• The Korean Journal of Pharmacology
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• v.21 no.2
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• pp.119-127
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• 1985

The renal function is under regulatory influence of the central nervous system, mainly through activation of sympathetic nerve to the kidney, and it was recently reported that clonidine, an agonist to ${\alpha}_2$-adrenoceptors, induces diuresis and natriuresis when injected directly into a lateral ventricle of the rabbit brain (i.c.v.). This study was undertaken, therefore, to obtain further information as to the role of the central ${\alpha}_2$-adrenoceptors in regulating renal function, by observing the effects of i.c.v. yohimbine, a specific antagonist of adrenoceptors of ${\alpha}_2$-type, on the rabbit renal function, and to elucidate the mechanism involved in it. With 10 ${\mu}g/kg$ i.c.v. of yohimbine sodium excretion transiently increased along with increasing tendency of urine flow, renal plasma flow and glomerular filtration rate. These responses decreased with increasing doses. With 100 and 300 ${\mu}g/kg$ i.c.v. marked antidiuresis and antinatriuresis as well as profound decreases of renal perfusion and glomerular filtration were noted. Systemic blood pressure transiently increased. In reserpinized rabbits, 100 ${\mu}g/kg$ yohimbine i.c.v. did not produce any significant changes in urine flow, sodium excretion as well as in renal hemodynamics. The pressor response was also abolished. In preparations in which one kidney was denervated and the other left intact as control, i.c.v. yohimbine elicited typical antidiuretic antinatriuretic response in the innervated control kidney, whereas the denervated experimental kidney responded with marked diuresis and increases in excretory rates of sodium and potassium and in osmolar clearance in spite of absence of increased filtration and perfusion . Systemic blood pressure responded as in the normal rabbits. These observations indicate that i.c.v. yohimbine affects renal function in dual ways in opposite directions, the first being the antidiuretic antinatriuretic effects which results from decreased renal perfusion and glomerular filtration due to sympathetic activation and which is predominantly expressed in the normal rabbits, and the second less apparent effect being the diuretic and natriuretic action which is not mediated by nerve pathway but brought about by some humoral mechanism and which is effected by decreased sodium reabsorption in the tubules, possibly of the proximal portion.

• Journal of Life Science
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• v.18 no.3
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• pp.291-297
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• 2008

We investigated whether 1) the combined capsaicin (75 mg), sesamin (30 mg), and L-carnitine (900 mg) (CCSC) ingestion enhances autonomic nervous system (ANS) activities including thermogenic sympathetic activity as energy metabolic modulator, 2) ${\beta}_3-AR$ polymorphism of each subject influences with ANS activity. Seven healthy males $(22.0{\pm}0.5\;yr)$ volunteered for this study. The cardiac autonomic nervous activities evaluated by means of heart rate variability of power spectral analysis were continuously measured during 5 min every 30 min for total 120 min resting condition with CCSC or placebo oral administration chosen at random. The results indicated that, there are not $Arp/Arg^{64}$ variants of the ${\beta}_3-AR$ genotypes in our subjects. There were not also significant differences in heart rate during rest between both trials. The difference of ANS activity did not reach the statistical significance between both trials. However, the significant improvement showed TOTAL power, HF component, and the indices of SNS and PNS activities before and at 30 min after CCSC ingestion (p<0.05, respectively). In conclusions, although each component of combined CCSC is associated with lipolysis and/or fat oxidation, the combined CCSC consumption is not influenced in stimulation of thermogenic sympathetic activity as modulator of energy metabolism. In rather, our results suggested that CCSC ingestion improves the balance of both SNS and PNS activities. Therefore, it will be considered many combined nutrient components for ergogenic and/or lipolysis effects as well as genetic variants affecting ANS activity in further studies.

• The Korean Journal of Pharmacology
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• v.26 no.1
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• pp.13-23
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• 1990

Methylene Blue (MeB) and gentian violet $(10^{-6}{\sim}10^{-4}\;M)$ produced contractions in isolated thoracic aortic preparations of rabbits in a dose-dependent fashion, while other dyes, evans blue and eosine yellowish, did not affect the basal tension in the same range of doses. Porcine mesenteric arterial rings also responded to MeB with dose-dependent contractions. Single dose of $10^{-4}$ M MeB produced a biphasic response: contraction followed by relaxation. The contraction developed slowly within $2{\sim}4$ min and peaked in about 20 minutes and then slowly relaxed to the basal level. Tyramine $(10^{-4}\;M)$ also induced contraction but it developed faster and was more persistent than that of MeB. While the tyramine-induced tension was reproducible, the MeB-induced one wat not reiterable until 3 to 5 hours after washing out the MeB. Adding $10^{-4}$ M MeB further potentiated the contraction induced by $10^{-4}$ M tyramine. However, the MeB contraction was not affected by further addition or tyramine. Both tyramine- and MeB-induced tensions were abolished or significantly inhibited by pretreatment with various drugs acting on the sympathetic nervous system. The tyramine-induced tension was more sensitive to guanethidine and 6-hydroxydopamine than the MeB-induced tension, while the latter was more sensitive to $Ca^{2+}-free$ PSS and reserpine. But they have similar sensitivity to prazosin. The MeB-induced tension was significantly inhibited but not abolished by 6-hydroxydopamine pretreatment. However, either tyramine or 6-hydroxydopamine could not affect the basal tension of the ring that MeB once had been tested. These results suggest that MeB-induced contractions of rabbit thoracic aorta and porcine mesenteric artery result from a release of endogenous norepinephrine from adrenergic nerve endings and are dependent in part on extracellular calcium, and that the potency of MeB to release or to deplete norepinephrine is greater than that of either tyramine or 6-hydroxydopamine.

• The Korean Journal of Pharmacology
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• v.1 no.1 s.1
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• pp.17-36
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• 1965

Besides it's all important analgesic action, morphine has, among others, hyperglycemic effect, though not important clinically, which is believed to be resulted from augmented glycogenolysis in the liver and muscles due to the increased liberation of epinephrine from the adrenal medulla upon the stimulation of the posterior part of hypothalamus. It is known that adrenergic blocking agents are acting inhibitory to this sort of hyperglycemia. Much, however, should as yet be studied for the drugs which affect central nervous system and release of endogenous catecholamine as far as their effects on hyperglycemia are concerned. Much is still not known about the effect of ginseng, which has been highly regarded in the Herb Medicine, as far as it's influence on the blood sugar is concerned. Author investigated the effects of chlorpromazine, reserpine and ginseng on epinephrine induced, and morphine-induced hyperglycemiae. Animals used in this experiment were healthy albino rabbits weighing approximately 2.0 kg of body weight and were all fasted for 24 hours, before the experiment undertaken. Blood sugar determination was carried out by Nelson-Somogy method. Results obtained are summarized as follows; 1. The groups of rabbits administered intravenously with epinephrine 0.02 mg/kg, and 0.05 mg/kg, showed marked and transient hyperglycemia within 15 minutes after injection. The maximal rate of elevation in blood sugar to the control level, were 28% and 57% respectively. The blood sugar returned to the control level within 3 hours. Thus, the hyperglycemic responses were paralleled with epinephrine doses. 2. The hyperglycemic responses by morphine were different according to the doses. The groups of rabbits in which 4 mg/kg of morphine was administered, did not show any hyperglycemic effect, but, in which 10 mg/kg of morphine administered, showed severe hyperglycemic effect, resulting in the maximal level within 2 hours after injection. The maximal rate of increasing in blood sugar ,level was 88%. Compared .with epinephrine-injected groups, morphjne-injected groups showed more persistent hyperglycemic effect, but returned to control blood sugar .level in 6 hours after injection. 3. The intravenous injection of chlorpromazine 2 mg/kg and 8 mg/kg evoked a slight, and persistent hyperglycemia. The maximal rate of increasing in blood sugar level were 15% and 23% respectively. These hyperglycemia gradually returned to the normal level in 5 or 6 hours after injection. Thus, the intensity of response was paralleled with the dose of chlorpromazine. 4. The intravenous injection of reserpine 0.2 mg/kg and 0.5mg/kg, showed the most persistent but steady elevation of blood sugar level in this experiments, resulting in the maximal level in 5 hours after injection. The maximal rate of increasing of blood sugar level were 18% and 39% respectively. 5. The blood sugar level from 24 hours to 30 hours after intraperitoneal administration of reserpine 1.0mg/kg, did not show statistically significant difference, compared with control groups. 6. The oral administration of ginseng extract 15 ml/kg did not. show any :change in blood sugar level. 7. The intravenous administration of epinephrine 0.05 mg/kg or morphine 4 mg/kg to the group pretreated with ginseng extract 15 ml/kg $20{\sim}30$ minutes before the experiment, evoked more marked hyperglycemic effect than the non-pretreated group. 8. The intravenous administration of epinephrine 0.02 mg/kg, morphine 4 mg/kg, or morphine 10 mg/kg to the groups pretreated with reserpine 0.2 mg/kg or 0.5 mg/kg $20{\sim}30$ minutes before experiment, produced more marked and persistent hyperglycemic effects than the groups injected with single epinephrine or morphine injection. 9. When epinephrine 0.05 mg/kg or morphine 10 mg/kg administered intravenously to the groups pretreated with the intraperitoneal administration of reserpine 1 mg/kg 24 hours before experiment morphine-induced hyperglycemia was inbibited, but epinephrine-induced hyperglycemia was augmented. 10. When epinephrine 0.05mg/kg or morphine 10 mg/kg administered intravenously to the groups pretreated with chlorpromazine, 2 mg/kg, 4 mg/kg, and 8 mg/kg $20{\sim}30$ minutes before the experiment, morphine-induced hyperglycemia was inbibited, but epinephrine-induced hyperglycemia was more persistent.