scholarly journals Effects of veratridine on Ca fluxes and the release of oxytocin and vasopressin from the isolated rat neurohypophysis.

1978 ◽  
Vol 72 (3) ◽  
pp. 297-304 ◽  
Author(s):  
J J Nordmann ◽  
R E Dyball
Keyword(s):  
Calcium Antagonists ◽  
Incubation Medium ◽  
Hormone Release ◽  
45Ca Uptake ◽  
Regulation Of Secretion ◽  
45Ca Efflux ◽  
Isolated Rat

Uptake of radioactive calcium, 45Ca efflux, and hormone release from the isolated rat neurohypophysis were monitored in vitro after the addition of veratridine to the incubation medium. Veratridine dramatically increased hormone release, but the release was not sustained and had declined by about 90% after 2 h. Removal of external Na+ prevented hormone release as did addition to the incubation medium of tetrodotoxin or the calcium antagonists D600 and Mn2+ ions. Veratridine increased 45Ca uptake into the isolated neurohypophysis and the increase could be prevented by addition of tetrodotoxin or D600 to the medium. Efflux of 45Ca was not changed by addition of veratridine. The results underline the importance of both Na+ and Ca+2 channels in the regulation of secretion of neurosecretory products.

Evidence for calcium inactivation during hormone release in the rat neurohypophysis

1976 ◽  
Vol 65 (3) ◽  
pp. 669-683
Author(s):  
J. J. Nordmann
Keyword(s):  
Hormone Secretion ◽  
Calcium Ionophore ◽  
High Rate ◽  
Hormone Release ◽  
45Ca Uptake ◽  
High K ◽  
K Concentration ◽  
The Relationship ◽  
Internal Calcium

1. A study has been made of the relationship between 45Ca uptake into and hormone release from isolated rat neurohypophyses incubated in vitro. 2. Hormone secretion is triggered by high-K (56 mM) but long exposure to the stimulus does not generate a maintained release of hormone. 3. When hormone release began to wane, addition of Ba of La increased hormone output which suggests that the decline in output did not result from depletion of the neurosecretory granules at the nerve terminals. 4. 45Ca uptake is enhanced in the presence of high-K concentration, but the initial high rate declines during long exposure to the potassium stimulus with a time constant similar to that of the decline in hormone release. 5. After a period of incubation in a K-rich, calcium-free medium, addition of calcium to the medium induced hormone release. The magnitude of this release was dependent on the time of exposure to excess potassium. 6. After inactivation of secretion, mobilization of internal calcium by means of a calcium ionophore increased hormone release.

Reversal of renal and smooth muscle actions of the thromboxane mimetic U-44069 by diltiazem

1986 ◽  
Vol 250 (4) ◽  
pp. F619-F626 ◽  
Author(s):  
R. Loutzenhiser ◽  
M. Epstein ◽  
C. Horton ◽  
P. Sonke
Keyword(s):  
Smooth Muscle ◽  
Rat Kidney ◽  
Tension Development ◽  
45Ca Uptake ◽  
Aortic Smooth Muscle ◽  
Control Value ◽  
Potent Vasoconstrictor ◽  
Isolated Rat

U-44069 is a stable prostaglandin (PG) H2 analogue and a potent vasoconstrictor. Its in vivo and in vitro actions mimic those of thromboxane A2. We have studied the effects of the calcium antagonist diltiazem upon the vasoconstriction induced by U-44069 using isolated rat aortic smooth muscle and isolated perfused rat kidney (IPRK). The administration of 10(-6)M U-44069 elicited maximally effective contractions in isolated aortic rings and increased 45Ca uptake from a control value of 285 +/- 6 mumol/kg to 344 +/- 8 mumol/kg. Diltiazem reduced U-44069-induced tension development and 45Ca uptake of isolated aortic smooth muscle 73 +/- 2 and 91 +/- 3%, respectively. The dose dependency of each of these effects of diltiazem was similar (EC50 = 369 nM and 334 nM for tension and 45Ca flux, respectively). When administered to the IPRK, 10(-6) M U-44069 caused a 82 +/- 3% decrease in glomerular filtration rate (GFR) and a 80 +/- 4% decrease in filtration fraction but reduced renal perfusate flow (RPF) only 13 +/- 8% (P less than 0.005). Diltiazem completely reversed the actions of U-44069 on the IPRK (EC50 = 288 nM and 323 nM for GFR and RPF, respectively). Diltiazem thus inhibited U-44069-induced tension development and 45Ca uptake by vascular smooth muscle and increased GFR within identical dose ranges. The contractile response of isolated rat glomeruli was also assessed. U-44069 reduced the volume of isolated glomeruli, but this action was neither prevented nor reversed by diltiazem. These results are consistent with the hypothesis that diltiazem increased GFR by inhibiting U-44069-induced Ca influx at preglomerular vessels.

Alterations in cellular Ca2+ regulation in the liver in endotoxic shock

1986 ◽  
Vol 250 (5) ◽  
pp. R884-R891 ◽  
Author(s):  
M. M. Sayeed
Keyword(s):  
Salmonella Enteritidis ◽  
Hepatic Glucose Production ◽  
Endotoxic Shock ◽  
Saline Control ◽  
Adrenergic Stimulation ◽  
45Ca Uptake ◽  
Intracellular Pool ◽  
Liver Slices ◽  
45Ca Efflux

Effects of Salmonella enteritidis endotoxin on cellular Ca2+ regulation were studied in the liver. Rats were given intravenous injections of saline (control) or endotoxin (15 mg/kg). They were killed 5 h later, at which time endotoxin-injected rats showed signs of shock. Liver slices were used to measure Ca2+ efflux from the intracellular Ca2+ pool and the size of that pool. 45Ca uptake was measured in isolated endoplasmic reticulum (ER) from livers. 45Ca efflux and uptake were also measured in control liver slices and ER in the presence of endotoxin (250 micrograms/ml) in vitro. In control livers, 45Ca efflux from the intracellular pool was sensitive to iodoacetate and 45Ca uptake by ER was ATP dependent. These active Ca2+ movements were significantly attenuated by endotoxin in vitro but were unaltered in livers of endotoxic rats. However, the intracellular Ca2+ pool size and norepinephrine (NE) regulation of cellular Ca2+ were adversely affected in endotoxic shock. Though the application of 1 microM NE to control liver slices significantly stimulated 45Ca efflux, it failed to stimulate efflux in liver slices of endotoxic rats. The intracellular Ca2+ pool in endotoxic livers (mean +/- SE = 553 +/- 23 mumol/kg tissue) was significantly larger than in controls (413 +/- 17). These results suggest that during endotoxic shock there is a depletion of the NE-mobilized activator Ca2+ in liver that could lead to a failure of alpha-adrenergic stimulation of hepatic glucose production. The increased sequestration of Ca2+ in the intracellular pool in endotoxic rat liver cells could be due to an influx of extracellular Ca2+ and may predispose these cells to Ca2+ overload.

Effect of Treatment with Calcium Antagonists in Vitro and in Vivo on the Contractile Response of Isolated Rat and Human Detrusor Muscle

1996 ◽  
Vol 91 (4) ◽  
pp. 467-474 ◽  
Author(s):  
Ruth A. Elliott ◽  
Robert I. Norman ◽  
Stuart G. Parker ◽  
R. Paul Whitaker ◽  
C. Mark Castleden
Keyword(s):  
Single Dose ◽  
Calcium Antagonists ◽  
Contractile Response ◽  
Detrusor Muscle ◽  
Significant Difference ◽  
Effect Of Treatment ◽  
Human Detrusor ◽  
Isolated Rat

1. The effect of calcium antagonists on the contractile response of human and rat isolated detrusor muscle in vitro was investigated. The effect of treatment with nimodipine on rat detrusor muscle in vivo was also examined. 2. Nimodipine 0.1 μmol/l, nifedipine 0.1 μmol/l, nifedipine 0.25 μmol/l and verapamil 1.5 μmol/l reduced the maximum contractile response of isolated human detrusor muscle to carbachol by 42%, 35%, 41% and 28% respectively (P < 0.01). Verapamil 0.1 μmol/l had no significant effect on contractile response. 3. Nimodipine 0.1 μmol/l reduced the maximum contractile response of isolated rat detrusor muscle in vitro to electrical field stimulation and carbachol by 53% and 84% respectively (P < 0.01). 4. Rats were pretreated with nimodipine for 8 days (5 mg day−1 kg−1) or with a single dose. Serum nimodipine concentrations were higher in rats treated for 8 days. In rats treated with nimodipine for 8 days there was no significant difference in detrusor contractile response compared with controls. However, after one dose of nimodipine the maximum contractile response was significantly reduced compared with controls (P < 0.05). 5. At the concentrations studied, nimodipine had a greater inhibitory effect on the contractile response of isolated human detrusor muscle. Nimodipine significantly reduced the contractile response of rat detrusor muscle in vitro and after a single dose in vivo, but had no significant effect after 8 days' treatment in vivo. It is possible that chronic oral treatment with nimodipine caused an up-regulation of 1,4-dihydropyridine-sensitive calcium channels, which may explain the lack of clinical effect of chronic treatment with calcium antagonists in patients with detrusor instability.

Calcium Antagonists and Hormone Release

1984 ◽  
Vol 66 (3) ◽  
pp. 249-255 ◽  
Author(s):  
J. A. Millar ◽  
A. D. Struthers
Keyword(s):  
Calcium Antagonists ◽  
Inhibitory Effect ◽  
Calcium Flux ◽  
Channel Blockers ◽  
Hormone Release ◽  
Calcium Dependent ◽  
Transmembrane Flux ◽  
Slow Channel

Introduction: Calcium (Ca2+) has been aptly entitled the ‘universal provocateur’ [1] in recognition of its many indispensable metabolic actions. The class of drugs popularly known as calcium antagonists (calcium slow channel blockers) provokes a variety of pharmacological effects and these drugs are useful as probes of calcium-dependent mechanisms. One area where such application appears particularly appropriate is the study of hormone release, since it has been demonstrated that secretion of at least some hormones is dependent on translocation of extracellular Ca2+ across the cell membrane. Furthermore, specific physiological stimuli to secretion of most hormones can be applied in vivo or mimicked in vitro, and hormone levels may be measured by specific assays. Calcium antagonists also provide a possible means of studying the role of Ca2+ in hormone release in the intact organism. In many studies an inhibitory effect of a calcium antagonist on hormonal responses to secretory stimuli has been taken as evidence that transmembrane flux of Ca2+ is an obligatory event in the response. Such a conclusion begs several questions, which will be discussed in this review. For example, it is important to define the extent to which calcium antagonists represent a homogeneous class of drugs, whether ‘antagonism’ is restricted to inhibition of inward calcium flux, and whether the pharmacological actions vary according to the agent used or the cell type under study. Answers to such questions are necessary to exclude actions of calcium antagonists other than prevention of calcium uptake which may inhibit hormone release.

Metabolism of thyroid hormones in isolated rat hepatocytes: studies on the influences of carbamazepine and phenytoin

1983 ◽  
Vol 104 (4) ◽  
pp. 479-484 ◽  
Author(s):  
Sylvi Aanderud ◽  
Jarle Aarbakke ◽  
Johan Sundsfjord
Keyword(s):  
Thyroid Hormones ◽  
Cellular Uptake ◽  
Incubation Medium ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

Abstract. The in vitro handling of thyroid hormones was studied in isolated rat hepatocytes by measuring 1) the cellular uptake of T4, 2) the conversion of T4 to T3 and 3) the degradation of T4 and T3. The in vitro conversion of T4 to T3 increased significantly by adding ethanol 2% or carbamazepine (CBZ) 400 μm in ethanol 2% to the incubation medium. As there was no difference between ethanol and CBZ/ethanol on the T3 formation, this effect was probably caused by ethanol. The T3 formation was unaffected by phenytoin (PHT) in conc. up to 400 μm, while propylthiouracil (PTU) 100 and 400 μm inhibited the conversion completely. The T4 to T3 conversion in hepatocytes from rats pretreated with CBZ or PHT for 2 weeks was not significantly different from untreated controls. The cellular uptake of T4 was reduced by about 30% in the presence of PHT and unaltered by CBZ and ethanol. The degradation of T4 and T3 was not influenced by the in vitro addition of CBZ or PHT, nor was the degradation of T4 and T3 significantly different from untreated controls in hepatocyte suspensions from CBZ or PHT pretreated rats. Our findings suggest that the handling of thyroid hormones in isolated rat hepatocytes is not influenced by the in vitro or in vivo exposure to CBZ or PHT.

SENSITIVITY OF THE RAT DIAPHRAGM TO GROWTH HORMONE.

1967 ◽  
Vol 54 (4) ◽  
pp. 645-662 ◽  
Author(s):  
Å. Hjalmarson ◽  
K. Ahrén
Keyword(s):  
Growth Hormone ◽  
Inhibitory Effect ◽  
Rat Diaphragm ◽  
Intracellular Accumulation ◽  
Slight Effect ◽  
Kidney Capsule ◽  
Muscle Tissues ◽  
Hypophysectomized Rats ◽  
Isolated Rat

ABSTRACT The effect of growth hormone (GH) in vitro on the rate of intracellular accumulation of the non-utilizable amino acid α-aminoisobutyric acid (AIB) was studied in the intact rat diaphragm preparation. Bovine or ovine GH (25 μg/ml incubation medium) markedly stimulated the accumulation of AIB-14C by diaphragms from hypophysectomized rats, while there was no or only a very slight effect on diaphragms from normal rats. In diaphragms from rats with the pituitary gland autotransplanted to the kidney capsule GH in vitro stimulated the accumulation of AIB-14C significantly more than in diaphragms from normal rats but significantly less than in diaphragms from hypophysectomized rats. Injections of GH intramuscularly for 4 days to hypophysectomized rats made the diaphragms from these rats less sensitive or completely insensitive to GH in vitro. These results indicate strongly that the relative insensitivity to GH in vitro of diaphragms from normal rats is due to the fact that the muscle tissues from these rats has been exposed to the endogenously secreted GH. The results show that GH can influence the accumulation of AIB-14C in the isolated rat diaphragm in two different ways giving an acute or »stimulatory« effect and a late or »inhibitory« effect, and that it seems to be a time-relationship between these two effects of the hormone.

ALDOSTERONE STIMULATION IN VITRO

1965 ◽  
Vol 50 (2) ◽  
pp. 301-309 ◽  
Author(s):  
Jürg Müller
Keyword(s):  
Ammonium Chloride ◽  
Human Urine ◽  
Incubation Medium ◽  
The Other ◽  
Ammonium Ions ◽  
Response Curves ◽  
Urine Extract ◽  
Similar Dose ◽  
Aldosterone Production

ABSTRACT An extract of human urine, which was previously shown to stimulate aldosterone production by rat adrenal sections, was further purified. Evidence was obtained that its aldosterone-stimulating effect was due to the presence of ammonium ions. Addition of ammonium chloride and of urine extract to the incubation medium caused identical increases in aldosterone production in vitro. In addition to ammonium ions, rubidium and caesium ions also stimulated aldosterone production up to 250% that of control values without a significant effect on corticosterone production. Similar dose-response curves were obtained when increasing concentrations of potassium, ammonium, rubidium and caesium ions were tested. Aldosterone production was maximal at concentrations of 7 mval/1 and was significantly lower at higher concentrations. When ammonium chloride and ACTH were simultaneously added to the incubation medium, the production of aldosterone and of corticosterone was lower than with ACTH alone. On the other hand, the stimulating activity on aldosterone and corticosterone production by »TPN« (NADP) and glucose-6-phosphate was enhanced by the simultaneous addition of ammonium chloride.

IN VITRO UPTAKE OF TRITIATED OESTRADIOL BY THE ANTERIOR HYPOTHALAMUS AND HYPOPHYSIS OF THE RAT

1970 ◽  
Vol 64 (4) ◽  
pp. 687-695 ◽  
Author(s):  
Junzo Kato
Keyword(s):  
Incubation Medium ◽  
Posterior Hypothalamus ◽  
Anterior Hypothalamus ◽  
Ovariectomized Rats ◽  
Free Medium ◽  
Cortex Cerebri ◽  
Anterior Hypophysis ◽  
In Vitro Uptake

ABSTRACT The anterior, middle, and posterior hypothalamus, the cortex cerebri, the anterior hypophysis as well as the diaphragm of adult ovariectomized rats were incubated in vitro with tritiated 17β-oestradiol. The uptake of tritiated oestradiol was differentially distributed intracerebrally with higher accumulation in the anterior hypothalamus and the hypophysis. Lowering the temperature of the incubation medium caused a reduction in the uptake of radioactivity by the anterior hypothalamus as compared to that found in other brain tissues. Tritiated oestradiol taken up in vitro by the anterior hypothalamus and the hypophysis tended to be retained after further incubation in a steroid-free medium. The addition of non-radioactive 17β-oestradiol to the medium inhibited the uptake of tritiated oestradiol by these tissues. Moreover, pretreatment with non-radioactive 17β-oestradiol in vivo prevented the preferential accumulation of tritiated oestradiol in vitro in the anterior hypothalamus and the hypophysis. These results indicate that oestradiol is preferentially taken up in vitro by the anterior hypothalamus and the hypophysis of the rat.

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