scholarly journals Dissimilar mechanisms of Ca2+response to bradykinin in different types of juxtamedullary glomerular arterioles

1999 ◽  
Vol 277 (5) ◽  
pp. F697-F705 ◽  
Author(s):  
F. Praddaude ◽  
J. Marchetti ◽  
F. Alhenc-Gelas ◽  
J.-L. Ader
Keyword(s):  
Tyrosine Kinases ◽  
Maximal Response ◽  
Lower Sensitivity ◽  
Free Medium ◽  
Herbimycin A ◽  
Intracellular Calcium Level ◽  
Different Types ◽  
Intracellular Ca ◽  
Induced Changes ◽  
Glomerular Arterioles

Bradykinin (BK)-induced changes in intracellular calcium level ([Ca2+]i) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex. A distinction was made between thin and muscular EA. In AA and both types of EA, BK increased [Ca2+]ithrough activation of B2 receptors located only on the endothelium. The responses were not affected by nifedipine (10−6 M) and were smaller in a Ca2+-free medium, providing evidence that BK opens voltage-independent Ca2+ channels and mobilizes intracellular Ca2+. Thin EA differed from AA and muscular EA by a lower sensitivity to BK (EC50 = 6.95 ± 3.81 vs. 0.21 ± 0.08 and 0.18 ± 0.13 nM, respectively; P < 0.05), a higher maximal response (89 ± 5 vs. 57 ± 5 and 44 ± 7 nM; P < 0.001), and a spontaneous return to basal Ca2+ level, even in the presence of BK. Genistein (10−4 M) and herbimycin A (25 × 10−6M), specific inhibitors of tyrosine kinases, inhibited the [Ca2+]iresponses exclusively in AA. Genistein reduced the peak and plateau phases of responses by 69 ± 9 and 82 ± 6%, respectively, in a medium with Ca2+ and the peak by 48 ± 9% in a Ca2+-free medium. Similar reductions were observed with herbimycin A. These results show that dissimilar signal transduction pathways are involved in BK effects on juxtamedullary arterioles and that a tyrosine kinase activity could participate in the regulation of BK effect on AA but not on EA.

Involvement of protein kinase C, tyrosine kinases, and Rho kinase in Ca2+ handling of human small arteries

2000 ◽  
Vol 279 (3) ◽  
pp. H1228-H1238 ◽  
Author(s):  
M. Carmen Martínez ◽  
Voahanginirina Randriamboavonjy ◽  
Patrick Ohlmann ◽  
Narcisse Komas ◽  
Juan Duarte ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Tyrosine Kinases ◽  
Rho Kinase ◽  
Free Medium ◽  
Kinase C ◽  
Intracellular Ca ◽  
Pkc Inhibitors ◽  
Continuous Presence

The mechanisms of Ca2+ handling and sensitization were investigated in human small omental arteries exposed to norepinephrine (NE) and to the thromboxane A2 analog U-46619. Contractions elicited by NE and U-46619 were associated with an increase in intracellular Ca2+ concentration ([Ca2+]i), an increase in Ca2+-independent signaling pathways, or an enhancement of the sensitivity of the myofilaments to Ca2+. The two latter pathways were abolished by protein kinase C (PKC), tyrosine kinase (TK), and Rho-associated protein kinase (ROK) inhibitors. In Ca2+-free medium, both NE and U-46619 elicited an increase in tension that was greatly reduced by PKC inhibitors and abolished by caffeine or ryanodine. After depletion of Ca2+ stores with NE and U-46619 in Ca2+-free medium, addition of CaCl2 in the continuous presence of the agonists produced increases in [Ca2+]i and contractions that were inhibited by nitrendipine and TK inhibitors but not affected by PKC inhibitors. NE and U-46619 induced tyrosine phosphorylation of a 42- or a 58-kDa protein, respectively. These results indicate that the mechanisms leading to contraction elicited by NE and U-46619 in human small omental arteries are composed of Ca2+ release from ryanodine-sensitive stores, Ca2+ influx through nitrendipine-sensitive channels, and Ca2+ sensitization and/or Ca2+-independent pathways. They also show that the TK pathway is involved in the tonic contraction associated with Ca2+ entry, whereas TK, PKC, and ROK mechanisms regulate Ca2+-independent signaling pathways or Ca2+sensitization.

ACE and non-ACE mediated effect of angiotensin I on intracellular calcium mobilization in rat glomerular arterioles

2003 ◽  
Vol 284 (6) ◽  
pp. H1933-H1941 ◽  
Author(s):  
Jeannine Marchetti ◽  
Claudia M. B. Helou ◽  
Catherine Chollet ◽  
Rabary Rajerison ◽  
François Alhenc-Gelas
Keyword(s):  
Maximal Response ◽  
Ang Ii ◽  
Angiotensin I ◽  
Cysteine Protease Inhibitors ◽  
Peritubular Capillaries ◽  
Intracellular Calcium Mobilization ◽  
Intracellular Ca ◽  
Glomerular Hemodynamics ◽  
Chymase Inhibitor ◽  
Glomerular Arterioles

Because renin and angiotensin I (ANG I) level are high in the renal circulation, the conversion of ANG I is a critical step in the regulation of glomerular hemodynamics. We studied this conversion by investigating the effect of ANG I on intracellular Ca2+concentration ([Ca2+]i) in rat juxtamedullary glomerular afferent and efferent arterioles (AA and EA, respectively). Two types of EA were considered, thin EA and muscular EA, terminating as peritubular capillaries and vasa rectae, respectively. In all arterioles, ANG I elicited [Ca2+]i elevations. Maximal responses of 171 ± 28 (AA), 183 ± 7 (muscular EA), and 78 ± 11 nM (thin EA) ( n = 6), similar to those obtained with ANG II, were observed with 100 nM ANG I. The EC50 values were 20 times higher for ANG I than for ANG II in AA (10.2 vs. 0.5) and muscular EA (6.8 vs. 0.4 nM) and 150 times higher in thin EA (15.2 vs. 0.1 nM). ANG I effect was blocked by losartan, indicating that AT1 receptors were involved. The ANG-converting enyzme (ACE) inhibitor lisinopril inhibited the maximal response to ANG I in AA and muscular EA by 75 ± 9% ( n = 13) and 70 ± 7% ( n = 13), respectively, but had no effect in thin EA ( n = 14). The serine protease inhibitor aprotinin, the chymase inhibitor chymostatin, and the cysteine protease inhibitors E64 and leupeptin had no effect on ANG I action. These data show that ANG I effects are mainly mediated by ACE in AA and muscular EA but not in thin EA. The lisinopril-insensitive response may be related to conversion by unknown enzyme(s) and/or to activation of AT1 receptors by ANG I.

Methacholine-induced bronchoconstriction in dogs: effects of lung volume and O3 exposure

1988 ◽  
Vol 65 (6) ◽  
pp. 2679-2686 ◽  
Author(s):  
S. T. Kariya ◽  
S. A. Shore ◽  
W. A. Skornik ◽  
K. Anderson ◽  
R. H. Ingram ◽  
...  
Keyword(s):  
Lung Volume ◽  
Maximal Response ◽  
Maximal Effect ◽  
Response Curves ◽  
Lung Volumes ◽  
Before And After ◽  
Residual Capacity ◽  
Induced Changes ◽  
Conducting Airways ◽  
Concentration Response Curve

The maximal effect induced by methacholine (MCh) aerosols on pulmonary resistance (RL), and the effects of altering lung volume and O3 exposure on these induced changes in RL, was studied in five anesthetized and paralyzed dogs. RL was measured at functional residual capacity (FRC), and lung volumes above and below FRC, after exposure to MCh aerosols generated from solutions of 0.1-300 mg MCh/ml. The relative site of response was examined by magnifying parenchymal [RL with large tidal volume (VT) at fast frequency (RLLS)] or airway effects [RL with small VT at fast frequency (RLSF)]. Measurements were performed on dogs before and after 2 h of exposure to 3 ppm O3. MCh concentration-response curves for both RLLS and RLSF were sigmoid shaped. Alterations in mean lung volume did not alter RLLS; however, RLSF was larger below FRC than at higher lung volumes. Although O3 exposure resulted in small leftward shifts of the concentration-response curve for RLLS, the airway dominated index of RL (RLSF) was not altered by O3 exposure, nor was the maximal response using either index of RL. These data suggest O3 exposure does not affect MCh responses in conducting airways; rather, it affects responses of peripheral contractile elements to MCh, without changing their maximal response.

scholarly journals Herbimycin A Induces the 20 S Proteasome- and Ubiquitindependent Degradation of Receptor Tyrosine Kinases

1995 ◽  
Vol 270 (28) ◽  
pp. 16580-16587 ◽  
Author(s):  
Laura Sepp-Lorenzino ◽  
Zhengping Ma ◽  
David E. Lebwohl ◽  
Alexander Vinitsky ◽  
Neal Rosen
Keyword(s):  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Herbimycin A

scholarly journals The Role of Sequestrene 138 in Highbush Blueberry (Vaccinium corymbosum L.) Micropropagation

HortScience ◽  
2018 ◽  
Vol 53 (10) ◽  
pp. 1487-1493 ◽  
Author(s):  
Doina Clapa ◽  
Claudiu Bunea ◽  
Orsolya Borsai ◽  
Adela Pintea ◽  
Monica Hârța ◽  
...  
Keyword(s):  
Culture Media ◽  
Iron Concentration ◽  
Vaccinium Corymbosum ◽  
Carotenoid Content ◽  
Free Medium ◽  
Axillary Shoots ◽  
Different Types ◽  
The Media ◽  
Dark Green

The current research was carried out to investigate the effects of iron source in the culture media for Vaccinium corymbosum L. ʻBluerayʼ, ʻDukeʼ, and ʻPatriotʼ cultivars grown on five different types of medium (Woody Plant Medium supplemented with 1.0 mg·L−1 zeatin and 0, 25, 50, 75, and 100 mg·L−1 Sequestrene 138). After 10 weeks of culture, seven physiological parameters were measured, such as the number and length of axillary shoots, rooting and acclimatization percentage, as well as chlorophyll (a, b, a/b) and carotenoid content of the leaves. Adding Sequestrene 138 to the culture media led to a slight decrease of the proliferation rate but increased the length of the shoots. The chlorophyll and carotenoid content in all of the three cultivars was considerably increased as the iron concentration of the media increased. The shoots developed on the Sequestrene 138–free medium were chlorotic and short, whereas at different concentrations of iron in the culture medium the shoots were dark green and vigorous, providing a greater acclimatization success than those grown in iron-free medium.

Relationship between flow rate and NO production in postnatal mesenteric arteries

2001 ◽  
Vol 280 (1) ◽  
pp. G43-G50 ◽  
Author(s):  
Kristina M. Reber ◽  
Gennifer M. Mager ◽  
Charles E. Miller ◽  
Philip T. Nowicki
Keyword(s):  
Flow Rate ◽  
Kinase Inhibitor ◽  
Age Groups ◽  
Mesenteric Arteries ◽  
No Production ◽  
Herbimycin A ◽  
Wide Range ◽  
Intracellular Ca ◽  
Controlled Flow

We studied mesenteric arterial arcades from 3- and 35-day-old swine to determine the relationship between perfusate flow rate and release of nitric oxide (NO) into mesenteric effluent. Mesenteric arterial arcades were perfused under controlled-flow conditions with a peristaltic pump using warm oxygenated Krebs buffer. Basal rates of NO production were 43.6 ± 4.2 vs. 12.1 ± 2.5 nmol/min in 3- vs. 35-day-old mesentery during perfusion at in vivo flow rates (9 vs. 20 ml/min, respectively). Rate of NO production was directly related to flow rate over a wide range of flows (5–40 ml/min) in 3- but not 35-day-old mesentery. Both age groups demonstrated a brisk, albeit brief, increase in NO production in response to infusion of NO-dependent vasodilator substance P (10−8 M/min). Tyrosine kinase inhibitor herbimycin A andl-arginine analog l-NMMA significantly attenuated flow-induced increase in NO production, and phosphatase inhibitor phenylarsine oxide increased magnitude of flow-induced increase in NO production in 3-day-olds. Removal of extracellular Ca2+ and depletion of intracellular Ca2+ stores (Ca2+-free Krebs with EGTA plus thapsigargin) had no effect on NO production in either group. Thus, basal rate of NO production is greater in mesenteric arterial arcades from 3- than from 35-day old swine, a direct relationship between flow rate and NO production rate is present in mesentery from 3- but not 35-day-olds, and phosphorylation events are necessary for this interaction to occur.

Activation of pp60(src) is critical for stretch-induced orienting response in fibroblasts

1999 ◽  
Vol 112 (9) ◽  
pp. 1365-1373 ◽  
Author(s):  
X. Sai ◽  
K. Naruse ◽  
M. Sokabe
Keyword(s):  
Tyrosine Kinase ◽  
Tyrosine Phosphorylation ◽  
Tyrosine Kinases ◽  
Time Course ◽  
Kinase Inhibitor ◽  
Orienting Response ◽  
Cyclic Stretch ◽  
Wild Type ◽  
Herbimycin A ◽  
Molecular Masses

When subjected to uni-axial cyclic stretch (120% in length, 1 Hz), fibroblasts (3Y1) aligned perpendicular to the stretch axis in a couple of hours. Concomitantly with this orienting response, protein tyrosine phosphorylation of cellular proteins (molecular masses of approximately 70 kDa and 120–130 kDa) increased and peaked at 30 minutes. Immuno-precipitation experiments revealed that paxillin, pp125(FAK), and pp130(CAS) were included in the 70 kDa, and 120–130 kDa bands, respectively. Treatment of the cells with herbimycin A, a tyrosine kinase inhibitor, suppressed the stretch induced tyrosine phosphorylation and the orienting response suggesting that certain tyrosine kinases are activated by stretch. We focused on pp60(src), the most abundant tyrosine kinase in fibroblasts. The kinase activity of pp60(src) increased and peaked at 20 minutes after the onset of cyclic stretch. Treatment of the cells with an anti-sense S-oligodeoxynucleotide (S-ODN) against pp60(src), but not the sense S-ODN, inhibited the stretch induced tyrosine phosphorylation and the orienting response. To further confirm the involvement of pp60(src), we performed the same sets of experiments using c-src-transformed 3Y1 (c-src-3Y1) fibroblasts. Cyclic stretch induced a similar orienting response in c-src-3Y1 to that in wild-type 3Y1, but with a significantly faster rate. The time course of the stretch-induced tyrosine phosphorylation was also much faster in c-src-3Y1 than in 3Y1 fibroblasts. These results strongly suggest that cyclic stretch induces the activation of pp60(src) and that pp60(src) is indispensable for the tyrosine phosphorylation of pp130(CAS), pp125(FAK) and paxillin followed by the orienting response in 3Y1 fibroblasts.

Chronic Lung Disease of Prematurity

PEDIATRICS ◽  
1985 ◽  
Vol 76 (4) ◽  
pp. 652-652
Author(s):  
JAMES B. SCHICK ◽  
BOYD W. GOETZMAN
Keyword(s):  
Lung Disease ◽  
Premature Infants ◽  
Chronic Lung Disease ◽  
Potential Usefulness ◽  
Maximal Response ◽  
Days Of Therapy ◽  
Different Types ◽  
Toxic Drugs

To the Editor.— The paper by Avery et al,1 further demonstrates the potential usefulness of corticosteroids in chronic lung disease of prematurity. However, initial reports in 1974 and 1975 met with criticism for the use of potentially toxic drugs in premature infants.2,3 In 1983 we retrospectively reviewed 23 infants with chronic lung disease of prematurity who received corticosteroids and identified distinct differences between responders and nonresponders which suggested different types of lung disease.4 Our responders all showed a greater than 30% decrease in AaPo2 by day 6 and showed maximal response by ten days of therapy.

Multiple calcium mobilization pathways in single avian salt gland cells

1990 ◽  
Vol 258 (2) ◽  
pp. C289-C298 ◽  
Author(s):  
E. L. Stuenkel ◽  
S. A. Ernst
Keyword(s):  
Salt Gland ◽  
Transient Increase ◽  
Secretory Cells ◽  
Free Medium ◽  
Subsequent Removal ◽  
Intracellular Pool ◽  
Gland Cells ◽  
Agonist Stimulation ◽  
Induced Changes ◽  
Sustained Increase

Agonist-induced changes in intracellular Ca2+ concentration ([Ca2+]i) in individual secretory cells from the avian salt gland were detailed using dual-wavelength microspectrofluorimetry of the Ca2(+)-sensitive fluorescent probe fura-2. Resting [Ca2+]i averaged 42 +/- 5 nM. Stimulation with the cholinergic agonist carbachol (1 microM) resulted in a rapid increase in [Ca2+]i to 308 +/- 26 nM, which was sustained at a nearly constant elevated level (328 +/- 31 nM) throughout agonist application. In the absence of extracellular Ca2+ or in the presence of an inorganic blocker of Ca2+ entry (Ni2+, 1 mM), only a transient increase in [Ca2+]i occurred on agonist stimulation, whereas subsequent readmission of Ca2+ or washout of Ni2+ reinitiated a sustained increase in [Ca2+]i. The initial transient response results from Ca2+ release from intracellular stores, whereas the sustained phase represents entry of extracellular Ca2+ into the cytoplasm. Repetitive stimulations in Ca2(+)-free medium alternating with Ca2(+)-containing medium were performed to examine the mechanisms involved in refilling of the agonist-sensitive intracellular pool. After depletion of the intracellular pool by stimulation in Ca2(+)-free medium, removal of the agonist and readmission of Ca2+ resulted in a rapid transient increase in [Ca2+]i that could be blocked by Ni2+, La3+, or elevated K+. Subsequent removal of extracellular Ca2+ and restimulation nonetheless showed that complete refilling of the intracellular pool had occurred in each case. These results suggest that two separate Ca2(+)-entry mechanisms, one sensitive to Ni2+, La3+, and elevated K+ and responsible for the agonist-induced increase in [Ca2+]i and one insensitive to the blockers and involved in refilling of the intracellular pool, may exist in salt gland cells. Spontaneous oscillations of [Ca2+]i that are independent of extracellular Ca2+ have also been observed in 10% of the cells. The abolition of the oscillations by depletion of the agonist-sensitive pool suggests this pool as the Ca2+ source for the oscillations.

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