Effects of a selective and a nonselective muscarinic cholinergic antagonist on heart rate and intestinal motility in dogs

1997 ◽  
Vol 20 (5) ◽  
pp. 387-395 ◽  
Author(s):  
P.K. Hendrix ◽  
E.p. Robinson
Keyword(s):  
Heart Rate ◽  
Intestinal Motility ◽  
Cholinergic Antagonist ◽  
Muscarinic Cholinergic

scholarly journals Induction of long-lasting depolarization in medioventral medulla neurons by cholinergic input from the pedunculopontine nucleus

2005 ◽  
Vol 99 (3) ◽  
pp. 1127-1137 ◽  
Author(s):  
Keiko Mamiya ◽  
Kevin Bay ◽  
R. D. Skinner ◽  
E. Garcia-Rill
Keyword(s):  
Action Potential ◽  
Pedunculopontine Nucleus ◽  
Intracellular Recordings ◽  
Stable States ◽  
Cholinergic Agonist ◽  
Firing Rates ◽  
Cholinergic Antagonist ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states by activation of such descending targets as the caudal pons and the medioventral medulla (MED). Previously, PPN stimulation was reported to induce prolonged responses (PRs) in intracellularly recorded caudal pontine neurons in vitro. The present study used intracellular recordings in semihorizontal slices from rat brain stem (postnatal days 12–21) to determine responses in MED neurons following PPN stimulation. One-half (40/81) of MED neurons showed PRs after PPN stimulation. MED neurons with PRs had shorter duration action potential, longer duration afterhyperpolarization, and higher amplitude afterhyperpolarization than non-PR MED neurons. PR MED neurons were significantly larger (568 ± 44 μm2) than non-PR MED neurons (387 ± 32 μm2). The longest mean duration PRs and maximal firing rates during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. The muscarinic cholinergic agonist carbachol induced depolarization in all PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked carbachol- and PPN stimulation-induced PRs in all MED neurons tested. These findings suggest that PPN stimulation-induced PRs may be due to activation of muscarinic receptor-sensitive channels, allowing MED neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs in large MED neurons using parameters known best to induce locomotion.

Isolated parietal cells: [3H]QNB binding to putative cholinergic receptors

1980 ◽  
Vol 239 (3) ◽  
pp. G204-G209
Author(s):  
R. Ecknauer ◽  
W. J. Thompson ◽  
L. R. Johnson ◽  
G. C. Rosenfeld
Keyword(s):  
Specific Binding ◽  
Cholinergic Receptors ◽  
Parietal Cells ◽  
Cholinergic Antagonists ◽  
Single Population ◽  
Muscarinic Cholinergic Receptors ◽  
Cholinergic Antagonist ◽  
Muscarinic Cholinergic ◽  
Quinuclidinyl Benzilate

The tritiated muscarinic cholinergic antagonist quinuclidinyl benzilate, [3H]QNB, was used as a direct probe for the detection and characterization of muscarinic cholinergic receptors associated with the particulate fraction of isolated and purified rat gastric muscosal parietal cells. Specific binding is saturable (Bmax = 55 fmol/mg protein, KD = 0.78 nM), shows a single population of binding sites, and has appropriate pharmacological specificity. Nanomolar concentrations of muscarinic cholinergic antagonists, such as atropine and scopolamine, inhibit [3H]QNB binding by 50%, whereas micromolar concentrations are needed for agonists, such as acetylcholine, oxotremorine, and carbamylcholine. Binding is also stereoselective as shown by the more than 1,000-fold difference in inhibitory potencies of the stereoisomers of benzetimide. Noncholinergic agents, including pentagastrin, histamine, and the H2-receptor antagonists cimetidine and metiamide, have little or no effect on [3H]QNB binding at concentrations of 100 microM. These data support the existence of specific parietal cell muscarinic cholinergic receptors with which the secretagogue acetylcholine may directly interact to initiate gastric acid secretion.

scholarly journals Global Disturbances in Autonomic Function Yield Cardiovascular Instability and Hypertension in the Chromogranin A Null Mouse

Endocrinology ◽  
2009 ◽  
Vol 150 (11) ◽  
pp. 5027-5035 ◽  
Author(s):  
Jiaur R. Gayen ◽  
Yusu Gu ◽  
Daniel T. O'Connor ◽  
Sushil K. Mahata
Keyword(s):  
Chromogranin A ◽  
Baroreflex Sensitivity ◽  
Autonomic Function ◽  
Plasma Catecholamines ◽  
Conscious State ◽  
Null Mouse ◽  
Wild Type ◽  
Cholinergic Antagonist ◽  
Adrenergic Antagonist ◽  
Muscarinic Cholinergic

We reported previously that chromogranin A (Chga) knockout (KO) mice are hypertensive and hyperadrenergic. Here we sought to determine the basis of such alterations by probing physiological, biochemical, and pharmacological responses to perturbations of the autonomic nervous system. In the conscious state, KO mice had substantially elevated basal high blood pressure (BP) and heart rate (HR); immobilization stress caused increments in systolic BP and HR in both wild-type (WT) and KO mice, with higher maxima but blunted increments in the KO state. Catestatin (CST; CHGA352–372) selectively diminished stress-induced increments in BP and HR in KO mice, implicating CST as an antihypertensive peptide, even in stressful conditions. Heightened plasma catecholamines in KO mice returned to WT level after CST. Stress caused further increments in catecholamines in WT mice but no change in KO mice. KO mice displayed diminished baroreflex sensitivity in response to either phenylephrine or sodium nitroprusside, accounting for exaggerated pressor and depressor responses to these compounds; baroreceptor function was normalized by CST. To probe the relative roles of endogenous/basal sympathetic vs. parasympathetic tone in control of BP and HR, we used the muscarinic-cholinergic antagonist atropine or the β-adrenergic antagonist propranolol; HR and BP responses to each antagonist were exaggerated in KO animals. We conclude that ablation of Chga expression results in global disturbances in autonomic function, both sympathetic and parasympathetic, that can be abrogated (or rescued), at least in part, by replacement of CST. The results point to mechanisms whereby CHGA and its CST fragment act to control cardiovascular homeostasis.

Activation of the hypothalamic dorsomedial nucleus stimulates intestinal motility in rats

1995 ◽  
Vol 268 (3) ◽  
pp. G514-G521 ◽  
Author(s):  
B. Greenwood ◽  
J. A. DiMicco
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Gabaa Receptors ◽  
Intestinal Motility ◽  
Colonic Motility ◽  
Cardiovascular Effects ◽  
Behavioral Changes ◽  
Dorsomedial Nucleus ◽  
Cholinergic Pathways ◽  
Gaba Antagonist

Blockade of gamma-aminobutyric acidA (GABAA) receptors in the dorsomedial nucleus of the hypothalamus (DMH) in rats induced cardiovascular and behavioral changes resembling those associated with emotional stress. The purpose of this study was to test the hypothesis that microinjection of the GABA antagonist bicuculline methiodide (BMI) into the DMH of anesthetized rats would produce increases in intestinal motility measured manometrically with saline-filled cannulas. Arterial pressure and heart rate were also recorded. Microinjection of BMI (15-30 pmol/15 nl) into the region of the DMH elicited reproducible and dose-related increases in jejunal motility, colonic motility, heart rate, and arterial pressure. Similar microinjection at sites anterior to the DMH into or nearer to the hypothalamic paraventricular nucleus elicited significantly attenuated cardiovascular effects accompanied by either no change in intestinal function or changes that were significantly reduced. Either vagotomy or treatment with atropine methyl bromide (1 mg/kg i.v.) blocked the increase in jejunal motility and reduced but did not abolish the colonic stimulation. Increases in heart rate and arterial pressure were essentially unaffected by either intervention. The observations suggest that disinhibition of neurons in the DMH increases jejunal motility through vagal cholinergic pathways and enhances colonic motility through vagal and nonvagal cholinergic and noncholinergic pathways.

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