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At least 235 records · Page 13Linked to original sources
PubMed1986

Effect of angiotensin II on mechanical and electrical responses of frog, chick and rat skeletal muscle.

The effect of angiotensin II (AII) on neuromuscular transmission and muscle contraction was investigated by analyzing its effect on electrically-evoked twitch and tetanic contractions in response to motor nerve stimulation at 0.2 Hz and 20 Hz, respectively, the amplitude and duration of frog sciatic nerve compound action potential (NCAP), the uptake (and release) of 3H-methylcholine into/by the nerve-muscle preparation, and the contractures produced by depolarizing agents, e.g. acetylcholine (ACh) and tetraethylammonium (TEA) in the chick, frog and rat skeletal muscle. The results showed that AII, in low concentrations (0.1-10 nM), may facilitate neuromuscular transmission by increasing the amplitudes of indirectly-elicited twitch and tetanic contractions, by increasing the uptake of 3H-methylcholine, and by increasing the duration of the frog NCAP, by about 86%. In high concentrations (greater than 1 microM), AII had inhibitory effects on neuromuscular transmission and produced a small contracture on its own in the muscle (0.4 +/- 0.01 g of tension, n = 6).

Acetylcholine↗
PubMed2001

Sparks and puffs in oligodendrocyte progenitors: cross talk between ryanodine receptors and inositol trisphosphate receptors.

Investigating how calcium release from the endoplasmic reticulum (ER) is triggered and coordinated is crucial to our understanding of how oligodendrocyte progenitor cells (OPs) develop into myelinating cells. Sparks and puffs represent highly localized Ca(2+) release from the ER through ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP(3)Rs), respectively. To study whether sparks or puffs trigger Ca(2+) waves in OPs, we performed rapid high-resolution line scan recordings in fluo-4-loaded OP processes. We found spontaneous and evoked sparks and puffs, and we have identified functional cross talk between IP(3)Rs and RyRs. Local events evoked using the IP(3)-linked agonist methacholine (MeCh) showed significantly different morphology compared with events evoked using the caffeine analog 3,7-dimethyl-1-propargylxanthine (DMPX). Pretreatment with MeCh potentiated DMPX-evoked events, whereas inhibition of RyRs potentiated events evoked by low concentrations of MeCh. Furthermore, activation of IP(3)Rs but not RyRs was critical for Ca(2+) wave initiation. Using immunocytochemistry, we show OPs express the specific Ca(2+) release channel subtypes RyR3 and IP(3)R2 in patches along OP processes. RyRs are coexpressed with IP(3)Rs in some patches, but IP(3)Rs are also found alone. This differential distribution pattern may underlie the differences in local and global Ca(2+) signals mediated by these two receptors. Thus, in OPs, interactions between IP(3)Rs and RyRs determine the spatial and temporal characteristics of calcium signaling, from microdomains to intracellular waves.

Aniline Compounds↗
PubMed1991

Characterization of bradykinin receptors in peripheral organs.

Bradykinin (BK) and related kinins are potent stimulants of the rabbit jugular vein, the hamster urinary bladder, and the guinea pig trachea. The characterization of kinin receptors in these tissues was made with agonists and antagonists. Results obtained with agonists indicate that bradykinin and kallidin are much more active than des-Arg9-BK and suggest the presence of B2 receptors in the three organs. Some new agonists were also tested and the BK analogue, [Hyp3,Tyr(Me)8]BK, was found to be a potent and selective stimulant of the three preparations, with pD2 values of 8.56, 8.00, and 8.39, respectively, but inactive on the rabbit aorta (a B1-receptor system). Contractile effects of kinins in the rabbit jugular vein and hamster urinary bladder were reduced or eliminated by B2-receptor antagonists but at different concentration levels; e.g., acetyl-D-Arg[Hyp3,D-Phe7]BK showed pA2 values of 7.78 on the rabbit jugular vein but only 5.72 on hamster urinary bladder. This compound contracted the guinea-pig trachea and was found to be inactive as an antagonist on this preparation. Contractions of the hamster urinary bladder and the guinea-pig trachea in response to bradykinin were markedly reduced or eliminated by indomethacin and by BW 755C, while those of the rabbit jugular vein were not modified. The present findings indicate that the myotropic effect of kinins on the rabbit jugular vein depends on the activation of B2 receptors and suggest that B2 receptors are largely responsible also for the response of the hamster urinary bladder. B2 receptors and (or) a nonreceptor mechanism appear to be involved in the stimulant effects of the kinin agonists and some antagonists in the guinea-pig trachea.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1985

Actions of polypeptides at the neuromuscular junction.

The effects of several polypeptides, e.g. angiotensin II, substance P, oxytocin and vasopressin, on the isolated frog gastrocnemius, chick biventer cervicis and rat hemodiaphragm preparations were studied using electrophysiological and neurochemical techniques. The effects of angiotensin II, substance P, oxytocin and vasopressin on neuromuscular transmission and muscle contraction were investigated by studying the following parameters: the directly and indirectly-elicited twitch and tetanic contractions, nerve compound action potential, uptake of 3H-methylcholine into nerve-muscle preparations, the contractures produced by depolarizing drugs, e.g. ACh or TEA. The results showed that angiotensin II (10(-10)-10(-6) M) and substance P (10(-7)-10(-6) M) enhanced neuromuscular transmission and muscle contraction by increasing the amplitudes of the indirectly-elicited twitch and tetanic contractions. Oxytocin and vasopressin (1-100 mU/ml-1) both depressed neuromuscular transmission by reducing the contractile and electrical response in the frog, chick and rat skeletal muscle. It was concluded that, like their effects on ganglionic transmission, the peptides can modify neuromuscular transmission. The mechanism by which these peptides produce their effects may be dependent on external calcium concentration. These peptides may affect both pre- and postjunctional mechanisms; prejunctionally by increasing/decreasing the release of ACh, and postjunctionally by affecting the sensitivity of the postjunctional membrane to depolarizing drugs and/or producing a contracture in the skeletal muscle.

Action Potentials↗
PubMed1975

Two cases of acute pandysautonomia.

Two men had acute nonprogressive pandysautonomia. Both of them showed orthostatic hypotension, fainting in upright position, pupillary disturbances, diminished sweating, anacidity, and impotence. Case 1 showed considerable but inadequate improvement within 31 months. Case 2 recovered completely after 11 months. Clinical and pharmacodynamic investigations suggested that the main lesion was located in postganglionic fibers in case 1 and in preganglionic fibers in case 2. The cause of this disorder is unknown, although both patients had undergone substantial weight loss.

Acetylcholine↗
PubMed1975

Myotonic pupils in Charcot-Marie-Tooth disease. Successful relief of symptoms with 0.025% pilocarpine.

Twenty-seven members of a family with dominantly inherited Charcot-Marie-Tooth disease (CMTD) were examined. Fifteen members had CMTD and 13 of these had varying amounts of myotonic pupillary abnormalities similar in some ways to Adie tonic pupil syndrome. Those with graver neurologic disease showed greater pupillary abnormalities. Ten of the 15 patients had pupillary constriction with methacholine chloride (Mecholyl) and some of these had extensive iris atrophy. Several affected patients received symptomatic relief from 0.025% pilocarpine. Seven other patients with CMTD who were not related to our initial family were checked for myotonic pupils; two had findings similar to our initial family. Pupillary abnormalities in certain patients with CMTD appear secondary to a parasympathetic denervation of the iris sphincter and ciliary muscle, as shown by a positive methacholine test, and probably represent part of the autonomic nervous system dysfunction associated with the polyneuropathy in CMTD.

Adult↗
PubMed1982

Medical therapy for experimental hypotony.

Experimental hypotony was induced in rhesus monkeys by the following procedures: ciliochoroidal detachment, retinal detachment, or cyclodialysis. Two days later, at the time of greatest hypotony, 10% methacholine chloride was deposited in the cornea by iontophoresis, and 0.25% physostigmine salicylate ointment was applied topically to each eye. The intraocular pressure rose to normal levels in all eyes for eight to 24 hours. The peak rise in IOP occurred one to four hours after drug administration and was 7.2, 6.8, and 11.3 mm Hg higher than the pretreatment levels in eyes with ciliochoroidal detachment, retinal detachment, and cyclodialysis, respectively. In a group of normal eyes, this drug combination caused a transient 5.7 mm Hg fall in IOP. The mechanism of pressure elevation by methacholine and physostigmine probably is caused by stimulation of aqueous humor formation or reduced uveoscleral outflow, or both.

Administration, Topical↗
PubMed1986

Cholinergic receptors in the upper respiratory system of the rat.

Radioligand receptor binding might give more detailed information on the innervation pattern of the nasal mucosa and the character of the various neuroreceptors involved. With respect to the cholinergic receptors, this technique reveals that specific binding of tritiated I-quinuclidinyl benzilate to rat nasal mucosa homogenates occurs to a homogeneous class of binding sites, with a dissociation constant of 0.06 +/- 0.02 nM and a receptor density of 8 +/- 2 pmole/g of tissue. Binding is stereoselectively inhibited by benzetimide hydrochloride enantiomers. Pirenzepine displacement (inhibition constant = 0.5 X 10(-6) M) classifies tritiated I-quinuclidinyl benzilate binding sites as M2-muscarinic receptors. Methylfurthrethonium inhibits tritiated I-quinuclidinyl benzilate binding at high concentrations, pointing to the presence of low-affinity agonist binding sites, probably admixed with a small proportion of high-affinity agonist binding sites. These data obtained in the rat open new perspectives for studying muscarinic receptors in the human nose to elucidate the supposed disturbance of autonomic nerve regulation in nasal hyperreactivity.

Animals↗