Biomedical subjects

Tomio Okamura

Publications and source records attributed to Tomio Okamura.

22 records · Page 2Linked to original sources

PubMed2002

[Nitroxidergic (nitrergic) nerve and erectile dysfunction].

In vascular tissues including the corpus cavernosum, the organ function is reciprocally regulated by noradrenergic and non-adrenergic, non-cholinergic (NANC) nerves. NANC nerves innervating the corpus cavernosum is thought to be nitroxidergic (nitrergic) nerves which liberate nitric oxide (NO) produced by neuronal NO synthase, and liberated NO activates soluble guanylate cyclase (sGC) in cavernous smooth muscle cells. Intracellular increase in cyclic (c) GMP by activation of sGC dilates cavernous smooth muscle and then induces penile erection. Nitroxidergic (nitrergic) vasodilator nerves also innervate cavernous arteries and veins which regulate the blood volume in the corpus cavernosum. The order of potency of nitroxidergic nerve functions in these tissues (cavernosum > artery >> vein) may be suitable for producing the erection. Therefore, obstruction of the arteries and impairment of nitroxidergic (nitrergic) nerve function are speculated to be one of the causes for erectile dysfunction (ED). On the other hand, NO derived from the cavernous endothelium may partly contribute to erectile function. Sildenafil (Viagra) is one of the potent therapeutics for ED. The agent is a selective phosphodiesterase type 5 (PDE-V) inhibitor that inhibits degradation of cGMP elevated by NO mainly derived from the nerves. To develop more selective and safer therapeutics for ED, further systematic investigations are required.

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PubMed2002

Neurogenic cerebral vasodilation mediated by nitric oxide.

In cerebral arteries isolated from most of mammals, nerve stimulation produces relaxations in contrast to contractions in peripheral arteries. The relaxant mechanism is found to be non-adrenergic and non-cholinergic, but the neurotransmitter is not clarified until recently. Based on several functional and histological studies with isolated cerebral arteries, nitric oxide (NO) is now considered to be a neurotransmitter of the vasodilator nerve and the nerve has been called a nitroxidergic (nitrergic) nerve. Upon neural excitation, calcium influxed through N-type Ca2+ channels activates neuronal NO synthase, and then NO is produced by the enzyme from L-arginine. The released NO activates soluble guanylate cyclase in smooth muscle cells, resulting in relaxation with a cyclic GMP-dependent mechanism. The functional role and neuronal pathway have also been investigated in anesthetized dogs and Japanese monkeys. The nitroxidergic (nitrergic) nerves innervating the circulus arteriosus, including the anterior and middle cerebral and posterior communicating arteries, are found to be postganglionic nerves originated from the ipsilateral pterygopalatine ganglion and tonically dilate cerebral arteries in the resting condition. Our findings suggest that the nitroxidergic (nitrergic) nerve plays a physiologically important role to maintain a steady blood supply to the brain.

Animals↗

PubMed2002

Functional study on nitroxidergic nerve in isolated dog pulmonary arteries and veins.

In dog pulmonary arterial and venous strips without endothelium under treatment with prazosin, nicotine induced relaxation that was abolished by N(G)-nitro-L-arginine, hexamethonium and methylene blue. L-Arginine antagonized the N(G)-nitro-L-arginine action. Neurogenic relaxations tended to be more evident in the vein. Nitric oxide (NO)-induced relaxations were greater in the veins than in the arteries. Concentrations of NO to induce the same magnitude of relaxation as that to nicotine were higher in the arteries. In conclusion, dog pulmonary arteries and veins are innervated by nitroxidergic (nitrergic) nerves, and NO is released by nerve stimulation with nicotine in a larger amount in the artery than the vein.

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PubMedDate not supplied

Comparison of the responses to thrombin in monkey renal and uterine arteries.

OBJECTIVE: Thrombin is known to regulate vascular tone. We analyzed and compared mechanisms of thrombin action in primate renal and uterine arteries. METHODS: Isolated Japanese monkey renal and uterine arteries were suspended in Ringer-Locke solution for tension recordings. RESULTS: Renal arteries responded to thrombin with relaxation, which was inhibited by N(G)-nitro-L-arginine or indomethacin and reversed to contractions by the combination. The relaxations were also reversed to contractions by endothelial denudation. Conversely, thrombin caused uterine arterial contractions that were unaffected by endothelial denudation. Relaxations in both renal arteries and contractions in uterine arteries were suppressed by hirudin (a specific thrombin inhibitor). Relaxant responses to A23187 (Ca(2+) ionophore), nitroprusside sodium (nitric oxide donor), and beraprost sodium (prostacyclin analogue) did not differ between renal and uterine arteries. CONCLUSION: Thrombin-induced relaxation of renal arteries appears to be mediated by nitric oxide and vasodilator prostaglandins liberated from the endothelium, whereas uterine arterial contraction is caused by an endothelium-independent mechanism.

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