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Biomedical subjects

K Adachi

Publications and source records attributed to K Adachi.

At least 703 records · Page 39Linked to original sources
PubMed1975

Prostaglandins and cyclic AMP in epidermis. Evidence for the independent action of prostaglandins and adrenaline on the adenyl cyclase system of pig and human epidermis, normal and psoriatic.

Prostaglandins E1 and E2 stimulate cyclic AMP accumulation in pig epidermis and in human epidermis from patients with psoriasis. Prostaglandins A1,A2 and F2alpha are relatively ineffective. The fact that this stimulation is not inhibited by a beta-blocker (propranolol) and that the stimulation by prostaglandin E2 and adrenaline is additive indicates that each drug acts independently on the epidermal adenyl cyclase system. In other words, prostaglandins E1 and E2 act on a site other than the beta-receptor of adenyl cyclase in epidermis. The stimulation by prostaglandins E1 and E2 is not additive; hence they probably act on the same site. Concentrations of prostaglandin E above 3X10(-7) M are effective in causing stimulation. This concentration may be within the physilogical range and the contribution of endogenous prostaglandin levels in the control of intracellular cyclic AMP levels cannot be disregarded.

Adenylyl Cyclases↗
PubMed1975

On the lack of response to catecholamine stimulation by the adenyl cyclase system in psoriatic lesions.

When epidermis from the uninvolved skin of psoriatic patients was incubated for 5 min in Hank's medium containing adrenaline and theophylline, the cyclic AMP level consistently increased 20-30 times over the level observed when adrenaline was not added to the medium. On the other hand, when epidermis from the involved skin of psoriatic patients was incubated under the same experimental conditions, the cyclic AMP level increased only 2-5 times. Even when theophylline, and inhibitor of specific cyclic AMP-phosphodiesterase, was omitted from the medium, a clearly demonstrable difference in sensitivity to adrenaline was evident in normal appearing and lesional psoriatic epidermis. These results indicate a faulty adenyl cyclase system in the involved epidermis of psoriatic lesions rather than a defective degradation process by the specific phosphodiesterase. Since the Km for adrenaline activation of adenyl cyclase was approximately the same in both the uninvolved and the involved epidermis and since the cyclic AMP increase by adrenaline was abolished by the addition of propranolol, the basic nature of the beta-receptor (specifically the binding affinity to adrenaline) in the involved epidermis does not appear to be defective. On the other hand, the finding that the Vmax for adrenaline activation is 10-20 times higher in the uninvolved than in the involved epidermis suggests that the poor response in the involved epidermis may be due to fewer available binding sites for adrenaline in the psoriatic lesion.

Adenylyl Cyclases↗
PubMed1975

The effects of catecholamine and related compounds on the adenyl cyclase system in the epidermis.

The effect of various hormones and drugs on the adenyl cyclase system of pig and human epidermal slices was studied in vitro. Adrenaline and isoproterenol in the presence of theophylline increased the epidermal cyclic AMP level 20-fold in 5 min. Noradrenaline also stimulated cyclic AMP accumulation but to a much lesser degree. The adrenaline stimulation was marked even in the absence of the phosphodiesterase inhibitor, theophylline. Theophylline potentiated the effect of adrenaline at the concentration of 2-10 mM although theophylline alone did not elevate the cyclic AMP level significantly. The Km for adrenaline stimulation of the adenyl cyclase system of pig epidermis was 7-7 X 10(-7) M. A beta-adrenergic antagonist, propranolol, markedly inhibited the adrenaline stimulation while alpha-antagonists, phentolamine or priscoline, showed little effect. The results are in accord with the view that the epidermis possesses an active adenyl cyclase system with beta-adrenergic receptors.

Adenylyl Cyclases↗
PubMed1975

Is the cyclic AMP in psoriatic epidermis low?

A deficiency of epidermal cyclic adenosine 3', 5'-monophosphate (cyclic AMP) has been implicated as the cause of the incomplete differentiation, increased mitosis and increased glycogen concentration which characterize the psoriatic lesion. This communication contains our data on the epidermal concentration of cyclic AMP in the lesional and 'normal' (non-involved) skin of patients with psoriasis. In these studies we have introduced the following improvement in methodology: (1) Local ischaemia in the biopsy specimens was prevented by not giving any injections prior to removal of the tissues and by freezing the tissues prior to removal. (2) The epidermis was microdissected from the dermis prior to cyclic AMP assay as as to give as pure an epidermal specimen as possible. Epidermal cyclic AMP was found to be 20-25% higher in the skin lesion than in the uninvolved skin when compared on a dry weight or protein basis but essentially when compared on the basis of DNA content. Our conclusion is that the cyclic AMP level in the psoriatic lesion is not lower than that in the 'normal' skin and thus these characteristics in psoriatic lesions cannot be related simply to a cyclic AMP deficiency.

Adult↗
PubMed1975

On the transportation of spermatozoa in the vas deferens.

In this report the intraluminal pressure of the vas deferens was measured in vivo in male cross-bred dogs. The measurement of the pressure elucidated that the vas deferens repeated autonomic contraction. This contraction was not the so-called peristalsis but the entire portion of the vas deferens contracted simultaneously. Stimulation of the hypogastric nerves resulted in a prominent elevation of the pressure in the proximal portion of the vas deferens, i.e., the portion approximate to the epididymis, followed 5-10 seconds later by a rise in the distal portion, i.e., the portion approximate to the prostate. These results suggest that the spermatozoa present near the proximal end of the vas deferens are transported littly by little by the autonomic movements of the vas deferens and that on ejaculation the spermatozoa are pressed forward from the proximal end of the vas deferens to its peripheral end by the stimuli through the hypogastric nerves.

Animals↗
PubMed1975

Peripheral nerves controlling the closure of internal urethral orifice during ejaculation.

The peripheral nervous pathways controlling seminal emission and closure of the internal urethral orifice during ejaculation were examined experimentally using male adolescent dogs. The experimental methods were measurement of the contraction of the internal urethral orifice and measurement of the change of the posterior urethral pressure induced by selective stimulation of the nerves related to the hypogastric nerve. Further, the change of actual ejaculation caused by manual stimulation of the penis was observed after excision of the nerves. Results included the following: (1) The seminal emission and the closure of the internal urethral orifice on ejaculation were controlled by the hypogastric nerve. (2) The nerve fibers which controlled these two phenomena took different paths above the lower mesenteric plexus. (3) Seminal emission was controlled by the splanchnic nerves which originated from the lower thoracic and upper lumbar ganglia of the sympathetic trunk, and the closure of the internal urethral orifice by those which originated from the lower lumbar ganglia of the trunk.

Animals↗
PubMed1975

Role of alpha-adrenergic receptor mechanism in closure of the internal urethral orifice during ejaculation.

The effects of autonomic drugs on closure of the internal urethral orifice during ejaculation were investigated in dogs. The closure of the internal urethral orifice was induced by the electric stimulation of the lateral fibers of the lower mesenteric plexus. The closing state of the orifice was measured with a latex balloon inserted into the orifice. The autonomic drugs were given into the aorta just above its bifurcation. From the results obtained in this study it was concluded that the closure of the internal urethral orifice during ejaculation is predominantly under the influence of the adrenergic nervous system, particularly through an alpha-adrenergic receptor mechanism.

Adrenergic alpha-Agonists↗
PubMed1975

The intranuclear binding of 17 beta-hydroxy-5 alpha-androstan-3-one and testosterone by hamster sebaceous glands.

After the administration of 3-H-testosterone to castrated hamsters, extracts from crude nuclei were separated into bound and free fractions by gel filtration of Sephadex G-25, Subsequent analysis by thin-layer chromatography and recrystallization showed that dihydrotestosterone was the predominant radioactive steroid in the bound fraction and that it increased steadily with time until 1 hr after the injection. Further purification of the nuclear fraction showed an abundance of dihydrotestosterone in the nuclei. The binding was significantly decreased by pronase treatment, only slightly affected by deoxyribonuclease, and remained unaffected by ribonuclease. From the elution pattern on Sephadex G-200, the molecular weight of the binding macromolecule was estimated to be 3 times 10-4 daltons.

Animals↗