PubMed HealthSearch

PubMed · 7713355

Endothelium-derived hyperpolarizing factor does not contribute to the decrease in endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic rats.

Abstract

1. We examined the contribution of endothelium-derived hyperpolarizing factor (EDHF) to the impairment of endothelium-dependent relaxation caused by acetylcholine (ACh) in the aorta of streptozotocin-induced diabetic rats, by using N omega-L-nitro-arginine methylester (L-NAME) and tetraethylammonium chloride (TEA) to inhibit nitric oxide (NO) and EDHF, respectively. 2. ACh-induced relaxation of the aorta decreased in diabetic rats. In contrast, sodium nitroprusside-induced relaxation was the same in diabetic rats and control rats. 3. Treatment with 5 x 10(-7) M L-NAME resulted in a right shift of the dose-response curves of ACh-induced relaxation in the aorta. The shift was greater in the control aorta. 4. Treatment with 5 x 10(-4) M TEA resulted in a similar right shift in both the control and diabetic aorta. 5. Therefore, while endothelium-derived NO appears to contribute to the impairment of ACh-induced endothelium-dependent relaxation in the aorta of diabetic rats, EDHF does not.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K Endo, T Abiru, H Machida, Y Kasuya, K Kamata. 1995. Endothelium-derived hyperpolarizing factor does not contribute to the decrease in endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic rats.. https://doi.org/10.1016/0306-3623(94)00159-k

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Local circuit for the computation of object approach by an identified visual neuron in the locust.

The lobula giant movement detector (LGMD) neuron in the locust visual system is part of a motion-sensitive pathway that detects objects approaching on a collision course. Here we show that the retinotopic units presynaptic to the LGMD make synapses directly with each other and these synapses are immediately adjacent to their outputs onto the LGMD. Synapses occur along the fine dendrites of the LGMD in the distal lobula, often in large numbers and completely covering the LGMD processes. Gamma aminobutyric acid (GABA) was eliminated as a possible neurotransmitter at these synapses when immunogold-tagged monoclonal GABA antibody did not specifically label the afferent processes. We used a histochemical method to demonstrate that acetylcholine esterase, the enzyme that hydrolyses acetylcholine at cholinergic synapses, was present in the synaptic clefts between the retinotopic units and along the membrane of the LGMD. It is well established that acetylcholine has both excitatory and inhibitory effects and we propose that these retinotopic units excite the LGMD, but inhibit each other; and that the synapses form the substrate for a critical race between excitation caused by edges moving out over successive photoreceptors, and inhibition spreading laterally. This results in the selective response to objects approaching on a collision course.

Acetylcholine

Presynaptic calcium channels mediating synaptic transmission in submucosal neurones of the guinea-pig caecum.

1. Intracellular recording techniques were used to examine the voltage-activated calcium channels mediating neurotransmitter release from nerve terminals of extrinsic, sympathetic origin and intrinsic (enteric) origin innervating submucosal neurones of the guinea-pig caecum. 2. The noradrenergic slow inhibitory postsynaptic potential (IPSP) was abolished by superfusion of omega-conotoxin (omega-CTX) GVIA (3-300 nM), with an apparent IC50 of 8.6 nM. Superfusion of omega-CTX MVIIC (500 nM) also suppressed the amplitude of slow IPSPs, but both omega-agatoxin IVA (100 nM) and nicardipine (1-10 microM) were ineffective. The hyperpolarization induced by exogenous noradrenaline was not affected by omega-CTX GVIA (100 nM). 3. In contrast to the slow IPSP, the amplitude of the cholinergic fast excitatory postsynaptic potential (EPSP) was partially inhibited, but not abolished, by omega-CTX GVIA (0.1-1 microM). Furthermore, omega-agatoxin IVA (0.1-1 microM) or omega-CTX MVIIC (0.1-1 microM) also affected the fast EPSP, but nicardipine (1-10 microM) was ineffective. In combination, omega-CTX GVIA (100 nM) and omega-agatoxin IVA (100 nM) inhibited the fast EPSP by 74 +/- 6 %; the residual fast EPSP was not affected by omega-CTX MVIIC (100 nM). The fast EPSP was completely abolished by low Ca2+, high Mg2+ Krebs solution or Krebs solution containing Co2+ (2 mM) and Cd2+ (400 microM). The depolarization induced by exogenous acetylcholine was not affected by either omega-CTX GVIA (100 nM), omega-agatoxin IVA (100 nM) or omega-CTX MVIIC (100 nM). 4. Taken together, these results suggest that, in the submucosal plexus of the guinea-pig caecum, release of noradrenaline from extrinsic nerve terminals is regulated by N-type calcium channels, whereas release of acetylcholine from intrinsic nerve terminals involves several types of calcium channel.

Acetylcholine

Release of acetylcholine from embryonic myocytes in Xenopus cell cultures.

1. Acetylcholine (ACh) is important as the transmitter responsible for neuromuscular transmission. Here we report the non-quantal release of ACh from embryonic myocytes. 2. Co-cultures of spinal neurons and myotomal muscle cells were prepared from 1-day-old Xenopus embryos. Single channel currents were recorded in the non-innervated myocytes. When the patch pipette was filled with Ringer solution alone, spontaneous single channel currents occurred, which were inhibited by d-tubocurarine (d-Tc). 3. The channel conductance appearing in Ringer solution (37.3 pS) was similar to that of an embryonic-type ACh channel (36.9 pS), indicating that ACh is probably released from myocytes in normal Ringer solution. 4. When the patch pipette was filled with anticholinesterase alone to prevent hydrolysis of ACh released from myocytes, both physostigmine and neostigmine in a concentration-dependent manner increased channel open probability; it was reduced by d-Tc or alpha-bungarotoxin. 5. Vesamicol and quinacrine, vesicular transporter inhibitors, reduced the channel open probability caused by ACh released from myocytes in the presence of neostigmine or physostigmine. 6. Intracellular alkalinization with NH4Cl inhibited the ACh release from myocytes, whereas, extracellular alkalinization, brought about by replacing normal Ringer solution, with pH 8.6 Ringer solution enhanced ACh release. 7. The immunocytochemistry of choline acetyltransferase (ChAT) showed that ChAT exists in both myocytes and neuronal cells but not in fibroblasts. 8. These results suggest that embryonic myocytes are capable of synthesizing and releasing ACh in a non-quantal manner. Extracellular alkalinization enhanced and intracellular alkalinization inhibited ACh release from myocytes.

Acetylcholine