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Biomedical subjects

K Takeda

Publications and source records attributed to K Takeda.

At least 1,261 records · Page 70Linked to original sources
PubMed1983

Cardiovascular and sympathetic nerve responses induced by intracerebroventricular injections of prostacyclin in rats.

Intracerebroventricular (ICV) injections of prostacyclin (PGI2) produced biphasic blood pressure responses consisting of an initial hypotensive phase followed by a sustained pressor phase in awake rats. Heart rate increased following such injections in either awake or anesthetized rats. PGI2, 1 microgram, produced biphasic responses and, 10 micrograms, purely vasodepressor responses in anesthetized rats, but abdominal sympathetic nerve firing recorded was consistently increased. Hypophysectomy did not affect the hypotensive phase of the responses. These results indicate that the initial hypotension can not be explained by centrally-induced changes in sympathetic nerve activity or vasopressin release, but may be due to peripheral effects of PGI2 leaking from the injection site.

Animals↗
PubMed1983

Effects of drugs on the cerebral circulation of the dog in relation to the cerebral oxygen consumption.

Drug effects were studied on the cerebral circulation by measuring the sagittal sinus outflow in the anaesthetized dog following the method of Michenfelder and by monitoring cerebral oxygen consumption. Systemic aortic pressure, heart rate and spinal fluid pressure were also studied. Since dilatation of cerebral vessels was observed in nearly all the preparations after inhalation of CO2, it was thought that gross extracerebral contamination was virtually eliminated in this preparation. A close correlation was observed between the oxygen consumption of the brain as a whole and the sagittal sinus outflow (r = 0.93, P less than 0.001); therefore it became feasible to differentiate the direct effects of drugs on cerebral blood vessels from indirect ones attributable to changes in the cerebral oxidative metabolism. Sodium pentobarbitone (5 mg kg-1, i.v.), reduced the cerebral venous outflow and caused a decrease in the oxygen consumption. Pentylenetetrazol (30 mg kg-1 i.v.) and bemegride (5 mg kg-1 i.v.) produced an increase in the blood flow and a corresponding increase in the cerebral oxygen consumption. Thus, it was concluded these substances had no direct effects on the cerebral blood vessels. Acetazolamide (10 mg kg-1, i.v.), a carbonic anhydrase inhibitor, produced a marked and sustained vasodilatation after a latent period of 0.5-1 min. There was no increase in the cerebral oxygen consumption. A similar pattern was seen after CO2 had been inhaled. Methylergometrine and dihydroergotamine (20 micrograms kg-1 i.v.) induced a prolonged vasoconstriction of the cerebral vascular bed without any changes in the oxygen consumption of the brain. Therefore this method can discriminate between indirect or direct effects of drugs on cerebral vascular outflow.

Acetazolamide↗
PubMed1983

The effects of 2-nicotinamidoethyl nitrate on smooth muscle cells of the dog mesenteric artery and trachea.

The effects of 2-nicotinamidoethyl nitrate (nicorandil; 2-NN), a synthesized coronary vasodilator, on smooth muscle cells of dog mesenteric artery or trachea were investigated using microelectrode, double sucrose gap and isometric tension recording methods. Nicorandil hyperpolarized the smooth muscle membrane of the mesenteric artery (5 X 10(-6)M) and the trachea (5 X 10(-5)M). In both these smooth muscle cells, the nicorandil-induced hyperpolarization remained constant in various concentrations of [Cl-]o, but changed with various concentrations of [K+]o. This hyperpolarization was partly inhibited following pretreatment with tetraethylammonium (TEA greater than 1 mM) and was completely inhibited following pretreatment with procaine (1 mM or 5 mM), indicating that the nicorandyl-induced hyperpolarization is due to increase in the K-conductance, in both these membranes. Following pretreatment with TEA (5 mM), outward current pulses evoked an action potential in tracheal smooth muscle cells. Nicorandil inhibited the generation of action potential due to the hyperpolarization of the membrane but not due to inhibition of the spike generating mechanism. Nicorandil (10(-6)M) inhibited the contracture evoked by excess [K]o, in both tissues. The contracture evoked by noradrenaline or repetitive field stimulation with short duration (50 microseconds) pulses was also inhibited in the mesenteric artery, while a higher dose of nicorandil (10(-5)M) was required to inhibit the contracture evoked by acetylcholine or repetitive field stimulation in the trachea. Excitatory junction potentials (e.j.ps) evoked by field stimulation in the mesenteric artery due to the release of noradrenaline, or in the trachea due to release of acetylcholine, were suppressed by 10(-5)M or 5 X 10(-5)M nicorandil, respectively. The reduction in the amplitude of e.j.p. was mainly due to the hyperpolarization of the membrane with increase in the membrane conductance. In the mesenteric artery, following pretreatment with TEA (1 mM) an action potential was generated on the e.j.p.. Nicorandil suppressed the generation of the action potential by reduction in the amplitude of the e.j.p., below the threshold required for generation of the action potential. These results indicate that nicorandil hyperpolarizes the membrane by increasing K-conductance and inhibits the generation of contraction, in both tissues. Higher concentrations of nicorandil are required to suppress the mechanical response in the trachea than in the mesenteric artery. Depression of the mechanical responses in both tissues is partly due to suppression of Ca-mobilization inside the muscle cells and partly to hyperpolarization of the membrane.

Animals↗
PubMed1983

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats.

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

Animals↗
PubMed1983

Arterial pressure-urinary output relationship in DOCA-saline hypertensive rats.

To know the role played by the kidney in the genesis of deoxycorticosterone acetate (DOCA)-saline hypertension, the arterial pressure-urinary output (AP-UO) relationship was compared in unanesthetized, unrestrained uninephrectomized (1-K) control and normal Wistar-Imamichi (W-I) rats according to the method of Norman et al. [Am. J. Physiol. 234 (Regulatory Integrative Comp. Physiol. 3): R98-R103, 1973]. The gradient of AP-UO relationship was slightly decreased in 1-K control rats compared with that in W-I rats. However, the AP-UO relationship of DOCA-saline hypertensive rats underwent only a parallel shift to higher blood pressure ranges compared with that of 1-K control rats. There was no significant change in the urinary volume, urinary sodium excretion, and urinary osmolarity. Furthermore, the AP-UO relationship was shifted back to the lower pressure range under the influence of hydralazine, a preferential renal arteriolar dilator, suggesting that constriction of the renal artery caused the rise of the arterial pressure in DOCA-saline hypertensive rats.

Animals↗
PubMed1983

Effects of spinasterol and sitosterol on plasma and liver cholesterol levels and biliary and fecal sterol and bile acid excretions in mice.

Effects of spinasterol and sitosterol on plasma and liver cholesterol levels and biliary and fecal sterol and bile acid excretions were examined with male mice. Both phytosterols were added to the diet at a 1% concentration and fed to mice for 15 days. Spinasterol increased the fecal cholesterol excretion and decreased the plasma and liver cholesterol levels, the bile acid pool size and the fecal bile acid excretion, especially those derived from chenodeoxycholic acid. Fecal coprostanol excretion remained unchanged. These changes were similar to those produced by sitosterol. These data led to the conclusions 1) that spinasterol, as well as sitosterol, inhibits cholesterol absorption, resulting in decreases of the plasma and liver cholesterol levels and 2) that when cholesterol absorption is inhibited, the synthesis of bile acids, especially that of chenodeoxycholic acid, decreases, suggesting that the dietary cholesterol is preferentially metabolized to chenodeoxycholic acid in mice.

Animals↗
PubMed1983

Changes in stenosis resistance and myocardial blood flow after a brief coronary occlusion in the dog.

Stress-induced changes in the resistance due to coronary arterial stenosis of a fixed diameter and in the myocardial blood flow distal to the stenosis were investigated in the open-chest dog. Myocardial blood flow in the inner and outer third of the left ventricular wall was continuously measured with heated cross-thermocouples. The circumflex coronary artery was constricted with a thick string so that myocardial reactive hyperemia was nearly eliminated. Without constriction, a 15-second occlusion of the artery produced no significant changes in the resistance of large coronary arteries. On the contrary, in the presence of coronary constriction, a brief coronary occlusion caused a sustained decrease in distal coronary pressure and subendocardial myocardial flow during reactive hyperemia, while coronary flow returned quickly to the pre-occlusion level with significant reactive hyperemia of subepicardial flow. This change resulted in a long-lasting increase in the stenosis resistance. These results suggest that stenosis resistance changes dynamically, resulting in additional myocardial ischemia especially in the subendocardial myocardial layers.

Animals↗
PubMed1983

Increase in the resistance of stenotic coronary segment by intravenous infusion of isoproterenol.

The effects of intravenous infusion of isoproterenol on stenosis resistance were studied in the anesthetized open-chest dog. The circumflex coronary artery (LCx) was isolated near its origin and an electromagnetic flow transducer was placed around the vessel for measuring coronary flow. A polyethylene catheter was inserted into the small branch of LCx for monitoring distal coronary pressure. LCx was constricted with a thick cotton string to a degree of obstruction that eliminated reactive hyperemia following a 20-second coronary occlusion. The coronary resistance across the stenotic segment (RL) was calculated as the pressure gradient across the stenosis divided by coronary flow. Isoproterenol was infused intravenously in a dose to keep the heart rate at a level 25-30% above the control with and without coronary constriction. For maintaining the ascending aortic pressure at the pre-isoproterenol level, the descending thoracic aorta was constricted with a tape. In the absence of coronary constriction, the vascular resistance of large coronary arteries was not affected by isoproterenol with a significant increase in coronary flow. In the presence of coronary stenosis, isoproterenol markedly increased RI regardless of additional aortic constriction. The magnitude of the increase in RL during aortic constriction varied directly with the percent increase in the pressure gradient across the coronary stenosis. Pacing-tachycardia essentially did not affect RL. These results suggest that isoproterenol increased the vascular resistance of the stenotic segment with fixed caliber.

Animals↗
PubMed1983

Extraction, cloning and physical maps of plasmid DNAs from Streptomyces noursei.

Three plasmids, pSCY 2, pSCY 3 and pSCY 4, were detected in Streptomyces noursei B3, a producer of cycloheximide and nystatin. pSCY 3 and pSCY 4 had molecular sizes of 15.1 megadaltons (Md) and 3.2 Md, respectively. When covalently closed circular (ccc) DNAs were extracted from the mycelia during the course of cultivation, the yield of ccc DNA extracted per mycelium reached the highest value at the starting point of the exponential growth phase and decreased rapidly during exponential phase; the yield increased gradually in stationary phase. The smallest plasmid, pSCY 4, could not be detected after 42 hours of cultivation. To purify and characterize DNA of the major plasmid pSCY 3, it was cloned into Escherichia coli using pACYC 184 as a vector, and the physical maps of the composite plasmids were constructed.

Base Sequence↗
PubMed1983

Basic techniques for DNA cloning and conditions required for streptomycetes as a host.

To develop a host-vector system in streptomycetes for DNA cloning, we examined the technical problems encountered and the conditions required for use of Streptomyces kasugaensis MB273 as the host. Basic techniques, such as plasmid DNA isolation, regeneration of mycelia from protoplasts and elimination of plasmids from cells were investigated. These techniques were found to be useful for many streptomycetes. Strain M518, a derivative of S. kasugaensis MB273, was found to have the following useful characteristics as a host. The plasmids of MB273 were easily cured by regeneration of mycelia from protoplasts. The protoplasts prepared from M518 regenerated mycelia at high frequency using an improved method and were efficiently transformed by plasmid DNA. The extra and intra cellular DNase activities were very weak, and no restriction endonuclease activity was detected. The sensitivity to various antibiotics was determined. This strain did not show any pathogenicity in mice nor suvival in the digestive organs of rats. MB273 and its derivatives died rather quickly in natural soil. M518 still forms aerial mycelial conidia. These results indicate that S. kasugaensis M518, derived from MB273, has useful characteristics as a host for DNA cloning. The techniques thus developed were found to be useful in other streptomycetes.

Animals↗
PubMed1983

[Effects of several beta-blockers and penfluzide, a thiazide diuretic, on the blood pressure, urinary water output and excretion of Na and K in DOCA-saline-induced hypertension in rats].

Effects of beta-blockers on the blood pressure (BP), urinary output (V) and excretion of Na% (UNaV) and K+ (UKV) were studied in DOCA-saline hypertensive rats in comparison with those of a thiazide diuretic drug, penfluzide. Pindolol produced a hypotension at all infusion rates of Ringer's solution used and a decrease in V with a retention of Na+ and K+ at a low infusion rate. There was a parallel shift of Guyton's renal function curve back to the lower pressure ranges. Similar effects were observed with labetalol. Propranolol induced an increase in UKV at all infusion rates and had a diuretic action at a high infusion rate without producing a significant fall of BP. UKV tended to be increased after atenolol, with essentially no change in other parameters. A new beta-blocker with alpha-blocking action, K-351, produced a hypotension at intermediate and high infusion rates and an increase in UNaV (low infusion rate) and UKV (low and high rates). UKV tended to be increased with another new beta-blocker, N-696, with a fall of BP at high infusion rate. Penfluzide produced a significant decrease in BP at intermediate and high infusion rates and an increase in UKV at all infusion rates.

Adrenergic beta-Antagonists↗
PubMed1983

Ventricular performance in congenital left-to-right shunt: temporal Fourier analysis of gated blood-pool data.

Using global time-activity curves, the phase and amplitude at fundamental frequency were calculated, and emptying patterns of the right and left ventricles (RV,LV) were evaluated by phase difference [D(phase) = RV phase minus LV phase] and RV/LV amplitude ratio [R(amp)]. In 21 subjects with normal cardiac function, D(phase) was minimal (mean 2.2 +/- 6.1 degrees), regardless of heart rate, and R(amp) was distributed from 0.31 to 0.92 (mean 0.57 +/- 0.20). In 19 patients of ventricular septal defect (VSD), R(amp) remained within the normal range, whereas D(phase) became larger in proportion to the ratio of pulmonary-to-systemic blood flow, Qp/Qs (p less than 0.001). Especially, cases with Qp/Qs over 2.0 showed a significant RV phase lag. By contrast, nine patients with patent ductus arteriosus (PDA), showed no RV phase lag, but--particularly in cases with Qp/Qs greater than 2.0--R(amp) was smaller than normal (p less than 0.001). Thus this method is valuable for pathophysiologic investigation of diseases with L-to-R shunt, and can help in the noninvasive differential diagnosis between VSD and PDA.

Adolescent↗
PubMed1983

Cardiac actions of vanadium.

Vanadate produces positive or negative inotropic effects in isolated cardiac muscle preparations, depending on species, type of the muscle, and experimental conditions. In intact animals, vanadate decreases the force of left ventricular contraction, presumably because of a coronary vasoconstriction, and decreases the heart rate. The blood pressure may be elevated or lowered by vanadate. Although vanadate is a potent inhibitor of isolated Na,K-ATPase, the above actions of vanadate are not associated with sodium pump inhibition, because vanadate is incapable of inhibiting the sodium pump in intact myocardial or vascular smooth muscle cells. In addition to inhibiting isolated Na,K-ATPase, vanadate is capable of affecting many, but not all, biochemical reactions involving formation of phosphorylated intermediates. Whether these effects occur in intact cells, however, should be carefully evaluated. In cardiac muscle preparations, vanadate seems to affect a superficial Ca2+ pool; its augmentation and inhibition corresponding to the positive and negative inotropic effects, respectively. The mechanism for the actions of vanadate on such a superficial Ca2+ pool, however, is presently unknown.

Animals↗