Modulation of noradrenergic transmission in the guinea‐pig mesenteric artery: an electrophysiological study.

1983

British J Pharmacology

1 Effects of 3,4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-nitroxy-2H-1-benzopyran (K-351) and its derivative, 3,4-dihydro-8-(2-hydroxy-3-isopropylaminopropoxy)-3-hydroxy-2H-1-benzopyran (K-351 (N-)) on the electrical and mechanical properties of smooth muscles of the dog coronary and mesenteric arteries were investigated, and the findings were compared with data obtained with nitroglycerine. 2 In both proximal and distal regions of the coronary arteries, K-35 1 and nitroglycerine reduced the resting tone and suppressed the contractions produced by high-potassium solution or by current passage to the same extent, with no remarkable change in the electrical properties of the smooth muscle membrane. 3 In the proximal regions of the descending coronary irtery, low and high concentrations of noradrenaline (NA) produced relaxation and contraction of the muscle, respectively. In the distal region, NA consistently relaxed the muscle with concentrations up to 10-5M. In both regions, the contraction or relaxation was suppressed by phentolamine or propranolol, respectively. 4 K-351 suppressed the NA-induced contraction. K-351(N-) potentiated the NA-induced contraction and suppressed the relaxation, but these actions were weaker than those of propranolol. Nitroglycerine suppressed the NA-induced contraction and the potency was weaker than that of K-351. 5 In the mesenteric artery, K-35 1 depressed excitatory junction potentials, spikes and contractions evoked by perivascular nerve stimulation, while K-351(N-)

Section: Introductionmentioning

confidence: 99%

The effects of 3,4‐dihydro‐8‐(2‐hydroxy‐3‐isopropylaminopropoxy)‐3‐nitroxy‐2H‐1‐benzopyr an (K‐351) and its denitrated derivative on smooth muscle cells of the dog coronary artery

Kou

1983

British J Pharmacology

“…The es j.p.s observed in these muscular arteries are not suppressed by a-adrenoceptor antagonists, and application of phentolamine increases the amplitude of the e. j.p.s (HOLMAN and SURPRENANT, 1980;KOU et al, 1982;KURIYAMA and MAKITA, 1983). In the mesenteric vein or the main pulmonary artery of the guinea-pig, perivascular nerve stimulation generates a slow depolarization which is suppressed by a-adrenoceptor antagonists (SUZUKI, 1981(SUZUKI, , 1983.…”

mentioning

confidence: 98%

Electrical components contributing to the nerve-mediated contractions in the smooth muscles of the rabbit ear artery.

Kou

1983

Jpn.J.Physiol

Adrenergic transmissions were investigated by recording electrical and mechanical responses of the smooth muscle cells in the rabbit ear artery. Perivascular nerve stimulation generated an excitatory junction potential (e) j.p.) and a slow depolarization. The latter but not the former was suppressed by prazosin or phentolamine. Both the e.j.p. and slow depolarization were suppressed by tetrodotoxin (TTX) or guanethidine. Facilitation processes of e.j.p.s produced by repetitive stimulation of the nerves were not modified by prazosin, phentolamine, or yohimbine. Increasing the stimulus frequency increased the amplitude of es j.p.s and slow depolarizations and, at high frequencies (>5 Hz) generated a spike potential. Nicardipine (10-7 M) blocked the spike potential and reduced the e.j.p. amplitude, but did not affect the slow depolarization. Amplitude of muscle contractions produced by transmural nerve stimulation increased with increase in the stimulus frequency. The nerve-mediated contractions produced by high-frequency stimulation (10 Hz) were reduced to 49 % of the control value by prazosin (10-6 M), to 79 % by nicardipine (10-i M), to 34 by prazosin (10-6 M) plus nicardipine (10-i M), and to 1.2% by TTX (3 x 10-~ M). Exogenously applied noradrenaline depolarized the smooth muscle membrane and produced the muscle contraction. These effects of noradrenaline were antagonized by prazosin or phentolamine. Thus, in the rabbit ear artery, perivascular nerve stimulation produced three types of electrical responses, i.e., e, j.p., spike potential, and slow depolarization. The latter but not the former two was produced through activation of al-adrenoceptors. Nerve-mediated muscle contractions were the results of stimulation of al-adrenoceptors, generation of spike potentials, and of e. j.p.s.

“…Application of a-adrenoceptor antagonists such as phentolamine, yohimbine or phenoxybenzamine enhances the ej.p. amplitude generated by repetitive stimulation of nerves, presumably due to inhibition of a-autoinhibition mechanisms at the prejunctional membrane (Kuriyama & Makita, 1983). Activation of the a-autoinhibition mechanism by exogenously applied noradrenaline decreased the e.j.p.…”

Section: Discussionmentioning

confidence: 93%

“…In perivascular adrenergic nerve terminals of the mesenteric artery, a2-and P-adrenoceptors are present, and stimulation of the former decreases and of the latter increases the ej.p. amplitude (Kuriyama & Makita, 1983). In the portal vein, stimulation of the o1-adrenoceptor depolarizes and of the P-adrenoceptor hyperpolarizes the muscle membrane (Takata, 1980).…”

Section: Introductionmentioning

confidence: 99%

“…Smooth muscle membranes of the mesenteric artery (Kuriyama & Makita, 1983), main pulmonary artery (Suzuki, 1983) and portal vein (Takata, 1980) possess o1-adrenoceptors, through which exogenously applied noradrenaline depolarizes the membrane. In perivascular adrenergic nerve terminals of the mesenteric artery, a2-and P-adrenoceptors are present, and stimulation of the former decreases and of the latter increases the ej.p.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of amosulalol on the electrical responses of guinea‐pig vascular smooth muscle to adrenoceptor activation

Fujioka

1985

British J Pharmacology

1The effects of amosulalol, a newly synthesized sulphonamide-substituted phenylethylamine derivative, on electrical responses of smooth muscle cells of the guinea-pig vascular tissues to noradrenaline, isoprenaline and perivascular nerve stimulation were investigated. 2 Amosulalol (10--10-M) did not alter the resting membrane potential of smooth muscle cells of the mesenteric artery, the mesenteric vein, the main pulmonary artery and the portal vein. 3 In the mesenteric artery, main pulmonary artery and portal vein, but not in the mesenteric vein, membrane depolarizations produced by noradrenaline were antagonized by amosulalol. 4 In the portal vein, membrane hyperpolarizations produced by isoprenaline were antagonized by amosulalol. 5 In the mesenteric artery, amosulalol (over 10-6M) enhanced the amplitude of excitatory junction potentials (ej.ps) produced by perivascular nerve stimulation. 6 Amosulalol antagonized the noradrenaline-induced decrease in the ej.p. amplitude; this effect was much weaker than that of phentolamine. Amosulalol also antagonized the isoprenaline-induced enhancement of the ej.p. amplitude. 7 In the mesenteric vein, the slow depolarizations produced by perivascular nerve stimulation were depressed by amosulalol (over 10-6M), but the effect was much weaker than that of prazosin, yohimbine or phentolamine. 8 Actions of amosulalol on electrical properties of vascular tissues can be summarized as follows:amosulalol blocks a,-and P-adrenoceptors. It also blocks a2-adrenoceptors, though weakly.