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Biomedical subjects

Y Misu

Publications and source records attributed to Y Misu.

At least 127 records · Page 7Linked to original sources
PubMed1986

Further evidence for tonically functioning presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries.

Effects of dl- and d-carteolol alone on the release of tritium evoked by transmural field stimulation at 1 Hz were investigated in spirally cut guinea-pig pulmonary arteries preloaded with [3H]-norepinephrine. Cumulatively applied dl-carteolol 10(-8) M, 10(-7) M and 10(-6) M readily inhibited the release of tritium in a concentration-dependent manner, whereas the same concentrations of d-carteolol produced no effect. In conclusion, presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries tonically function to facilitate the release of the transmitter norepinephrine.

Animals↗
PubMed1985

Involvement of central catecholamines in mediation of pressor responses of the rat to carotid occlusion.

Carotid occlusion evoked a pressor response in rats after transection of the spinal cord. Intraventricular pretreatment with 6-hydroxydopamine inhibited the pressor response. The pressor response to occlusion was also diminished by the intraventricular but not by the intravenous injection of guanethidine. Intravenous atropine or mecamylamine, or intraventricular captopril did not affect the pressor response. Thus, it appears that central catecholaminergic mechanisms are involved in the mediation of the pressor response to carotid occlusion.

Animals↗
PubMed1985

Caudal ventrolateral medulla. A region responsible for the mediation of vasopressin-induced pressor responses.

We localized glutamate-sensitive sites in the ventrolateral medulla of the rat with the spinal cord cut at C. When unilaterally injected into a circumscribed region of the caudal ventrolateral medulla, L-glutamate (30-300 ng) elicited a dose-dependent increase in arterial pressure. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral microinjections of kainic acid (50 ng) into the ventrolateral glutamate-sensitive area markedly reduced a vasopressin-induced pressor response to kainic acid (30 ng), injected bilaterally into the nucleus tractus solitarii. It is concluded that the glutamate-sensitive neurons in the caudal ventrolateral medulla are involved in mediation of the vasopressin-induced pressor response arising from the nucleus tractus solitarii.

Animals↗
PubMed1985

Autoregulation of endogenous epinephrine release via presynaptic adrenoceptors in the rat hypothalamic slice.

High-K+ (30 mM)-evoked release of endogenous epinephrine in hypothalamic slices from three rats in the presence of tetrodotoxin, 3 X 10(-7) M, was measured by high-performance liquid chromatography with an electrochemical detector. Spontaneous and evoked release of epinephrine was markedly reduced, when rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p., before decapitation. The amount of epinephrine released during the resting state was lower by a factor of approximately 2 orders than that of norepinephrine and dopamine but was consistently higher than the limit of the sensitivity of this assay system, 0.1 to 0.3 pmol. The evoked release of epinephrine was Ca++ dependent. Isoproterenol, 10(-8) M to 10(-7) M, dose dependently increased this parameter. I-Propranolol, 3 X 10(-8) M, shifted the dose-effect curve of isoproterenol to the right. Atenolol, 10(-6) M, and butoxamine, 3 X 10(-8) M, beta-1 and beta-2 antagonists, respectively, antagonized the action of isoproterenol, 3 X 10(-8) M. Tazolol, 3 X 10(-7) and 10(-6) M, a beta-1 agonist, and salbutamol, 10(-8) and 3 X 10(-8) M, a beta-2 agonist, dose dependently increased the evoked release of epinephrine. I-Propranolol, 3 X 10(-7) M and 3 X 10(-6) M alone, dose dependently decreased this parameter, but the d-isomer produced no effect. Clonidine, 10(-8) and 10(-7) M, an alpha-2 agonist, dose dependently decreased the parameter, and this decrease was antagonized by yohimbine, 10(-6) M, an alpha-2 antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed1985

Involvement of epinephrine in the presynaptic beta adrenoceptor mechanism of norepinephrine release from rat hypothalamic slices.

Using high-performance liquid chromatography with electro-chemical detector, we measured field impulse (5 or 2 Hz)- and high K+ (20 mM)-evoked release of endogenous norepinephrine from rat hypothalamic slices. Release by impulses at 5 Hz was tetrodotoxin-sensitive and both types of release were Ca++-dependent. Isoproterenol (10(-10) to 10(-8) M) dose-dependently facilitated impulse-evoked release and l-propranolol (10(-8) M) shifted dose-effect curve of isoproterenol to the right. Atenolol (10(-8) to 10(-6) M) or butoxamine (10(-9) to 10(-8) M), beta-1 and beta-2-antagonist, respectively, dose-dependently antagonized the facilitatory effect of isoproterenol (10(-8) M). Tazolol (10(-8) to 10(-7) M), beta-1-agonist, and salbutamol (10(-10) to 10(-8) M), beta-2-agonist, dose-dependently increased impulse-evoked release. Epinephrine (10(-9) M) also facilitated impulse-evoked release and the action was antagonized by l-propranolol (10(-8) M). Isoproterenol (10(-8) M) also facilitated high K+-evoked release in the presence of tetrodotoxin (3 X 10(-7) M) to exclude possible involvement of axonal conduction or neuronal loops. This facilitatory effect was antagonized by l-propranolol (10(-8) M). l-Propranolol (3 X 10(-7) M) alone decreased release by impulses at 2 Hz, but the d-isomer produced no effect. When rats were pretreated with 2,3-dichloro-alpha-methylbenzylamine, an inhibitor of phenylethanolamine N-methyltransferase, the enzyme catalyzing the formation of epinephrine from norepinephrine, 80 mg/kg i.p. before decapitation, the l-propranolol-induced decrease was abolished completely.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Presynaptic inhibitory dopamine receptors on noradrenergic nerve terminals: analysis of biphasic actions of dopamine and apomorphine on the release of endogenous norepinephrine in rat hypothalamic slices.

Electrical field stimulation (5 Hz)- or high K+ (20 mM)-evoked release of endogenous norepinephrine from superfused rat hypothalamic slices in the presence of cocaine (20 microM) was measured by high-performance liquid chromatography with an electrochemical detector. Apomorphine (10-1000 nM) dose-dependently facilitated the electrically evoked release. Apomorphine (1 microM)-induced facilitation was abolished by pretreatment with yohimbine (100 nM), was converted to inhibition by yohimbine (1 microM), but was not antagonized by propranolol (300 nM). Epinephrine (100 nM) decreased the electrically evoked release and the decrease was antagonized by yohimbine (100 nM) and by apomorphine (100 nM), but not by S-sulpiride (100 nM). In the presence of yohimbine (1 microM), apomorphine (10-1000 nM) dose-dependently inhibited the electrically evoked release. Furthermore, in the presence of tetrodotoxin (300 nM), apomorphine (100 nM) also decreased the high K+-evoked release and this decrease was antagonized by S-sulpiride (100 nM). Dopamine produced biphasic actions on the electrically evoked release, a dose-dependent decrease at 30 and 100 nM and an increase at 300 and 1000 nM. Dopamine (300 nM)-induced increase was antagonized by propranolol (300 nM) but not by yohimbine (100 nM). The dopamine (100 nM)-induced decrease was antagonized by S-sulpiride (1 nM), but not by the R-isomer. S-sulpiride (10 to 100 nM) alone dose-dependently increased the electrically evoked release, whereas the R-isomer had no effect. Haloperidol (100 nM) also increased the electrically evoked release.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Further studies on vasopressin-induced pressor responses to kainic acid injected into the nucleus tractus solitarii of the rat.

Kainic acid, an analogue of L-glutamate, was microinjected into the nucleus tractus solitarii of cordotomized rats. Kainic acid (30 ng) injected bilaterally into the nucleus elicited hypertension. The pressor response to kainic acid was restricted to sites in the intermediate one-third of the nucleus tractus solitarii. Plasma vasopressin levels were markedly increased during the kainic acid-induced pressor response. Intravenous injection of atropine sulphate or mecamylamine, or intraventricular injection of captopril did not affect the pressor response. It is concluded that in cordotomized rats the pressor response to kainic acid injected into the nucleus tractus solitarii is mainly mediated via increased release of vasopressin. It seems unlikely that the central cholinergic and angiotensin mechanisms are mainly responsible for the response to kainic acid.

Animals↗
PubMed1984

Adrenaline involvement in the presynaptic beta-adrenoceptor-mediated mechanism of dopamine release from slices of the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine (DA) was measured by high performance liquid chromatography combined with electrochemical detection. The K+ (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was facilitated by a beta-agonist, isoproterenol and this effect was completely abolished by a beta-antagonist, 1-propranolol. Isoproterenol also concentration-dependently facilitated the electrically (at 5Hz) evoked release of DA. The pretreatment with 1-propranolol, beta 1-antagonist, atenolol and beta 2-antagonist, butoxamine shifted the concentration-effect curve of isoproterenol to the right. On the other hand, beta 1-agonist, tazolol, beta 2-agonist, salbutamol and low concentration (10(-9) M) of adrenaline also facilitated the release. 1-Propranolol alone reduced the electrically (at 2 Hz) evoked release, and this effect was completely abolished when the adrenaline content in the brain was drastically reduced by use of a potent PNMT inhibitor, DCMB. These findings suggest that in the rat hypothalamus adrenaline released from adrenaline-containing nerve terminals probably modulates DA release via presynaptic beta 1- and beta 2-adrenoceptors on DA nerve terminals.

Action Potentials↗
PubMed1984

Vasopressin-induced pressor responses to carotid occlusion in the rat.

We studied the effect of carotid occlusion on blood pressure in cordotomized rats. Occlusion of both common carotid arteries resulted in an increase in blood pressure. This response was unaffected by denervation of the sinus and aortic nerves, and vagi. The response to occlusion was blocked by intravenous administration of a vasopressin antagonist, d(CH2)5Tyr(Me)arginine-vasopressin, but not by intravenous administration of hexamethonium or captopril. Further, microinjection of procaine into the paraventricular nuclei abolished the pressor response to occlusion. Thus, it appears that in cordotomized rats carotid occlusion causes release of vasopressin and this in turn results in an elevation of blood pressure. The arterial baroreceptors are not essential for the pressor response.

Animals↗
PubMed1984

Pharmacological properties of presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries.

Pharmacological properties of the facilitatory presynaptic beta-adrenoceptor mechanism were studied in superfused spiral preparations of guinea-pig pulmonary arteries preloaded with 3H-norepinephrine. (-)-Isoproterenol (0.3 microM)-induced increases in total 3H efflux per pulse evoked by transmural field stimulation (1, 5, 10 and 20 Hz, 10 V, 2 msec pulse width, 100 pulses and 30 min intervals) were neither dependent on impulse-frequencies nor selective at lower frequencies. Isoproterenol increased 3H efflux at 5 Hz in a concentration-dependent manner (1 nM to 1 microM): pD2 was 7.7. Salbutamol increased 3H efflux in a similar manner to isoproterenol: pD2 was 7.4. Prenalterol at 3 microM only slightly increased 3H efflux. Tazolol (10 nM to 3 microM) produced no increases. Atenolol (3 microM) and practolol (3 microM) did not antagonize isoproterenol (0.3 microM)-induced increases in 3H efflux. Butoxamine (3 microM) and H 35/25 (3 microM) did antagonize this parameter. (-)-Epinephrine (1 nM to 0.1 microM) decreased 3H efflux at 5 Hz and concentration-dependently increased this parameter in the presence of 10 microM phentolamine. (-)-Norepinephrine (10 nM to 1 microM) concentration-dependently inhibited evoked 3H efflux and did not increase the parameter in the presence of 10 microM phentolamine, 10 microM cocaine and 10 microM normetanephrine. Thus, there exist presynaptic beta 2-subtype receptors on noradrenergic nerve endings innervating guinea-pig pulmonary arteries.

Adrenergic beta-Agonists↗
PubMed1983

Presynaptic alpha 2- and dopamine-receptor-mediated inhibitory mechanisms and dopamine nerve terminals in the rat hypothalamus.

Slices of rat hypothalamus were superfused and endogenous release of dopamine was measured. The potassium (20 mM)-evoked release in the presence of tetrodotoxin was Ca2+-dependent. The evoked release was reduced by adrenaline 10(-7) M, with a potent alpha 2-agonist action, and was reduced by a dopamine receptor agonist, apomorphine 10(-7) M, in the presence of yohimbine 10(-6) M. These inhibitory effects were antagonized by an alpha 2-antagonist, yohimbine 10(-6) M, and a dopamine receptor antagonist, (-)-sulpiride 10(-7) M, respectively. The electrically evoked release of DA was enhanced by (-)-sulpiride but not by the (+)-isomer. Taking into consideration that yohimbine at a relatively high concentration (10(-6) M) increases the electrically evoked DA release, it is suggested that DA release in the rat hypothalamus may be mediated not only via autoreceptors but also in part via presynaptic alpha 2-receptors on the DA nerve terminals.

Animals↗
PubMed1983

Presynaptic mediation by alpha 2-, beta 1- and beta 2-adrenoceptors of endogenous noradrenaline and dopamine release from slices of rat hypothalamus.

Using high performance liquid chromatography with an electro-chemical detector, we studied effects of different compounds on the impulse-evoked release of endogenous noradrenaline (NA) and dopamine (DA) release from slices of the rat hypothalamus. Adrenaline (10(-7) M), with a potent alpha-agonistic action decreased both NA and DA release, and these effects were blocked by pretreatment with yohimbine (10(-7 M). The alpha 2-antagonist, yohimbine alone (10(-8) - 10(-6) M) concentration-dependently increased these releases, while alpha 1-antagonist, prazosin showed weak increase on NA but not DA release at 10(-6) M. Isoproterenol (10(-10) - 10(-8) M) concentration-dependently increased these releases and the effects were antagonized by pretreatment with a non-selective beta-antagonist, 1-propranolol, a beta 1-antagonist, atenolol or a beta 2-antagonist, butoxamine. 1-Propranolol (3 X 10(-7) M) alone, but not the d-isomer inhibited the releases. Thus, in the rat hypothalamus, the release of NA and DA may be mediated via presynaptic alpha 2-, beta 1- and beta 2-adrenoceptors.

Adrenergic alpha-Antagonists↗
PubMed1983

Further characterization of presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries.

Presynaptic beta-adrenoceptors were further characterized in spiral strips of guinea-pig pulmonary arteries preloaded with [3H]norepinephrine. l-Metoprolol (3 X 10(-6) M) inhibited isoproterenol (3 X 10(-7) M)-induced increases in 3H efflux by transmural field stimulation, whereas the d-isomer produced no inhibition. However, IPS 339, H 35/25, butoxamine and metoprolol (3 X 10(-6) M) antagonized salbutamol (3 X 10(-7) M)-induced increases in the parameter, whereas acebutolol, bevantolol and practolol (3 X 10(-6) M) produced no antagonism. Presynaptic beta-adrenoceptors in guinea-pig pulmonary arteries appear to have characteristics similar to those postsynaptic classical beta-adrenoceptors.

Albuterol↗