scholarly journals Purification of Histamine Receptor (III) Characterization of Receptor Rich Membrane Fraction of Small Intestinal Smooth Muscle of the Cat

1977 ◽  
Vol 27 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Masaatsu Uchida ◽  
Keijiro Takagi
Keyword(s):  
Smooth Muscle ◽  
Membrane Fraction ◽  
Histamine Receptor ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Role of stat6 in hypercontractility of murine small intestinal smooth muscle induced by nematode infection

2001 ◽  
Vol 120 (5) ◽  
pp. A534-A534
Author(s):  
A ZHAO ◽  
D MULLOY ◽  
J URBANJR ◽  
W GAUSE ◽  
T SHEADONOHUE
Keyword(s):  
Smooth Muscle ◽  
Nematode Infection ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Electrical activity of small intestinal smooth muscle and its temperature dependence

1975 ◽  
Vol 229 (5) ◽  
pp. 1268-1276 ◽  
Author(s):  
TY El-Sharkawy ◽  
EE Daniel
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Activity ◽  
Temperature Dependence ◽  
Intestinal Smooth Muscle ◽  
Plateau Phase ◽  
Control Activity ◽  
Electrical Control ◽  
Electrical Control Activity ◽  
Small Intestinal

Some important features of the intracellularly recorded electrical control activity of rabbit jejunal smooth muscle and its temperature dependence are reported in this study. This activity consisted of repetitive 18-mV depolarizations (control potentials (CP) or slow waves), which at 37degreesC lasted 2 s and had a frequency of 18/min and arose from a membrane potential of --55 mV. In some cells periods between CP's exhibited "diastolic" progressive depolarizations (intercontrol-potential depolarization), which may be the trigger of the CP in driving cells. While CP was usually monophasic, some cells persistently exhibited a notch early in the plateau phase. We suggest that CP consists of two components, an "initial depolarization" and a "secondary depolarization," which are usually fused together to give a monophasic potential. Cooling reduced CP frequency and prolonged its duration and caused more cells to show notching. While amplitude and rate of CP initial depolarization had low Q10's, duration and rates of onset and offset of the secondary depolarization had higher Q10's. Thus, the process responsible for secondary depolarization is more sensitive to temperature thant that underlying initial depolarization of the CP.

scholarly journals Improving Small Intestinal Motility in Experimental Acute Necrotising Pancreatitis by Modulating the CPI-17/MLCP Pathway Using Chaiqin Chengqi Decoction

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Ziqi Lin ◽  
Chenlong Zhang ◽  
Xiaoxin Zhang ◽  
Na Shi ◽  
Yongjian Wen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Intestinal Motility ◽  
Contractile Function ◽  
Specific Inhibitor ◽  
Intestinal Smooth Muscle ◽  
Fatty Acid Binding ◽  
Treatment Groups ◽  
Necrotising Pancreatitis ◽  
Acute Necrotising Pancreatitis ◽  
Small Intestinal

Protein kinase C-potentiated inhibitor protein of 17 kDa (CPI-17), a specific inhibitor of myosin light-chain phosphatase (MLCP) regulated by proinflammatory cytokines, is central for calcium sensitisation. We investigated the effects of chaiqin chengqi decoction (CQCQD) on the CPI-17/MLCP pathway in the small intestinal smooth muscle cells (SMCs) and strips (SMS) in an AP model. Necrotising AP was induced in rats by intraperitoneal injections (IPI) of L-ornithine (3.0 g/kg, pH 7.0; hourly × 2) at 1 hour apart; controls received saline. In treatment groups, carbachol (CCh; 60 μg/kg, IPI) or CQCQD (20 g/kg; 2-hourly × 3, intragastric) was administered. The necrotising AP model was associated with systemic inflammation (serum IL-1β and TNF-α) and worsened jejunum histopathology and motility (serum vasoactive intestinal peptide and intestinal fatty acid-binding protein) as the disease progressed. There was decreased intracellular calcium concentration ([Ca2+]i) SMCs. Contractile function of isolated SMCs was reduced and associated with down-regulated expression of key mRNAs and proteins of the CPI-17/MLCP pathway as well as increased IL-1β and TNF-α. CQCQD and CCh significantly reversed these changes and the disease severity. These data suggest that CQCQD can improve intestinal motility by modulating the CPI-17/MLCP pathway in small intestinal smooth muscle during AP.

Role of stat6 in hypercontractility of murine small intestinal smooth muscle induced by nematode infection

2001 ◽  
Vol 120 (5) ◽  
pp. A534 ◽  
Author(s):  
Aiping Zhao ◽  
Daniel P. Mulloy ◽  
Joseph F. Urban ◽  
William C. Gause ◽  
Terez Shea-Donohue
Keyword(s):  
Smooth Muscle ◽  
Nematode Infection ◽  
Intestinal Smooth Muscle ◽  
Small Intestinal

Responses of rabbit renal artery to histamine: receptor type and temperature dependence

1980 ◽  
Vol 58 (3) ◽  
pp. 306-309 ◽  
Author(s):  
D. A. Cook ◽  
D. M. Iwanow
Keyword(s):  
Smooth Muscle ◽  
Renal Artery ◽  
Histamine Receptor ◽  
Blocking Agent ◽  
Intestinal Smooth Muscle ◽  
Receptor Subtype ◽  
Temperature Dependent ◽  
Receptor Blocking ◽  
Dose Dependent ◽  
Reduced Temperature

The effects of histamine on spiral strips of rabbit renal artery have been recorded. Histamine causes dose-dependent contractions of this preparation which are not antagonized by the H2 receptor blocking agent metiamide, but which are blocked by the H1 antagonist diphenhydramine. The p42 for the latter agent is similar to that observed at 37 °C in intestinal smooth muscle. No evidence of a relaxant population of H2 receptors was encountered.Unlike that of intestinal smooth muscle, the response of strips of renal artery becomes progressively diminished at temperatures below about 20 °C, and the effect of reduced temperature on receptor subtype is thus more difficult to assess. It appears, however, that there is no change in type from the H1 receptor observed at 37 °C and thus the temperature-dependent transformation which has been reported previously does not occur in all H1 systems.

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