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Biomedical subjects

H Ijichi

Publications and source records attributed to H Ijichi.

197 records · Page 11Linked to original sources
PubMed1977

Studies on beta-pyridylcarbinol as a precursor of nicotinamide adenine dinucleotide.

The major part of orally administered beta-pyridylcarbinol was converted to nicotinic acid in the gastrointestinal tract, whereas that administered intraperitoneally was partially converted to nicotinic acid in the liver. The conversion of this compound to nicotinic acid in both the gastrointestinal tract and liver involved enzymatic processes. The converted nicotinic acid from beta-pyridylcarbinol may play a dominant role in the biological actions of beta-pyridylcarbinol and possibly involves in the synthesis of NAD via Preiss-Handler's pathway.

Animals↗
PubMedDate not supplied

Pressor responses to intracisternal injection of hypertonic NaCl in rats.

Hypertonic NaCl solution injected into the cisterna magna of anesthetized rats produced dose-dependent pressor responses accompanied by slight tachycardia. Similar injections of hypertonic urea solution were ineffective. Because the early phase of the pressor response to hypertonic NaCl was always accompanied by increased sympathetic nerve firing and was inhibited following alpha-adrenergic blockade with phentolamine, initial pressor response was attributed to sympathetic hyperactivity. On the other hand, because the later phase of the pressor response was unaffected either by adrenalectomy or by alpha-adrenergic blockade, but was significantly inhibited by hypophysectomy or by pretreatment with a vasopressin antagonist, the later pressor response was ascribed to an increased release of endogenous vasopressin. Thus, our findings indicate that central pressor responses to hypertonic NaCl solution involve two different mechanisms: sympathetic hyperactivity in the early phase and vasopressin release during the later phase. In spontaneously hypertensive rats (SHR), both pressor and sympathetic responses to intracisternally injected NaCl were greater than in Wistar-Kyoto rats (WKY). Our results further indicate hypersensitivity to NaCl around the brain stem in SHR, which could account for the increased sympathetic activity and cause SHR to develop hypertension.

Adrenalectomy↗
PubMedDate not supplied

Antihypertensive and hypothalamic depressant effects of tripamide in spontaneously hypertensive rats.

When tripamide was added to the food of spontaneously hypertensive rats (SHR), there were no appreciable effects on heart rate, body weight, or food intake. Tail-cuff systolic pressures measured weekly were also unaffected in normotensive control rats (WKY), but the elevation expected in SHR was significantly reduced. Pressor responses to hypothalamic stimulation were also reduced selectively only in SHR. A peripheral inhibition of cardiovascular reactivity was considered unlikely, since pressor responses to injected norepinephrine, tyramine, or vasopressin were unaltered. Diminished pressor responsiveness was considered to be due to concurrent reduction of central sympathetic vasomotor activity, because sympathetic nerve responses to hypothalamic stimulation were appreciably lessened in tripamide-treated SHR. Although neither the site nor the mechanism causing sympathetic inhibition was determined exactly, our results are in accord with the interpretation that antihypertensive effects of tripamide in SHR depend, at least partly, on sympathetic inhibition.

Animals↗
PubMedDate not supplied

Effect of xanthine oxidase inhibitor on myocardial ischemia.

The xanthine oxidase inhibitor, 4-hydroxypyrazolo(3,4-d) pyrimidine (HPP), Allopurinol, caused augmentation of myocardial uptake of [3H] hypoxanthine, which was eventually completely incorporated into ATP. The decrease of [32P] orthophosphate incorporation into ATP induced by isoproterenol was restored by HPP administration.

Adenosine Triphosphate↗