All issues
Volume 101 (1993)
- Issue 6 Pages 349-
- Issue 5 Pages 289-
- Issue 4 Pages 197-
- Issue 3 Pages 101-
- Issue 2 Pages 59-
- Issue 1 Pages 1-
Volume 101, Issue 4
Displaying 1-8 of 8 articles from this issue
- |<
- <
- 1
- >
- >|
-
Tetsuo OKA, Toyokazu HIRANUMA, Xiao-Fei LIU, Nobuyuki OHGIYA, Kayoko I ...1993 Volume 101 Issue 4 Pages 197-207
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe inhibitory effects of opioid peptides such as [Met5]-enkephalin and [Met5]-enkephalin-Arg6 on the electrically-evoked contractions of guinea-pig ileum, mouse vas deferens and rat vas deferens were enhanced by aminopeptidase inhibitors such as amastatin and bestatin, a peptidyl dipeptidase A inhibitor like captopril, and endopeptidase-24.11 inhibitors such as phosphoramidon and thiorphan. The magnitude of the enhancement by each peptidase inhibitor depended on both the preparation and opioid peptide employed. Additionally, enkephalin had been shown to be almost exclusively hydrolyzed at least in the ileal and striatal guinea pig membrane preparation by 3 kinds of enzymes, amastatin-sensitive aminopeptidase(s), captopril-sensitive peptidyl dipeptidase A and phosphoramidon-sensitive endopeptidase-24.11, which were indicated to be located very close to opioid receptors.View full abstractDownload PDF (17560K) -
Sachiko OH-ISHI1993 Volume 101 Issue 4 Pages 209-218
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSIt is well known that the kallikrein-kinin system expresses potent biological activities through its final product, bradykinin. However, bradykinin has an extremely short half life in biological fluids, so that it is difficult to quantitate the amount of bradykinin released in relevant pathological samples. Therefore investigators have attempted to prove its involvement or importance by measuring the precursor proteins, such as prekallikrein, kininogens, and glandular kallikreins. In this review, I would like to focus the discussion on a study of the kallikrein-kinin system in B/N Katholiek rats, a strain that has a congenital deficiency in plasma high molecular weight and low molecular weight kininogens. When experimental inflammation induced in the mutant deficient rats are compared to that induced in the normal rats (B/N-Kitasato), there was a significant difference; i.e., the deficient rats showed less swelling in the carrageenin-induced paw edema and less exudate accumulation in carrageenin-induced rat pleurisy. These results indicate that bradykinin may be released from kininogens and it may cause exudate formation in above inflammation. Furthermore, when experimental hypertension was induced by DOCA-salt loading, the blood pressure of the deficient rats rose faster than that of the normal rats. From the above findings, it is concluded that the plasma kallikrein-kinin system could be an important regulatory system in body defense mechanisms such as inflammation and blood pressure control.View full abstractDownload PDF (19624K) -
Yuji IMAIZUMI1993 Volume 101 Issue 4 Pages 219-231
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSMembrane ionic currents were recorded using whole cell and patch clamp techniques in smooth muscle cells isolated from various organs to clarify the mechanisms underlying the diversity of membrane excitability. Components of inward and outward currents upon depolarization were resolved from one another kinetically or pharmacologically and were analyzed and compared in these cells under the same conditions. Cells were isolated from the ureter (UT), urinary bladder (UB), vas deferens (VD), aorta (AT), pulmonary artery (PA), taenia caeci (TC) and ileum (IL) of the guinea pig; the femoral artery (FA), portal vein (PV) and iris sphincter (IS) of the rabbit; the stomach fundus (SF) of the rat; the trachea (TR) of the dog and the coronary artery (CA) of the pig. Action potentials were elicited by depolarization in cells from UT, UB, VD, TC, IL, SF and PV, but not in those from AT, PA, FA, IS, TR and CA. Currents identified included Ca2+ currents, Na+ current, Ca2+-dependent K+ current, two kinds of delayed rectifier K+ currents which were pharmacologically distinguished by sensitivity to 4-aminopyridine, and Ca2+-independent A-type transient K+ current. The membrane excitabitiy including the action potential configuration in each cell type can be roughly explained by a combination of these currents, taking their amplitude and features into consideration.View full abstractDownload PDF (25954K) -
Toshinori HIDAKA, Kazuo AISAKA, Tomochika OHNO, Takafumi ISHIHARA1993 Volume 101 Issue 4 Pages 233-251
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSEffects of carperitide (α-human atrial natriuretic peptide) on hemodynamics and renal function in dogs with congestive heart failure (CHF) produced by volume expansion and ligation of the left anterior descending coronary artery were compared with those of various anti-heart failure agents (cardiotonic, vasodilator and diuretic). Carperitide (0.1 ?? 1 μg/kg/min) dose-dependently decreased the elevated left ventricular end-diastolic pressure (LVEDP). No significant changes in cardiac contractility (LV dP/dtmax) and heart rate (HR) were noted, although cardiac output (CO) tended to reduce during the infusion of carperitide. Nitroglycerin (NG; 3 μg/kg/min) and furosemide (1 mg/kg) also decreased LVEDP, but the potency was less than that of carperitide. Sodium nitroprusside (SNP; 10 μg/kg/min) and dobutamine (10 μg/kg/min) caused a reduction in LVEDP and increased CO with an increase in HR. Hydralazine (H; 100 μg/kg/min) increased CO without reduction in LVEDP and induced a pronounced increase in HR. Double product (systolic blood pressure × HR), an index of myocardial oxygen consumption, was significantly reduced by carperitide, but significantly increased by DB and H. Carperitide, unlike NG, SNP, H and DB, increased urine volume and urinary electrolyte excretion. These results suggest that carperitide will be an useful therapeutic agent for the treatment of CHF.View full abstractDownload PDF (27035K) -
Masami SATO, Kazunori IMADA, Shigeo IIDA, Kiyokazu OHASHI, Shigeru KIM ...1993 Volume 101 Issue 4 Pages 253-267
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe general pharmacological properties of MHR-24 were studied in various experimental animals. Intravenously (i.v.)-administered MHR-24 at 8.6×102 JRU/kg or more produced fever in rabbits. MHR-24 at 3×104 JRU/kg or more caused tachycardia; and at 1×105 JRU/kg or more, it lowered arterial blood pressure in anesthetized monkeys. In rats, MHR-24 at 2.9×104 JRU/kg or more showed a diuretic action and inhibitory effects on gastric juice secretion and carrageenin-induced paw edema. Furthermore, MHR-24 at a large dose (8.6×104 or 2.9×105 JRU/kg, i.v.) decreased spontaneous locomotor activity, had an inhibitory effect on acetic acid-induced writhing and potentiated intestinal propulsion in mice; and it caused the appearance of rest wave on acute spontaneous electroencephalograms in rabbits. Pretreatment of the animals with the cyclooxygenase inhibitor indomethacin abolished the fever and potentiation of intestinal propulsion caused by MHR-24. Therefore, these data seem to indicate that some of the effects of MHR-24 are mediated via cyclooxygenase pathways. The results suggested that, except for the above results, MHR-24 has no noticeable effects on the central nervous, autonomic nervous, respiratory and cardiovascular systems and others in general pharmacological studies.View full abstractDownload PDF (28577K) -
Kensuke KISARA, Shinobu SAKURADA, Takeshi TADANO, Tsukasa SAKURADA, Ko ...1993 Volume 101 Issue 4 Pages 269-280
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSCentral effects of intravenously (i.v.)-administered iohexol were compared with those of iopamidol in a series of tests. Mannitol was used as a reference. As assayed by the primary screening test based on Irwin's method, i.v. administration of mannitol resulted in a score of 0 in ddY mice and a score of 0.6 in ICR mice in the startle response. These results were not different from the data of both iohexol and iopamidol. lopamidol at a dose of 1750 mgI/kg produced an inhibitory effect on the spontaneous locomotor activity. Iohexol at a dose of 7000 mgI/kg potentiated the duration of thiopental-induced narcosis. Hypothermia was caused by high doses of both iohexol and iopamidol. Electric stimulus increased the mortality of mice pretreated with high doses of iohexol and iopamidol. Both drugs had no notable activities in the anticonvulsant, electroencephalic, muscle relaxant and antinociceptive tests. These results indicate that both iohexol and iopamidol do not necessarily possess a similar pharmacological action. Judging from the LD50 of approximately 15000 mgI/kg for both drugs, they seem unlikely to have a specific pharmacological action on the central nervous system.View full abstractDownload PDF (19990K) -
Kumiko AOKI, Tadashi KISHIMOTO, Kiyotaka SUNAKAWA, Yoshiaki OKAMIYA, K ...1993 Volume 101 Issue 4 Pages 281-288
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSInhibitions by palonidipine hydrochloride (TC-81), a new Ca entry blocker, of the contractile responses to norepinephrine (NE), serotonin (5-HT), prostaglandin F2α (PGF2α) and U-46619, a thromboxane A2 analog, were investigated in isolated rat aorta strips and compared with the inhibition of the high K+ response. TC-81 and nicardipine inhibited the contractile responses to NE, 5-HT, PGF2α, and U-46619 in a concentration-dependent manner, but their relative inhibitions were less than 50% at 10-8 M. In a Ca2+-free medium, 2-hr pretreatment with TC-81 or nicardipine did not inhibit the contractile responses to various vasoconstrictors, but it inhibited the responses to the addition of Ca. Their inhibitory potencies were less than the inhibition with high K+. Also, the treatment with TC-81 or nicardipine at 10-7M did not affect the tissue level of cyclic AMP. These results suggest that in isolated rat aorta, the inhibition by TC-81 of the contractile responses to NE, 5-HT, PGF2α and U-46619 is not due to inhibition of intracellular Ca2+ release or an increase in cyclic AMP; rather, it is due to inhibition of the Ca2+ influx. This inhibitory effect was less than that seen on the high K+ response.View full abstractDownload PDF (11899K) -
[in Japanese]1993 Volume 101 Issue 4 Pages 289-291
Published: 1993
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSDownload PDF (5657K)
- |<
- <
- 1
- >
- >|