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Biomedical subjects

Y Misu

Publications and source records attributed to Y Misu.

At least 145 records · Page 8Linked to original sources
PubMed1983

The nucleus reticularis dorsalis: a region sensitive to physostigmine.

Microinjection of physostigmine (3 micrograms) into the nucleus reticularis dorsalis of the rat produced hypertension. Little or no increases in blood pressure were found at the other areas of the medullary reticular formation. The pressor effect following injection of physostigmine into the nucleus reticularis dorsalis was sensitive to atropine (1 microgram) but resistant to hexamethonium (5 micrograms), similarly injected. Atropine (1 microgram) bilaterally injected into the nucleus decreased pressor responses to intravenous physostigmine (100 micrograms/kg). These data may indicate that there are muscarinic receptors responsible for pressor effects in the nucleus reticularis dorsalis. The medullary cholinoceptors may be involved in the systemic physostigmine effect on blood pressure.

Animals↗
PubMed1983

Modification of sympathetic nerve stimulation frequency-response relationship in rabbit ileum by guanethidine, bretylium and tetracaine.

Effects of low concentrations of guanethidine, bretylium and tetracaine were comparatively studied with regard to inhibitory responses of rabbit ileum to periarterial nerve stimulation at 5, 10 and 20 Hz. Guanethidine 2 X 10(-7) to 10(-6) M and bretylium 3 X 10(-6) to 3 X 10(-5) M dose-dependently and preferentially reduced responses to lower frequencies, whereas tetracaine 10(-5) to 3 X 10(-5) M reduced responses, in a dose- and frequency-dependent manner. In conclusion, the mode of adrenergic neuron blocking action of guanethidine and bretylium differs from that of local anesthetics.

Animals↗
PubMed1982

Presynaptic dual inhibitory actions of guanabenz on adrenergic transmission.

Actions of guanabenz, clonidine and guanethidine on adrenergic transmission were studied in rabbit atria and ilea with intact nerves. While guanabenz 3 X 10(-6) M and clonidine 3 X 10(-7) M inhibited to a similar degree atrial positive chronotropic responses to nerve stimulation at 2 Hz, no inhibition was seen at 10 Hz. Phentolamine 3 X 10(-6) M completely antagonized the inhibition by clonidine, but a partial antagonism was seen against guanabenz. Cocaine 10(-5) M prevented the phentolamine-resistant inhibition by guanabenz. Guanethidine 10(-5) M inhibited the responses to 2 and 10 Hz. In ilea, guanabenz 10(-5) M inhibited frequency-independent relaxation responses to 2-20 Hz. Clonidine 10(-5) M inhibited preferentially the responses to lower frequencies. After the temperature of the bathing solution was kept at 4 degree C during the period of drug application, guanabenz no longer produced an inhibition of the transmission, whereas clonidine produced the usual inhibition. Thus, guanabenz appears to have both presynaptic alpha-receptor stimulating and adrenergic neuron blocking actions.

Animals↗
PubMed1982

Comparative studies of cerebral vasodilators on relaxation activities in isolated basilar, mesenteric and pulmonary arteries of rabbits.

Effects of cerebral vasodilators such as bencyclane, cinnarizine, and papaverine were comparatively studied using helically cut basilar and superior mesenteric arteries and radial muscle preparations of pulmonary arteries with the sympathetic nerve isolated from rabbits. The order of relaxation activities on high K+-induced contractures was cinnarizine>bencyclane>papaverine in basilar strips and cinnarizine>papaverine>bencyclane in mesenteric strips. Relaxation responses of basilar strips to cinnarizine and bencyclane were faster and more marked than those seen in mesenteric strips. Responses to papaverine were equipotent in both preparations. The action of cinnarizine alone was irreversible. In mesenteric strips, the order of the sensitivity of contractile responses to cumulatively applied biogenic amines was serotonin>noradrenaline>histamine. Cinnarizine produced an antihistaminergic action, while bencyclane produced an antiserotonergic action. In pulmonary arteries, 6 x 10(-6) g/ml papaverine inhibited contractile responses to 2, 5, and 25 Hz nerve stimulation in a frequency-independent manner together with inhibition of responses to noradrenaline. Bencyclane at 6 x 10(-6) and 10(-5) g/ml selectively inhibited in a dose-dependent manner contractile responses only to 25 Hz without inhibition of responses to noradrenaline. These results were discussed in comparison with findings of the cerebral vasodilators obtained using other experimental techniques. Spiral strips of basilar arteries from rabbits in combination with peripheral arteries may be used as a simple quantitative, and reproducible screening method in a preclinical stage for drug evaluation of cerebral vasodilators.

Animals↗
PubMed1981

Pharmacological characterisation of the alpha-adrenoceptors responsible for a decrease of blood pressure in the nucleus tractus solitarii of the rat.

The effects of various alpha-adrenoceptor agonists, microinjected into the area of the nucleus tractus solitarii (NTS) at the level of the obex, on blood pressure, and the interaction between noradrenaline and some alpha-antagonists in the area of the NTS were investigated in anaesthetized male rats. A dose-dependent decrease in blood pressure was induced by noradrenaline. The relative potencies of the substances were adrenaline greater than noradrenaline greater than alpha-methylnoradrenaline greater than clonidine greater than tyramine. In contrast, phenylephrine was ineffective. The hypotensive effect of noradrenaline, alpha-methylnoradrenaline and clonidine was not affected by pretreatment with 6-hydroxydopamine given intraventricularly, while the effect of tyramine was blocked by the pretreatment. Prior application of phentolamine at the same site antagonized the hypotensive response to noradrenaline. Prazosin was about 10 times less potent than yohimbine in antagonizing the noradrenaline-induced hypotension. The present data suggest that the alpha-adrenoceptors in the area of the NTS responsible for the decrease in blood pressure are the same type as the peripheral presynaptic alpha 2-adrenoceptors but may be located postsynaptically. It appears that the noradrenergic neurons in the NTS can play a role in blood pressure regulation.

Adrenergic alpha-Agonists↗
PubMed1981

Comparative studies of (--)-, (+/-)-propranolol, atenolol, guanethidine, bretylium and tetracaine on adrenergic transmission.

1 Effects of (--)-, (+/-)-, and (+)-propranolol, atenolol, guanethidine, bretylium and tetracaine were studied on relaxation responses of rabbit ileum and contractile responses of rabbit pulmonary artery and guinea-pig vas deferens to electrical nerve stimulation (2 to 50 Hz). 2 In the ileum, inhibition by tetracaine 3.3 x 10(-6) M occurred at high frequencies of stimulation, while bretylium 1.2 x 10(-4) M and guanethidine 2 x 10(-5) M inhibited responses at all frequencies, the latter producing greater inhibition at low frequencies. 3 (+/-)-Propranolol 10(-5) M produced a tetracaine-type inhibition after 1 h and a bretylium-pattern after 2 h in the ilea and pulmonary arteries and a transition from bretylium- to guanethidine-pattern in the vas deferens, while atenolol 2 x 10(-5) to 10(-4) M produced guanethidine-type inhibition in all preparations. 4 (--)-, (+/-)-, and (+)-Propranolol 3 x 10(-6) to 3.3 x 10(-5) M were equipotent in the vas deferens and ileum. However, inhibition by (--)-propranolol 3.3 x 10(-5) M persisted in the ileum, while that by the (+)-isomer was partially restored by washing. 5 (--)- or (+)-Propranolol 3.3 x 10(-5) M or atenolol 2 x 10(-5) M did not inhibit relaxation of the ileum after the bath temperature was maintained at 4 degrees C for 2 h during drug application. 6 In conclusion, propranolol and atenolol both have gradually developing guanethidine-like adrenergic neurone blocking actions.

Animals↗
PubMed1981

Cardiovascular responses to intracisternal administration of nicotine in rats.

The administration of nicotine into the cisterna magna evoked a delayed depressor effect with an initial pressor effect in anaesthetized rats. The depressor response was accompanied by a bradycardia. The cardiovascular effects of nicotine were abolished after intracisternal administration of hexamethonium but not after atropine given via the same route. Intravenous administration of methylatropine abolished the bradycardic response to nicotine but did not affect the blood pressure responses. The pressor effect of nicotine was abolished by intravenous administration of phenoxybenzamine. The cardiovascular effects of nicotine injected intracisternally were abolished when the diffusion of nicotine onto an area around the area postrema was interrupted using a polyethylene tube. In contrast, nicotine applied to the area produced a marked pressor--depressor response. It is concluded that the cardiovascular responses to intracisternal administration of nicotine result from the activation of central nicotinic receptor sites that may be present around the area postrema.

Animals↗
PubMed1981

Antihypertensive effects of nifedipine on conscious normotensive and hypertensive rats.

Hypotensive actions of single and repeated administrations of nifedipine were evaluated in comparison with hydralazine in normotensive, spontaneously hypertensive and renal hypertensive rats. Substantial and prolonged falls in blood pressure were observed following oral dosing with 3 mg/kg of nifedipine in renal hypertensive rats, with 10 mg/kg of nifedipine in normotensive and spontaneously hypertensive rats and with 10 mg/dg of hydralazine in all three groups of animals. The hypotensive effect of nifedipine was greater in both forms of hypertensive rats than the normotensive rats, while there was no difference in the hypotensive effect of hydralazine in normotensive and hypertensive animals. In spontaneously hypertensive rats tolerance to nifedipine and hydralazine was not observed with oral administrations for 4 weeks at a daily dose of 10 mg/kg. An increase in heart rate always accompanied the hypotension induced by both drugs, but this tachycardia was seen to a lesser extent with nifedipine than with hydralazine. The mechanism of the selective action of nifedipine in hypertensive rats in contrast to normotensive rats is discussed.

Animals↗
PubMed1981

Increased pressor responses to nicotine in spontaneously hypertensive rats.

Intraventricular administration of nicotine produced a biphasic effect, consisting of an initial rise than a slight fall in blood pressure in unanaesthetized rats. Spontaneously hypertensive rate (SHR) showed increased pressor responses, but these responses were within normal limits in renal hypertensive and DOCA-saline hypertensive rats. The blood pressure response to nicotine in SHR was abolished by intraventricular administration of hexamethonium, but not by atropine given via the same route. Central phentolamine and 6-hydroxydopamine did not affect the pressor response to nicotine. The pressor effect of nicotine in SHR was markedly diminished after removal of the adrenals and abolished after bilateral adrenalectomy plus peripheral 6-hydroxydopamine. These results indicate that the pressor response to intraventricular nicotine is increased in SHR. The pressor effect of nicotine may result from the activation of the central nicotinic receptor sites, which may cause the release of catecholamines both from the adrenal medulla and adrenergic nerve terminals.

Adrenalectomy↗
PubMed1981

Adrenergic transmission failure via the blockade of presynaptic beta receptors in guinea-pig pulmonary arteries.

Mechanisms related to the inhibitory actions of low concentrations of l- and d-propranolol on adrenergic transmission were investigated in isolated preparations of guinea-pig pulmonary arteries. In sympathetic nerve-radial muscle preparations, l-propranolol (3.3 X 10(-8) and 10(-7) M) dose-dependently inhibited by 15 to 20% contractile responses to nerve stimulation (1 Hz, 2-msec pulse width, 100-sec period and 30-min intervals) 30 and 60 min after the addition, whereas 3.3 X 10(-7) M produced a maximal inhibition. Contractile responses to cumulatively applied norepinephrine were not modified by pretreatment with l-propranolol (10(-7) - 10(-6) M). d-Propranolol (10(-7) M) produced no inhibition of adrenergic transmission. In superfused spiral preparations preloaded with [3H]norepinephrine, l-isoproterenol (3 X 10(-8) - 10(-6) M) dose-dependently facilitated total 3H efflux by transmural field stimulation by 10 to 35% under the same conditions; this facilitation was antagonized by l-propranolol (10(-7) M) but not by d-propranolol (10(-7) M). Phentolamine (3 X 10(-6) M) increased 3H efflux by approximately 3-fold. In the presence of phentolamine, l-propranolol (10(-7) M) significantly inhibited 3H efflux, whereas d-propranolol (10(-7) M) produced no effect. Presynaptic beta adrenoceptors are present on sympathetic nerve endings which innervate guinea-pig pulmonary arteries and low concentrations of propranolol inhibit adrenergic transmission via blockade of these receptors.

Adrenergic beta-Antagonists↗