• The Korean Journal of Pharmacology
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• v.26 no.2
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• pp.101-111
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• 1990

The effect of physostigmine (PS), which has been shown to act on the muscarinic receptors in the brains of the rat, dog and cat, on the arterial blood pressure (BP) was investigated in urethane-anesthetized rabbits. Intravenous (iv) PS, $25{\sim}300\;{\mu}g/kg$, caused little change in BP. However, after treatment of rabbits with either of chlorisondamine (CS), hexamethonium, intracerebroventricular (icv) clonidine, icv xylazine and icy reserpine iv PS produced a pressor response. Spinalization of the rabbit also caused iv PS to increase BP. The pressor effect of iv PS in CS-treated rabbits was markedly reduced after prazosin or pirenzepine. Iv PS inhibited the pressor response to McN-A-343 in CS-treated and in spinal rabbits; alternately during the infusion of McN-A-343 iv PS failed to produce the pressor response. The pressor response to DMPP was not affected by iv PS. Icv PS, $12{\sim}200\;{\mu}g/kg$, produced a pressor response which was accentuated after CS-treatment. This pressor effect was inhibited, though not complete, by prazosin or by pirenzepine. A simultaneous treatment of rabbits with both $[Sar^{1},\;Ala^{8}]-angiotensin$ II, an angiotensin II antagonist, and prazosin or pirenzepine almost completely abolished the pressor effect of icv PS, whereas the angiotensin II antagonist did not enhance the inhibitory effect of pirenzepine and prazosin on the pressor response to iv PS . Icv pirenzepine blocked the pressor response to icv PS without affecting that to iv PS. The present results show that the pressor response to iv PS in CS-treated and in spinal rabbits arises from stimulation of the muscarinic receptors in the sympathetic ganglia, whereas the pressor response by icv PS via activation of the muscarinic receptors in the brain which causes an enhancement in the outflow of sympathetic discharge and angiotensin. The results also suggest that iv PS is unable to produce a pressor response in the rabbit unless the sensitivity of the gangionic muscarinic receptors is altered by ganglionic nicotinic blockade, by the decrease of central sympathetic outflow on the sympathetic ganglia or by spinalization.

• Journal of Chest Surgery
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• v.23 no.5
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• pp.833-843
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• 1990

Vasomotor areas were identified by stimulating various sites of the medulla electrically in adult cats anesthetized with a-chloralose and their correlation with somatosympathetic pressor or depressor responses was investigated. Followings are the results obtained: 1. Pressor areas were found in the rostral ventrolateral, the caudal ventrolateral and the rostral dorsolateral medulla. 2. Separate depressor areas were found dorsal and ventral to the rostral ventrolateral pressor area. 3. Some areas showed biphasic responses: depressor responses to low frequency[1 \ulcorner2 Hz] and pressor responses to high frequency[20 \ulcorner100 Hz] stimulation 4. Lesions on the rostral ventrolateral pressor areas abolished the somatosympathetic pressor responses to the stimulation of peripheral afferent nerves, while the depressor responses remained. Lesions on the caudal ventrolateral pressor area affected neither the pressor nor depressor responses to the peripheral nerve stimulation. 5. Lesions on the depressor areas resulted in decreased depressor responses to the peripheral nerve stimulation, but to a lesser degree than that resulted from lesions on the pressor areas. 6. A microinjection of glutamate solution to the pressor area resulted in a prolonged pressor response, while glutamate injection to the depressor areas did not elicit depressor responses. From the above results, it is concluded that there are separate pressor and depressor areas in the rostral medulla of cats and each area plays a role in somatosympathetic pressor and depressor responses, respectively.

• YAKHAK HOEJI
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• v.30 no.3
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• pp.111-120
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• 1986

The influence of debrisoquine on pressor actions of norepinephrine (NE) and tyramine (TR) was investigated in rabbits. Debrisquine(D), in the doses of 1.0, 3.0 and 6.0.mu.g/kg, i.v. potentiated significantly the pressor actions of NE and TR, except the action of TR in the dose of 1.0mg/kg of debrisoquine. NE response potentiated by debrisoquine was not affected by tranylcypromine, a MAO inhabiter, or desipramine, a NE uptake blocking agent, but augmented by reserpine, a NE depleting agent, or bethanidine, a sympathetic neuronal blocking agent. NE response potentiated by tranylcypromine or desipramine was augmented by debrisoquine, while NE response potentiated by reserine or bethanidine was not affected by debrisoquine. TR response potentiated by debrisoquine was weakened by tranylcypromine, desipramine or reserpine, and not affected by bethanidine. TR response in rabbit pretreated with tranylcypromine, desipramine or reserpine was augmented by debrisoquine, but in rabbit pretreated with bethanidine was not affected by debrisoquine.

• Journal of Pharmaceutical Investigation
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• v.15 no.1
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• pp.22-31
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• 1985

The influence of some sympathetic blocking agents on pressor actions of norepinephrine and angiotensin was investigated in rabbits. 1. Phentolamine, sympathetic ${\alpha}-blocking$ agent, blocked the pressor action of norepinephrine, but did not affect the pressor action of angiotensin 2. Chlorisondamine, autonomic ganglionic blocking agent, potentiated the both actions of norepinephrine and angiotensin. 3. Guanethidine, bethanidine and debrisoquine, sympathetic neuronal blocking agents, potentiated the action of norepinephrine, while diminished that of angiotensin. 4. Reserpine, norepinephrine depleting agent, increased the pressor response of norepinephrine, but did not influence the pressor action of angiotensin.

• Journal of Chest Surgery
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• v.20 no.3
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• pp.439-450
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• 1987

The arterial blood pressure response elicited by stimulating the peripheral afferent fibers of different groups and origins was studied in cats. Experimental animals were anesthetized with a-chloralose [60mg/kg] and artificially ventilated with a respirator. The lumbosacral spinal cord was exposed through a laminectomy and L7 ventral root was isolated. The sural, medial gastrocnemius and common peroneal nerves were also exposed in the hindlimb. The arterial blood pressure was monitored continuously while the exposed peripheral nerves and L7 ventral root were being stimulated. Then, spinal lesions were made on the dorsolateral sulcus area, dorsolateral funiculus and other areas at the thoracolumbar junction. The arterial blood pressure responses were compared before and after making spinal lesions. The following results were obtained. 1. The mean arterial blood pressure was elevated from 103*7.3 to 129*8, 1 [mean*S.E.] mmHg [p<0.001] during stimulation of the sural nerve with C-strength [1000T], 20Hz. Stimulation with Ad-strength, 1Hz resulted in the depression of the arterial pressure by 8 mmHg [p<0.01]. 2. Stimulation of the medial gastrocnemius nerve with Ad-strength did not elicit any significant change in arterial blood pressure. Stimulation with C-strength, 20 Hz induced a pressor response from 102*6.2 to 117*6.4 mmHg [p<0.01] while that with C-strength, 1Hz induced a depressor response from 104*6.1 to 93*4.9 mmHg [p<0.001]. 3. A pressor response by 56 [from 107*7 5 to 163*9.4] mmHg [p<0.001] was induced during stimulation of the common peroneal nerve with C-strength, 20Hz stimuli. Stimulation with A4-strength, 1Hz depressed the arterial blood pressure from 111~9.3 to 94*7.8 mmHg [P<0.005]. The activation of the ventral root afferent fibers with C-strength, 20 Hz stimuli induced a pressor response by 22 mmHg [from 115*9.4 to 137*8.6 mmHg] [p<0.001]. 4. The pressor response elicited during stimulation of the sural nerve was abolished by making lesions on the dorsolateral sulcus area bilaterally. With the medial gastrocnemius nerve, the pressor response had not been abolished completely by the dorsolateral sulcus lesions. The pressor response disappeared completely with addition of the bilateral dorsolateral funiculus lesions. 5. The depressor response induced by stimulation of the sciatic nerve with Ad-strength, 1Hz was decreased by making lesions on the dorsolateral funiculus. 6. From the above results it is concluded that the difference in the blood pressure responses to the activation of the muscular afferent and the cutaneous afferent fibers is responsible for the groups of afferent fibers and the spinal ascending pathways.

• Journal of Korean Academy of Nursing
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• v.41 no.2
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• pp.191-196
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• 2011

Purpose: We investigated the effects of group III mechanoreceptors to cardiovascular responses in both pre-menopausal woman and post-menopausal woman during passive ankle dorsiflexion (PAD). Methods: Twenty healthy volunteers (10 post-menopausal women and 10 pre-menopausal women) were recruited for this study. Stroke volume (SV), heart rate (HR), cardiac output (CO), and total vascular conductances (TVC) were measured continuously throughout the experiment. To stimulate the group III mechanoreceptors, PAD was performed for one minute. Results: The results showed that mean arterial pressure (MAP) mediated by the mechanoreflex activation was significantly increased in both groups. However, this pressor response was significantly higher in post-menopausal women. This reflex significantly increased both SV and CO in pre-menopausal women, while there were no differences in post-menopausal women. There was no difference in HR in either group. The mechanoreflex significantly decreased TVC in post-menopausal woman, while there was no difference in pre-menopausal woman. Conclusion: The results indicate that the excessive pressor response mediated by the mechanoreflex occurs due to overactivity of group III mechanorecptors and the mechanism is produced mainly via peripheral vasoconstriction in post-menopausal women.

• The Korean Journal of Pharmacology
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• v.28 no.1
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• pp.61-74
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• 1992

Influence of the blockade of the three major pressor systems-sympathetic nervous system (SNS), renin-angiotensin system (RAS) and vasopressin system-on the pressor responsiveness to norepinephrine (NE), angiotensin II (AII), and vasopressin (VP) as well as on basal blood pressure (BP) levels was investigated in urethane-anesthetized rabbits. To block the SNS and RAS, chlorisondamine (CS) and pirenzepine (PZ), sympathetic ganglionic blockers, and enalapril (ENAL), an inhibitor of angiotensin converting enzyme, respectively were used. And for suppressing the VP system bremazocine (BREM), a kappa opiate receptor agonist shown to suppress plasma levels of VP, was employed. Each of CS (0.4 mg/kg), ENAL (2 mg/kg), and BREM (0.25 mg/kg) produced almost same levels of steady hypotensive state. The hypotensive effect of BREM was significantly attenuated by desmopressin, a synthetic VP-like analogue, suggesting the hypotension being at least in part due to suppression of plasma levels of VP. CS, ENAL and BREM elicited further fall of the BP which had been lowered by ENAL or BREM, CS or BREM, and CS or ENAL, respectively. The hypotension produced by both CS and PZ together with either of ENAL or BREM was more marked than that produced by the three drugs other than CS. CS potentiated the pressor response not only to NE but to AII and VP. The pressor effect of AII was increased by ENAL and BREM, too. The pressor response to VP was also enhanced by BREM. Blockade of ${\alpha}-adrenergic$ receptors with phentolamine or phenoxybenzamine potentiated the pressor response to AII and that to VP. The results on basal BP levels indicate that the three major pressor systems are all participating in control of BP, but SNS has the greatest potential for supporting BP. The finding that blockade of one of the pressor systems induced enhanced pressor responsiveness to the pressor hormone of that particular system as well as to the pressor hormone(s) of the other systems(s) provides evidence for important interactions among the three major pressor systems.

• Korean Journal of Pharmacognosy
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• v.7 no.3
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• pp.215-220
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• 1976

1. Nepetae Herba water extract (NHW) produced a fall of blood pressure in the rabbit. 2. The depressor effect of NHW was inhibited by atropine, but was not affected by propranolol, hexamethonium and diphenhydramine. 3. NHW showed pressor response in the rabbit treated with atropine. 4. The pressor response in the atropine treated rabbit was inhibited by phentolamine and guanethidine.

• YAKHAK HOEJI
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• v.22 no.3
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• pp.163-174
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• 1978

Plantaginis seed has been applied in Chinese medicine a as well as in folk remedy. It was advocated that Plantaginis S Semeη exerts good therapeutic effects as anti-inflammatory, antitussive, obstipant and diuretic agent in some cases of alimentary, respiratory a and renal disorders. This study was carried out in order to r re-evaluate the pharmacological action, especially the hypotensive a action of Plantaginis Semen and to elucidate the mechanism of its a action, making use of Plantaginis Semen methanol extract (PME), because its basic pharmacological action, i. e., hypotensive action is n not clear. 1) PME, when administered into intravenous route, elicited the h hypotensive response dependent on the dose of PME given to the rabbit anesthetized with urethane. 2) This hypotensive response of P PME was inhibited by atropine and potentiated by physostigmine, but not influ$\varepsilon$need by vagotomization. 3) Depressor effect of PME was blocked by chlorisondamine, phentolamine, and bethanicline, while not altered by cyproheptadine, diphenhydramine and propran¬olol. 4) The secondary pressor response after blocking the depressor e effect of PME by chlorisondamine was produced, but this pressor response was deminished by atropine. 5) PME augmented the pressor e effect of norepinephrine and angiotensin, on the other hand, reduced b blood pressure elevated by carotid occlusion reflex. 6) These observa¬t tions suggest that PME may induce the hypotensive response via dual mechanisms of parasympathomimetic and sympatholytic action, that the positions of this action are cholinergic peripheral site and sympathetic ganglia respectively, and that PME may possess the pressor activity caused by stimulation of "atropine-sensitive site" which seems to existsin the sympathetic ganglia.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.59-67
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• 1982

1) Oxymetazoline, which has been known as an agonist for${\alpha}_1-adrenoceptor$ in various peripheral tissues, caused a pressor response in urethane-anesthetized rabbits when given intra-ventricularly. This pressor response was little affected by pretreatment of rabbits with i.v. guanethidine or chlorisondamine, but it was weakened in rabbits pretreated with either of i.v. phentolamine or guanethidine and chlorisondamine and in guanethidine-pretreated adrenal-ligated rabbits. 2) The pressor to intraventricular oxymetazoline was markedly attenuated by intraventricular pretreatment with prazosin, whereas intraventricular pretreatment with yohimbine or piperoxan did not affect this response. 3) Reserpine-pretreated rabbits also responded with hypertension to intraventricular oxymetazoline, which was markedly diminished by pretreatment with intraventricular prazosin but not affected by yohimbine. 4) Oxymetazoline, given intravenously, produced a pressor response in both whole and spinal rabbits. Intravenous prazosin, phentolamine and yohimbine, in this order, showed greater antagonizing effect to this pressor response. 5) The results indicate that oxymetazoline acts an agonist for ${\alpha}_1-adrenoceptors$ in the rabbit brain participating in the regulation of the blood pressure and in the vasculature of rabbits.