Search PubMed⌕ Search

Biomedical subjects

T Kushiro

Publications and source records attributed to T Kushiro.

65 records · Page 4Linked to original sources
PubMed1984

[The effects of the intracerebroventricular administration of 5-hydroxytryptamine on hemodynamics in conscious rats. Participation of the serotonin receptor and the sympathetic nervous system].

We have previously reported that the intracerebroventricular (i.c.v.) administration of 5-hydroxytryptamine (5-HT) in conscious rats elicited significant pressor response, which was accompanied with an increase in plasma norepinephrine and the pressor response, was abolished by peripheral phenoxybenzamine pretreatment. For further investigation of the relationship between the serotonergic nervous system and the sympathetic nervous system, the effect of either i.c.v. or intravenous (i.v.) serotonin receptor antagonist, methysergide pretreatment on hemodynamic response to centrally administrated 5-HT was studied. Male Wistar rats weighing approximately 250g were used. On the day before the study, the unilateral carotid artery was cannulated (PE-50) to facilitate mean arterial pressure (MAP) and pressure triggered heart rate (HR) observation. Also, a cannula (PE-10) was inserted stereotaxically into the anterior horn of the lateral cerebral ventricle. The experiment was performed under a conscious and minimumly restrained state. After the observation of resting MAP and HR for at least 20 minutes, 5 microgram of 5-HT was given i.c.v. and MAP and HR were recorded for 50 minutes. Then, the rats were divided into two groups, one group (n = 9) received 1 microgram of i.c.v. methysergide and the other group (n = 10) received 1 mg/kg of i.v. methysergide. Ten minutes after either methysergide i.c.v. or i.v. treatment, 5 microgram of 5-HT was administrated i.c.v. again, and MAP and HR were observed for 30 minutes. Resting MAP and HR were 101.6 +/- 3.0mmHg and 413.8 +/- 20.0/min, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

BP changes in obese hypertensive subjects during rapid weight loss. Comparison of restricted v unchanged salt intake.

A controlled prospective study compared two groups of obese hypertensive subjects during 12 weeks of a hypocaloric protein-supplemented fast containing 40 mEq of sodium daily. One group received additional sodium chloride sufficient to maintain baseline sodium intake measured prior to the fast (210 m/Eq/day). Sodium restriction resulted in greater weight loss and slightly greater BP reduction only during the initial week of fasting. Thereafter, despite sodium equilibrium, further substantial weight loss and BP reduction were identical in both groups, the decrement in weight being linear (1.89 kg/wk) and the BP reduction asymptotic. Although the initial reduction in BP during the first week of supplemented fast may be attributable to negative salt and water balance, the further reduction in BP during a period of constant sodium balance must be caused by weight loss per se or by the triggering of other antihypertensive mechanisms associated with weight reduction.

Blood Pressure↗
PubMed1980

Effects of variations in sodium intake on the acute vasodepressor response to kininase II inhibition in rats with mild two-kidney, one-clip hypertension.

1. Unilateral renal artery constriction in rats maintained on a sodium-deplete, but not sodium-replete, diet induced an augmented acute vasodepressor response to kininase II inhibition produced by an intravenous injection of the dipeptidyl carboxypeptidase inhibitor captopril (250 microgram) during continuous saralasin-induced angiotensin II blockade (10 microgram/min). Dietary sodium restriction alone in sham-operated rats had no effect. 2. Acute bilateral adrenalectomy (18-24 h) did not preclude the demonstration of an augmented response to kininase II inhibition in sodium-depleted rats with benign two-kidney, one-clip hypertension. Neither did chronic administration of deoxycorticosterone acetate in intact rats elicit an augmented response. 3. The augmented acute vasodepressor response to kininase II inhibition in sodium-depleted rats with benign two-kidney, one-clip hypertension is probably due to bradykinin potentiation and secondary to an increased activity of the kallikrein-kinin system. The mechanism responsible for this apparent increase is not known, but neither hyperangiotensinemia nor hyperaldosteronism seems to play a role.

Adrenalectomy↗
PubMed1979

The kallikrein-kinin system in blood pressure homeostasis.

1. The acute effects of the kallikrein inhibitor aprotinin (498 ki.u./min), and the kininase II inhibitor SQ 14,225 (250 MICROGRAM), GIVEN INTRAVEnously during saralasin-induced angiotensin blockade, were studied in conscious sham-operated rats and rats with benign and malignant two-kidney, one-clip Goldblatt hypertension during dietary sodium restriction. 2. The blood pressure of conscious sham-operated rats increased significantly in response to aprotinin. It remained unchanged after SQ 14,225 in contrast to the significant vasodepressor effect seen when SQ 14,225 was given to the same rats under surgical stress and pentobarbital anaesthesia. 3. Benignly hypertensive rats showed a consistent vasopressor response to aprotinin and a marked vasodepressor response to SQ 14,225. The effects of both inhibitors were markedly and significantly blunted in malignantly hypertensive rats. 4. Our demonstration that two agents with known opposite actions on the kallikrein-kinin system produced predictable and opposite effects on blood pressure may indicate that this system is involved in the homeostatic regulation of blood pressure. It may play an important antihypertensive role in benign two-kidney, one-clip Goldblatt hypertension, a role which might be impaired in malignant hypertension.

Angiotensin-Converting Enzyme Inhibitors↗