Characterization of receptors for angiotensin in the rat vas deferens

1979 ◽  
Vol 57 (4) ◽  
pp. 417-423 ◽  
Author(s):  
J. Magnan ◽  
D. Regoli
Keyword(s):  
Smooth Muscle ◽  
Vas Deferens ◽  
Proteolytic Enzymes ◽  
Rabbit Aorta ◽  
Rat Vas Deferens ◽  
Converting Enzyme ◽  
Response Curves ◽  
Sympathetic Nerve Stimulation ◽  
The Right

Experiments were performed in the rat vas deferens to characterize the receptor for angiotensin mediating the potentiation of the sympathetic nerve stimulation by this peptide. For this purpose we measured the order of potency of various angiotensins, the affinity of two specific and competitive antagonists, and we compared the effects of several angiotensins in tissues desensitized by angiotensin II.The potency of natural angiotensins follows the order: ATII > ATI > ATIII the relative potency of a few analogues which resist degradation by proteolytic enzymes as well as the potency of three L-Ala analogues of ATII show similar changes as those observed in other smooth muscle preparations (e.g. the rabbit aorta).Affinity of antagonists was evaluated by measuring pA2 and is higher for [Leu8]-ATII than for [des-Asp1, Leu8]-ATII. Both antagonists appear to be competitive since they displace the dose-response curves of ATII and ATIII to the right without changing the slope of the curves. Desensitization with ATII renders the tissues insensitive to ATIII and to other angiotensins without changing the response of the tissues to substance P.ATII does not modify the action of exogenous NA on nonstimulated tissues. ATI has no direct effect since its action is completely blocked in the presence of an inhibitor of the converting enzyme (SQ. 14225), while the responses of the vas deferens to ATII and substance P are unaltered.It is concluded that the receptor for ATII in the rat vas deferens is of the same type as the receptor mediating contraction of the rabbit aorta.

Characterization of sulfidopeptide leukotriene responses in sheep tracheal smooth muscle in vitro

1991 ◽  
Vol 69 (6) ◽  
pp. 805-811 ◽  
Author(s):  
K. Tomioka ◽  
J. T. Jackowski ◽  
W. M. Abraham
Keyword(s):  
Smooth Muscle ◽  
Dose Response ◽  
Tracheal Smooth Muscle ◽  
Response Curves ◽  
Leukotriene Antagonist ◽  
Dose Response Curves ◽  
The Right ◽  
Glutamyl Transpeptidase

We have investigated the effects of leukotrienes (LTs) on isolated tracheal smooth muscle from sheep sensitive to Ascaris suum antigen. LTC4 and LTD4 produced dose-dependent contractions of sheep trachea, but LTE4 was virtually inactive. YM-17690, a non-analogous LT agonist, produced no contractile response up to 100 μM. Indomethacin (5 μM) had no effect on LTC4- and LTD4-induced contractions. L-Serine borate (45 mM), an inhibitor of γ-glutamyl transpeptidase, shifted the dose–response curve of LTC4 to the left by 161-fold, and L-cysteine (6 mM), an inhibitor of aminopeptidase, shifted the dose–response curves of LTC4 and LTD4 to the left by 67- and 23-fold, respectively. YM-16638 (1 μM), an LT antagonist, shifted the dose–response curves of LTC4 and LTD4 to the right with pKB values of 6.57 and 7.13, respectively. YM-16638 did not affect LTC4-induced contractions of L-serine borate-treated tissues, indicating that the compound acts only on LTD4 receptors in sheep trachea. LTE4 (1 μM) shifted the dose–response curves of LTC4 and LTD4 to the right with pKB values of 6.87 and 7.31, respectively. YM-17690 (10 μM) showed effects similar to LTE4, suggesting that the compound acts as an LTE4 agonist in sheep trachea. These results suggest that in sheep tracheal smooth muscle (a) LTC4 and LTD4 produce contractions, (b) these LT-induced contractions are not mediated by cyclooxygenase products, (c) LTC4 is converted to LTD4 and then to LTE4, and (d) the potency of the LTC4- and LTD4-induced contractions is increased when their conversion to LTE4 is inhibited. This potentiation may result from the inability of LTE4 to contract sheep trachea and (or) its antagonist actions.Key words: leukotriene antagonist, receptors, asthma.

scholarly journals Subcellular-membrane characterization of [3H]ryanodine-binding sites in smooth muscle

1993 ◽  
Vol 290 (1) ◽  
pp. 259-266 ◽  
Author(s):  
Z D Zhang ◽  
C Y Kwan ◽  
E E Daniel
Keyword(s):  
Smooth Muscle ◽  
Ryanodine Receptor ◽  
Binding Sites ◽  
Vas Deferens ◽  
Smooth Muscles ◽  
Rat Vas Deferens ◽  
Detailed Characterization ◽  
Release Channel ◽  
Subcellular Membrane

The plant alkaloid ryanodine, known to interact selectively with the intracellular Ca(2+)-release channel in skeletal and cardiac muscles, has been repeatedly reported to affect smooth-muscle contractile functions that are consistent with its intracellular action at the Ca(2+)-release channel sites. Direct evidence for the binding of [3H]ryanodine to smooth-muscle membranes is sparse. Following our recent detailed characterization of functional effects of ryanodine and a preliminary report on the presence of [3H]ryanodine binding sites in rat vas deferens smooth muscle, we now report in this study a detailed characterization of binding of [3H]ryanodine to smooth muscle at the subcellular-membrane level. The ryanodine receptor in rat vas deferens muscle layer is primarily of smooth-muscle origin and is localized at the subcellular membrane site that is consistent with its role as a Ca(2+)-release channel in the sarcoplasmic reticulum (SR). Ryanodine binding to its receptor is Ca(2+)-dependent, with half-maximal binding occurring within the physiologically relevant cytosolic Ca2+ concentration. It is also sensitive to many factors, including change in Mg2+ concentration, ionic strength and osmolarity across the membrane vesicles. Agents known to inhibit (Ruthenium Red, Mg2+) or enhance (caffeine, Na+, K+) the Ca(2+)-induced Ca2+ release also inhibit or enhance the binding of ryanodine. Quantitative differences in ryanodine receptors exist among smooth muscles and do not seem to parallel their SR contents. Results from the present study indicate both the need and the basis for future investigations of the functional role of the ryanodine receptor in different smooth muscles.

Characterization of a continuous smooth muscle cell line derived from rabbit aorta

1989 ◽  
Vol 25 (10) ◽  
pp. 892-898 ◽  
Author(s):  
Maurice Nachtigal ◽  
Madan L. Nagpal ◽  
Phillip Greenspan ◽  
Sidonia A. Nachtigal ◽  
Alain Legrand
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cell ◽  
Cell Line ◽  
Muscle Cell ◽  
Rabbit Aorta ◽  
Muscle Cell Line

Extracellular calcium-dependent and -independent effects of adenosine in bovine coronary artery

1990 ◽  
Vol 68 (5) ◽  
pp. 608-613 ◽  
Author(s):  
Mudumbi V. Ramagopal ◽  
S. Jamal Mustafa
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Extracellular Calcium ◽  
Free Medium ◽  
Response Curves ◽  
Coronary Smooth Muscle ◽  
Calcium Dependent ◽  
Relaxation Responses ◽  
The Right

Adenosine relaxes the coronary arteries of various species through A2 receptors. The aim of the present investigation was to evaluate the relaxing effects of adenosine in relation to the role of calcium in bovine coronary arteries by studying the vasodilatory effect of adenosine in normal and calcium-free medium and on calcium-45 efflux into calcium-free medium. Acetylcholine (ACh) and norepinephrine (NE) were used to induce tone in coronary artery rings. Adenosine, 5′-(N-ethylcarboxamido)adenosine (NECA), and N6-(L-phenylisopropyl)adenosine (L-PIA) produced concentration-dependent relaxations of the coronary artery rings. Both in normal and calcium-free medium, the order of potency for adenosine analogs (NECA > L-PIA > adenosine) was similar and 8-phenyltheophylline antagonized the relaxation responses to adenosine and its analogs. Removal of extracellular calcium shifted the concentration–response curves to the right in a parallel fashion, slowed the rate of relaxation, and in NE contracted rings reduced the maximum responses for adenosine and its analogs. In calcium-free medium, adenosine was without an effect on calcium-45 efflux in the presence of ACh. However, adenosine inhibited the stimulated calcium-45 efflux induced by NE. The data suggest that the vasodilatory action of adenosine in bovine coronary smooth muscle has both extracellular calcium-dependent and -independent components.Key words: adenosine receptors, calcium, coronary circulation, vascular smooth muscle, acetylcholine, norepinephrine.

Characterization of responses of neonatal sinus and AV nodes to critically timed, brief vagal stimuli

1991 ◽  
Vol 260 (2) ◽  
pp. H459-H464 ◽  
Author(s):  
S. Yamasaki ◽  
A. Stolfi ◽  
A. S. Pickoff
Keyword(s):  
Cycle Length ◽  
Cardiac Cycle ◽  
Gradual Increase ◽  
Latency Period ◽  
Atrial Pacing ◽  
Response Curves ◽  
Stimulus Train ◽  
Sinus Cycle Length ◽  
The Right

We studied the responses of sinus cycle length and atrioventricular (AV) nodal conduction to brief, critically timed vagal stimuli in 25 neonatal (9.6 +/- 3.1 days) canines. Vagal stimuli were delivered to the right or left decentralized cervical vagosympathetic trunk as either a single, brief stimulus train or a repetitive, phase-coupled train with both stimulation paradigms programmed to scan the entire cardiac cycle. The effects of brief vagal stimuli on cardiac cycle length were measured while the heart was beating spontaneously, and the vagal effects on AV nodal conduction were measured while the cycle length was held constant by atrial pacing at 300 ms. Neither changes in sinus cycle length nor AV nodal conduction demonstrated classical phase dependency, i.e., a gradual increase in the magnitude of the vagal response as stimuli are delivered progressively later in the cardiac cycle until the latency period (that point in the cardiac cycle at which vagal stimulation no longer affects the next cardiac cycle) is reached. Phase-response curves (PRCs) to single and repetitive stimuli typically exhibited either a flat response or a small decrease in magnitude as the latency period of the PRC was approached. Thus the neonatal sinus and AV node PRCs exhibit a different configuration than that reported in the adult.

Effect of NO donors on protein phosphorylation in intact vascular and nonvascular smooth muscles

2001 ◽  
Vol 280 (4) ◽  
pp. H1565-H1580 ◽  
Author(s):  
James K. Hennan ◽  
Jack Diamond
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Protein Phosphorylation ◽  
Vas Deferens ◽  
Smooth Muscles ◽  
Rat Aorta ◽  
Rat Vas Deferens ◽  
Two Dimensional Gel Electrophoresis ◽  
Relaxant Response ◽  
Underlying Mechanisms

It is generally well accepted that nitrovasodilator-induced relaxation of vascular smooth muscle involves elevation of cGMP and activation of a specific cGMP-dependent protein kinase [protein kinase G (PKG)]. However, the protein targets of PKG and the underlying mechanisms by which this kinase leads to a relaxant response have not been elucidated. Several types of smooth muscle, including rat myometrium and vas deferens, are not relaxed by sodium nitroprusside, even at concentrations that produce marked elevation of cGMP and activation of PKG. The main objective of our studies was to compare PKG-mediated protein phosphorylation in intact rat aorta, rat myometrium, and rat vas deferens using two-dimensional gel electrophoresis. In intact rat aorta, seven PKG substrates were detected during relaxation of the tissue. None of the PKG substrates identified in the rat aorta appeared to be phosphorylated in the myometrium or vas deferens after administration of various cGMP-elevating agents. Thus the failure of the rat myometrium and rat vas deferens to relax in the face of cGMP elevation and PKG activation may be due to a lack of PKG substrate phosphorylation.

Ca2+ handling properties of microsomal subfractions of rat vas deferens smooth muscle

1984 ◽  
Vol 62 (1) ◽  
pp. 76-79 ◽  
Author(s):  
A. K. Grover ◽  
C. Y. Kwan
Keyword(s):  
Smooth Muscle ◽  
Concentration Dependence ◽  
Vas Deferens ◽  
Membrane Vesicles ◽  
Rat Vas Deferens ◽  
Enzyme Marker ◽  
Isopycnic Centrifugation ◽  
Stimulation Of ◽  
Ph Profiles

The rat vas deferens smooth muscle microsomes on isopycnic centrifugation gave two fractions, namely F2 (15–30% sucrose) and F3 (30–40% sucrose), with comparable ATP-dependent azide-insensitive Ca2+-uptake capacities, although these fractions differed from each other in various enzyme marker activities. The fractions F2 and F3 also show similar pH profiles for the ATP-independent and ATP-dependent Ca2+ uptake, and similar ionized Ca2+-concentration dependence for the ATP-dependent Ca2+ uptake. However, the fractions F2 and F3 differ from each other in that: (a) F3 shows higher permeability to Ca2+, and (b) F3 shows higher stimulation of the ATP-dependent Ca2+ uptake by oxalate. The F3 fraction can also be used to obtain membrane vesicles loaded with Ca2+ oxalate in the presence of ATP. However, the yield of the Ca2+ oxalate enriched fraction is too low to permit their further characterization.

scholarly journals Regulation of smooth muscle contractility by the epithelium in rat vas deferens: role of ATP-induced release of PGE2

2008 ◽  
Vol 586 (20) ◽  
pp. 4843-4857 ◽  
Author(s):  
Ye Chun Ruan ◽  
Zhe Wang ◽  
Jian Yang Du ◽  
Wu Lin Zuo ◽  
Jing Hui Guo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vas Deferens ◽  
Rat Vas Deferens ◽  
Muscle Contractility ◽  
Smooth Muscle Contractility

Studies on antihypertensive and antispasmodic activities of Andropogon muricatus Retz.This article is one of a selection of papers published in this special issue (part 1 of 2) on the Safety and Efficacy of Natural Health Products.

2007 ◽  
Vol 85 (9) ◽  
pp. 911-917 ◽  
Author(s):  
Anwar H. Gilani ◽  
Abdul J. Shah ◽  
Khalid H. Janbaz ◽  
Shahida P. Ahmed ◽  
Muhammad N. Ghayur
Keyword(s):  
Calcium Channel ◽  
Rabbit Aorta ◽  
Natural Health Products ◽  
Response Curves ◽  
Medicinal Uses ◽  
Health Products ◽  
Rabbit Jejunum ◽  
The Right

The aqueous-methanolic crude extract of Andropogon muricatus (Am.Cr) was investigated pharmacologically to determine some of its medicinal uses in cardiovascular and gastrointestinal disorders. A series of in vivo and in vitro studies were conducted to evaluate dose-dependent effects of Am.Cr on mean arterial pressure (MAP), cardiac and vascular contractions, and to further investigate the potential mechanism of action. Intravenous administration of Am.Cr (10–50 mg/kg) caused a fall (18%–56%) in MAP in normotensive rats under anesthesia. When tested in isolated guinea pig atria, Am.Cr (0.03–5.0 mg/mL) exhibited a cardiodepressant effect on the rate and force of spontaneous contractions. In isolated rabbit aorta, Am.Cr caused inhibition of K+ (80 mmol/L)-induced contractions at a lower concentration than of phenylephrine. In isolated rabbit jejunum preparations, Am.Cr (0.01–0.10 mg/mL) caused relaxation of spontaneous and high K+ (80 mmol/L)-induced contractions, suggesting that the spasmolytic effect is mediated possibly through calcium channel blockade (CCB). The CCB activity was confirmed when pretreatment of the tissue with Am.Cr (0.03–0.1 mg/mL) shifted the Ca2+ dose–response curves to the right, similar to that caused by verapamil. These data indicate that the blood pressure-lowering and spasmolytic effects of Am.Cr are mediated possibly through a calcium channel blocking activity. Phytochemical screening of Am.Cr revealed the presence of phenols, saponins, tannins, and terpenes, which may be responsible for the observed vasodilator, cardiodepressant, and antispasmodic activities. This study shows potential with respect to its medicinal use in cardiovascular and gut disorders.

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