibits by 30 percent the short-circuit current across the isolated skin of a marine teleost. The effect appears to be specific and cannot be attributed to actions of epinephrine, urotensin I, or arginine vasotocin. The results strongly suggest that urotensin II may act directly on ion-transporting cells involved in teleostean hypoosmoregulation.

Animals↗

Mouse mammary epithelial cells on floating collagen gels: transepithelial ion transport and effects of prolactin.

Epithelial cells dissociated from midpregnant BALB/c mouse mammary glands were cultured for as long as 20 days as confluent monolayers on floating collagen gels. Detached gels bearing monolayers were placed in lucite Ussing chàmbers for measurement of transepithelial potential difference (PD), short-circuit current (I(sc)), resistance (R), and unidirectional fluxes of Na(+) and Cl(-) during short-circuit current conditions (PD = 0). With Hanks' solution bathing both sides of cultures maintained with insulin and cortisol, PD = -12.8 mV (serosal side ground), I(sc) = 24.6 muA/cm(2), and R = 507 omega.cm(2). Net absorption of Na(+) equaled I(sc), and there was no net Cl(-) transport. PD and I(sc) were reduced 50% by mucosal addition of 10 muM amiloride and to zero by metabolic inhibition with nitrogen gas or by serosal addition of 0.1 mM ouabain. In similar cultures supplemented with prolactin, PD and I(sc) increased to -15.8 mV and 48.0 muA/cm(2), respectively, and R decreased to 374 omega.cm(2). Inhibitor effects were similar to those seen in prolactin-free cultures. Prolactin exposure resulted in a 3-fold increase in net absorption of Na(+). Na(+) absorption was not equivalent to I(sc), and there was little Cl(-) absorption; therefore, prolactin induced active transport of other, as yet unidentified, ions. These effects of prolactin require at least 3 days to occur and cannot be attributed to the known contamination with neurohypophysial hormones. The prolactin-induced increase in Na(+) absorption parallels its Na(+)-retaining ability in lower vertebrates and could be part of the mechanism that keeps milk Na(+) concentration low in intact glands.

Animals↗