PubMed · 11094053
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B A Kingwell, G L Jennings, A M Dart. 2000-11-28. Exercise and endothelial function.. https://doi.org/10.1161/01.cir.102.22.e179
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To determine if vascular smooth muscle from teleost and agnathan fishes expresses receptors for signaling agents that are important in vascular tension in other vertebrates, we exposed rings of aortic vascular smooth muscle from the eel (Anguilla rostrata), the hagfish (Myxine glutinosa), and the lamprey (Petromyzon marinus) to a suite of putative agonists, including: acetylcholine, endothelin, nitric oxide, natriuretic peptides, and prostanoids. Acetylcholine constricted aortic rings from the eel, but had no effect on the rings from lamprey. On the other hand, endothelin constricted rings from all three species. Use of receptor-specific ET agonists demonstrated that only ET(A) receptors are expressed in the eel and lamprey aorta. The nitric oxide donor sodium nitroprusside or nitric oxide itself dilated rings from the eel, but both agonists constricted rings from the hagfish and NO produced a biphasic response (constriction followed by dilation) in the lamprey. Two natriuretic peptides, eel ANP and porcine CNP, produced marginally significant dilation in the eel aorta, human ANP dilated the hagfish rings, and pCNP and eANP dilated the lamprey rings. The prostanoids PGE(1) and PGE(2) both dilated the eel aortic rings, and PGE(1) and carbaprostacyclin (stable PGI(2) agonist) dilated the hagfish and lamprey rings. Our results suggest that receptors for a variety of vasoactive signaling agents are expressed in the aortic smooth muscle of the earliest vertebrates (lamprey and hagfish), as well as the more advanced teleosts (eel).
The synaptic input on myenteric Dogiel type II neurones (n = 63) obtained from the ileum of 17 pigs was studied by intracellular recording. In 77% of the neurones, electrical stimulation of a fibre tract evoked fast excitatory postsynaptic potentials (fEPSPs) with an amplitude of 6 +/- 5 mV (mean +/- S.D.) and lasting 49 +/- 29 ms. The nicotinic nature of the fEPSPs was demonstrated by superfusing hexamethonium (20 microM). High-frequency stimulation (up to 20 Hz, 3 seconds) did not result in a rundown of the fEPSPs, and did not evoke slow excitatory or inhibitory postsynaptic potentials. The effects of neurotransmitters, possibly involved in these excitatory responses, were investigated. Pressure microejection of acetylcholine (10 mM in pipette) resulted in a fast nicotinic depolarisation in 67%(18/27) of the neurones (13 +/- 9 mV, duration 7.0 +/- 7.2 seconds) as did 1,1-dimethyl-4-phenylpiperazinium iodide (DMPP) application (10 mM; 14 +/- 10 mV, duration 4.1 +/- 2.8 seconds) in 76% of the cells. The fast nicotinic response to acetylcholine was sometimes (6/27) followed by a slow muscarinic depolarisation (8 +/- 4 mV; duration 38.7 +/- 10.8 seconds). Immunostaining revealed 5-hydroxytryptamine hydrochloride (5-HT)- and calcitonin gene-related peptide (CGRP)-positive neuronal baskets distributed around and in close vicinity to Dogiel type II neuronal cell bodies. Microejection of 5-HT (10 mM) resulted in a fast nicotinic-like depolarisation (12 +/- 6 mV, duration 3.0 +/- 1.3 seconds) in 4 of 8 neurones tested, whereas microejection of CGRP (20 mM) gave rise to a slow muscarinic-like depolarisation (6 +/- 2 mV, duration 56.0 +/- 27.5 seconds) in 8 of 12 neurones tested. In conclusion, myenteric Dogiel type II neurones in the porcine ileum receive diverse synaptic input. Mainly with regard to the prominent presence of nicotinic responses, these neurones behave contrary to their guinea pig counterparts.
Dystrobrevins are protein components of the dystrophin complex, whose disruption leads to Duchenne muscular dystrophy and related diseases. The Caenorhabditis elegans dystrobrevin gene (dyb-1) encodes a protein 38 % identical with its mammalian counterparts. The C. elegans dystrobrevin is expressed in muscles and neurons. We characterised C. elegans dyb-1 mutants and showed that: (1) their behavioural phenotype resembles that of dystrophin (dys-1) mutants; (2) the phenotype of dyb-1 dys-1 double mutants is not different from the single ones; (3) dyb-1 mutants are more sensitive than wild-type animals to reductions of acetylcholinesterase levels and have an increased response to acetylcholine; (4) dyb-1 mutations alone do not lead to muscle degeneration, but synergistically produce a progressive myopathy when combined with a mild MyoD/hlh-1 mutation. All together, these findings further substantiate the role of dystrobrevins in cholinergic transmission and as functional partners of dystrophin.