The effect of several α-adrenoceptor antagonists on the response to histamine in various tissues

1980 ◽  
Vol 58 (1) ◽  
pp. 40-44 ◽  
Author(s):  
K. M. MacLeod ◽  
C. A. Krueger ◽  
D. Smith ◽  
D. M. Iwanow ◽  
D. A. Cook
Keyword(s):  
Guinea Pig ◽  
Portal Vein ◽  
Right Ventricle ◽  
Induced Response ◽  
Guinea Pig Ileum ◽  
Receptor System ◽  
Guinea Pig Heart ◽  
Rabbit Portal Vein ◽  
Histamine Response ◽  
Antagonist Effect

The effect of various α-receptor antagonists on the histamine-induced response of guinea pig ileum, guinea pig heart, and rabbit portal vein have been studied. In guinea pig ileum, an H1 receptor system, phenoxybenzamine and dibozane are effective antagonists, phentolamine is a weak antagonist, azapetine is without antagonist effect, and tolazoline is a weak agonist. In the H2 system of guinea pig right ventricle, phentolamine and azapetine are antagonists, phenoxybenzamine and dibozane are inactive, and tolazoline is an agonist. All antagonists except tolazoline block the histamine response in portal vein which is believed to be mediated by a receptor of low selectivity. Tolazoline is an agonist in portal vein.

scholarly journals Lowering of the extracellular Na+ concentration enhances high-K+-induced formation of inositol phosphates in the guinea-pig ileum

1988 ◽  
Vol 252 (3) ◽  
pp. 883-888 ◽  
Author(s):  
T Sasaguri ◽  
S P Watson
Keyword(s):  
Guinea Pig ◽  
Inositol Phosphates ◽  
Induced Response ◽  
Guinea Pig Ileum ◽  
Tissue Slices ◽  
Phospholipid Hydrolysis ◽  
Collagenase Treatment ◽  
High K ◽  
K Concentration ◽  
Dispersed Cells

1. Formation of inositol phosphates (InsPs) was measured in cross-chopped slices or dispersed cells, isolated by collagenase treatment, of guinea-pig ileum longitudinal smooth muscle pre-labelled with [3H]inositol. 2. Elevation of the extracellular K+ concentration by equimolar replacement of Na+ induced accumulation of InsPs in the dispersed cells and in the tissue slices. These effects were blocked by neither tetrodotoxin (1 microM) nor atropine (10 microM), and were approximately additive with carbachol-induced accumulation. 3. In the tissue slices, the response to K+ was partially inhibited by nifedipine (10 microM) and by CdCl2 (0.3 mM), but the carbachol-induced response was not altered. 4. Accumulation of InsPs induced by KCl-excess solution (high-K+ solution without Na+ replacement) was suppressed strongly by nifedipine and completely by CdCl2. The response to KCl excess was approx. 40% of that to high K+ with Na+ replacement. 5. Low-NaCl solution (replacement of NaCl with equimolar sucrose) also produced InsPs, and this was not blocked by either nifedipine (10 microM) or CdCl2 (0.3 mM). 6. The formation of InsPs by a maximally effective concentration of carbachol (1 mM) in the presence of KCl excess or low NaCl was greater than the additive effect of the two stimuli on their own. Enhancement of the carbachol-induced response by KCl excess disappeared in the presence of CdCl2 (0.3 mM). 7. These data suggest that formation of InsPs induced by high-K+ solution with equimolar replacement of Na+ consists of two components, i.e. high-K+-induced inositol-phospholipid hydrolysis by Ca2+ entry through voltage-sensitive channels, and low-Na+-induced formation of InsPs, insensitive to Ca2+ antagonists, but that both of them do not contribute significantly to the activation of phospholipase C by muscarinic stimuli.

Temperature and histamine receptor function—what is really happening?

1985 ◽  
Vol 63 (6) ◽  
pp. 751-755 ◽  
Author(s):  
D. A. Cook ◽  
C. A. Krueger ◽  
A. Michalchuk
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Low Temperatures ◽  
Histamine Receptor ◽  
Receptor Function ◽  
Guinea Pig Ileum ◽  
Abundant Evidence ◽  
Cast Doubt ◽  
Histamine Response ◽  
New Evidence

Early studies suggested that at low temperatures there was a transition of receptor type from an H1 to an H2 receptor when the temperature was reduced from 37 °C to temperatures below 20 °C. These original observations were based on the development of sensitivity of guinea-pig ileum to the H2 antagonist metiamide as the temperature was reduced. More recently, evidence from a number of laboratories has cast doubt on the existence of a simple H1–H2 receptor transition, but there is abundant evidence that there are major changes in the response of a variety of smooth muscle preparations to histamine at reduced temperatures. The evidence in regard to alterations in histamine response at low temperatures is reviewed, some new evidence presented, and a model which is consistent with most of the observations is suggested.

scholarly journals A poly(ADP-ribose) synthetase inhibitor, benzamide protects smooth muscle cells but not endothelium against ischemia/reperfusion injury in isolated guinea-pig heart.

2007 ◽  
Vol 54 (1) ◽  
pp. 199-204
Author(s):  
Andrzej Jakubowski ◽  
Magdalena Lomnicka
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Smooth Muscle Cells ◽  
Reperfusion Injury ◽  
Cellular Response ◽  
Coronary Circulation ◽  
Muscle Cells ◽  
Induced Response ◽  
Guinea Pig Heart ◽  
Coronary Smooth Muscle

Activation of the nuclear enzyme poly(ADP-ribose) synthetase (PARS) is important in the cellular response to oxidative stress. During ischemia and reperfusion (I/R) increased free radical production leads to DNA breakage that stimulates PARS which in turn results in an energy-consuming metabolic cycle and initiation of the apoptotic process. Previous studies have reported that PARS inhibition confers protection in various models of I/R-induced cardiovascular damage. The purpose of this study was to determine the role of PARS inhibition in I/R-induced injury of smooth muscle cells and endothelium in the coronary circulation of the isolated guinea-pig heart. Control hearts and those treated with a PARS inhibitor--benzamide (100 micromol L(-1)), were subjected to 30 min of subglobal ischemia and subsequent reperfusion (90 min). To analyze the functional integrity of smooth muscle cells and endothelium, one-minute intracoronary infusions of endothelium-independent (sodium nitroprusside, NaNP; 3 micromol L(-1)) and endothelium-dependent (substance P, SP; 10 nmol L(-1)) vasodilators were used before ischemia and at the reperfusion time. The degree of the injury of coronary smooth muscle and endothelial cells induced by I/R was estimated in terms of diminished vasodilator responses to NaNP (at 55 min and 85 min of reperfusion) and to SP (at 70 min of reperfusion), respectively, and expressed as the percentage of preischemic response. I/R reduced vasorelaxant responses to both vasodilators by half (to 54.1 +/- 5.1% and to 53.6 +/- 4.9% of preischemic value for NaNP at 55 min and 85 min of reperfusion, respectively and to 45.9 +/- 6.5% for SP at 70 min of reperfusion). PARS inhibition provided complete restoration of vasorelaxation induced by NaNP (107.6 +/- 13.3% and 104 +/- 14.4% of preischemic response at the two time points of reperfusion, respectively). However, there was no effect on the SP-induced response (48+12.1% of preischemic response). We conclude that pharmacological PARS inhibition with benzamide protects coronary smooth muscle cells but not endothelium against I/R-induced reperfusion injury in the coronary circulation of the guinea-pig heart.

New agonist and antagonist analogues of bradykinin

1984 ◽  
Vol 62 (6) ◽  
pp. 627-629 ◽  
Author(s):  
J. Barabé ◽  
S. Caranikas ◽  
P. D'Orléans-Juste ◽  
D. Regoli
Keyword(s):  
Guinea Pig ◽  
Jugular Vein ◽  
Rabbit Aorta ◽  
Guinea Pig Ileum ◽  
Receptor System ◽  
Relative Affinity ◽  
Agonist And Antagonist

Three new analogues of bradykinin (BK) have been tested for their agonistic and antagonistic actions on the rabbit jugular vein and the guinea pig ileum (B2 receptors), and six were studied on rabbit aorta strips (B1 receptors). Substitution of Gly4, Phe5, and Phe8 in BK with D-Trp gives analogues with a relative affinity lower than 1.0% as compared with BK. These analogues have no antagonistic properties on the rabbit jugular vein and on guinea pig ileum (B2 receptors). Substitution of Pro7 in des-Arg9-BK by Gly and by D-Ala give compounds that antagonise the effects of kinins on the rabbit aorta strips (B1-receptor system). These new antagonists are fairly potent with a pA2 value of 6.03 to 7.29 and seem competitive because the pA2 – pA10 values approximate 0.95. These results suggest that the orientation of Phe8 is critical for the activation of B1 receptors by kinins.

Mitochondrial Oxidation of p-N, N-Dimethylamino-β-Phenethylamine (DAPA)

1975 ◽  
Vol 33 ◽  
pp. 458-459
Author(s):  
W. Allen Shannon ◽  
Hannah L. Wasserkrug ◽  
andArnold M. Seligman
Keyword(s):  
Guinea Pig ◽  
Oxidase Activity ◽  
Amine Oxidase ◽  
Histochemical Demonstration ◽  
Guinea Pig Heart ◽  
Pig Kidney ◽  
Cytoplasmic Vacuoles ◽  
Liver And Kidney ◽  
Mitochondrial Oxidation ◽  
Amine Oxidase Activity

The synthesis of a new substrate, p-N,N-dimethylamino-β-phenethylamine (DAPA)3 (Fig. 1) (1,2), and the testing of it as a possible substrate for tissue amine oxidase activity have resulted in the ultracytochemical localization of enzyme oxidase activity referred to as DAPA oxidase (DAPAO). DAPA was designed with the goal of providing an amine that would yield on oxidation a stronger reducing aldehyde than does tryptamine in the histochemical demonstration of monoamine oxidase (MAO) with tetrazolium salts.Ultracytochemical preparations of guinea pig heart, liver and kidney and rat heart and liver were studied. Guinea pig kidney, known to exhibit high levels of MAO, appeared the most reactive of the tissues studied. DAPAO reaction product appears primarily in mitochondrial outer compartments and cristae (Figs. 2-4). Reaction product is also localized in endoplasmic reticulum, cytoplasmic vacuoles and nuclear envelopes (Figs. 2 and 3) and in the sarcoplasmic reticulum of heart.

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