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Biomedical subjects

M Seino

Publications and source records attributed to M Seino.

At least 109 records · Page 6Linked to original sources
PubMed1988

Effects of a competitive antagonist of bradykinin on blood pressure and renal blood flow in anesthetized rats.

To examine a possible role of endogenous bradykinin in the regulation of blood pressure (BP) and renal blood flow (RBF), a newly synthesized competitive antagonist of bradykinin (B4147) was studied in anesthetized rats. Also, the question of whether the hypotensive effect of the converting enzyme inhibitor, captopril, is mediated partly by an accumulation of endogenous bradykinin was considered. The intravenous infusion of B4147 (25 micrograms/min) inhibited the depressor effect of exogenous bradykinin (0.5 microgram, i.v.) by 69%. After an intravenous injection of B4147 at doses of 25, 50 and 100 micrograms, BP increased and RBF decreased in a dose-dependent fashion. The increase in BP was not blocked by pretreatment with an angiotensin II antagonist (1-Sar-8-Ile angiotensin II; 20 micrograms/kg per min) or an alpha 1-blocker (prazosin; 0.1 mg/kg). The administration of captopril (1 mg/kg) decreased mean BP from 110 +/- 3.5 to 71 +/- 1.9 mmHg (P less than 0.001). However, the injection of B4147 (50 micrograms) after the administration of captopril elicited an increase in BP of 43% of the initial decrease induced by captopril. These results suggest that the effects of B4147 on BP and RBF are not mediated through angiotensin II or sympathetic alpha 1-stimulation. Endogenous bradykinin could contribute to the maintenance of BP and RBF in anesthetized rats, probably counter-balancing the vasoconstrictor mechanisms. It is also suggested that bradykinin may partly participate in the acute hypotensive effect induced by the converting enzyme inhibitor captopril.

Animals↗
PubMed1988

Contribution of bradykinin to maintenance of blood pressure and renal blood flow in anaesthetized spontaneously hypertensive rats.

We used a newly synthesized competitive antagonist of bradykinin (B 4147) to determine whether bradykinin contributes to the maintenance of blood pressure and renal blood flow in anaesthetized Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The injection of B 4147 (50 micrograms, intravenously) caused an increase in blood pressure and a decrease in renal blood flow in both strains. However, the magnitude in the change in blood pressure was significantly lower in SHR than in WKY. The reduction of renal blood flow was greater in WKY than in SHR, but there was no significant difference in the basal renal blood flow. These results indicate that bradykinin contributes to the maintenance of blood pressure and renal blood flow in both strains. However, bradykinin antagonist produced a more prominent systemic effect in WKY than in SHR. This suggests that a deficiency in the bradykinin system in SHR contributes to the development or the maintenance of hypertension.

Animals↗
PubMed1988

A comparative study of absence status epilepticus between children and adults.

Based on the clinicoelectrographic data of 28 patients (14 children and 14 adults) with absence status epilepticus thoroughly documented by CCTV/EEG, it was found that there were significant differences between the children and adults. In childhood, absence status tended to occur in those who had experienced individual short-lived atypical absence seizures and also other types of generalized seizure. In contrast, there was a general tendency for absence status in adulthood to occur in females without individual absence seizure. With respect to the clinicoelectrographical manifestations, absence status with a decreased postural tone was prone to be associated with a more profound clouding of consciousness, whereas in those with myoclonic components there was a less profound clouding. The former was found solely in children while the latter was both in children and in adults. During absence status, the focal motor features with or without secondarily generalized convulsions were observed in 8 adult patients (57%). On the other hand, no focal motor manifestations were observed during absence status in children. Absence status is composed of two modalities: either a prolongation or repetition of absence seizures. It was demonstrated that, in children, either the prolongation or repetition of individual absence seizures developed into absence status. The short-lived absence was of an atypical nature, whereas in adults, absence status consisted of the prolongation of an absence seizure which occurred in patients with no experience of individual absence seizures. With respect to the drug treatment, antiabsence drugs had some effect in children, while none of the adult patients responded either to the antiabsence drugs or other antiepileptic drugs. The long-term seizure prognosis was not necessarily poor in children but invariably poor in adults. Four adult patients showed diffuse, but unilateral frontally accentuated asymmetrical paroxysmal activity during the status. Three of them showed initial localized spike-wave discharges in the unilateral frontal region followed by a generalized spike-wave rhythm. Furthermore, all of these 4 patients with focally accentuated ictal EEGs have shown partial motor seizures intermingled with absence status.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1988

A prospective WISC-R study in children with epilepsy.

A prospective intraindividual study of WISC-R testing in the 45 children with epilepsy revealed that: 1) antiepileptic drugs, phenobarbital in particular, resulted in a detrimental effect on the WISC-R scores, 2) of the WISC-R subtests, vocabulary tasks of the verbal test were the most susceptible indicators in children whose FSIQ scores either improved or deteriorated, and 3) in children whose antiepileptic drug dosage remained unchanged while the seizure frequency remained unchanged, both the VIQ and PIQ scores decreased. It was evident that either recurrent seizures or inappropriate medication may exert a detrimental effect on intelligence as expressed by the WISC-R testing. In addition, the possibility that the underlying cerebral pathology associated with the etiology of epilepsy may play a role in a progressive intellectual deterioration was suggested.

Brain Damage, Chronic↗
PubMed1988

A clinical study on frontal lobe epilepsy.

Of 30 patients whose epileptogenic focus was presumed to be located in the frontal lobe on the basis of a clinico-electrographic correlation, the principal seizure manifestation consisted of peculiar automatisms in about 40% of the cases. However, the nature of the automatisms was of a short duration lasting about one minute but in most cases it was accompanied by extremely violent movements, but this was not true in all cases. Of the 30 cases, only 5 cases showed marked improvement one year after being discharged from the hospital so that this type of seizure event is extremely intractable.

Adolescent↗
PubMed1988

Interaction between ANP and amiloride in renal tubular sodium handling in anesthetized rabbits.

To examine whether amiloride, an inhibitor of a conductive sodium channel in the distal tubule, modifies a possible tubular action of atrial natriuretic peptide (ANP), alpha-human ANP (0.05 micrograms.kg-1.min-1) was infused intravenously with or without pretreatment of amiloride (5 mg/kg + 0.04 mg.kg-1.min-1) in anesthetized rabbits. No significant changes in arterial pressure and renal blood flow were observed between two groups after ANP infusion. However, increases in filtered sodium load (FNa) and net tubular sodium reabsorption (RNa) induced by ANP were attenuated after the amiloride pretreatment. These attenuations in FNa and RNa could be due to the failure of increase in glomerular filtration rate, although the reason is not clear. Amiloride pretreatment abolished the ANP-induced kaliuresis, whereas ANP-induced increases in urinary sodium and fractional sodium excretion were additive after amiloride pretreatment. Thus, ANP elicited a further natriuretic effect even when the amiloride-sensitive component was blocked. This suggests that there is another mechanism by which ANP induces natriuresis, in addition to any ANP effects mediated by interference with sodium conductive channels.

Amiloride↗
PubMed1988

Nifedipine enhances the vasodepressor and natriuretic effects of atrial natriuretic peptide.

We examined a possible interaction between the calcium entry blocker nifedipine and atrial natriuretic peptide on blood pressure and natriuresis in anesthetized rabbits. The administration of atrial natriuretic peptide (0.05 micrograms/kg/min) produced a significant decrease in mean arterial pressure. Similar reductions in blood pressure were obtained during the administration of nifedipine (1.0 micrograms/kg/min). Atrial natriuretic peptide produced a consistent increase in glomerular filtration rate that was higher than the increase in renal blood flow; hence, the filtration fraction was significantly elevated. Atrial natriuretic peptide also elicited a significant increment in urine volume and urinary sodium excretion, while nifedipine was devoid of any significant effects on renal hemodynamics and renal excretory function during the experimental period. The administration of atrial natriuretic peptide superimposed on an ongoing infusion of nifedipine resulted in a greater fall of blood pressure than that seen during the administration of atrial natriuretic peptide or nifedipine alone. Sodium excretion was also potentiated, but there were no changes in renal hemodynamics or in the filtration fraction. These results suggest that calcium entry blockers potentiate the vasodepressor and the natriuretic effects of atrial natriuretic peptide but prevent its renal hemodynamic effects.

Animals↗
PubMed1988

Renal vein plasma renin activity in patients with unilateral renovascular hypertension.

Plasma renin activity in the renal veins (V) or infrarenal inferior vena cavae (IVC) of 20 patients with unilateral renovascular hypertension (RVH) was measured to determine how renal vein renin ratio (RVRR) compares with renin index (V-IVC/IVC) as a predictor of curability of RVH. Although there was no significant difference between them in predicting curability, 3 out of 4 patients with hypersecretion of renin (V-IVC/IVC greater than or equal to 0.48) in the stenosed side with contralateral suppression (V-IVC/IVC less than or equal to 0) on the normal side were cured. In addition, 7 out of 11 patients with contralateral suppression irrespective of values of renin index in the stenosed side were also cured. On the other hand, only one out of 6 patients who had neither hypersecretion nor contralateral suppression was cured. These results reconfirm that significant renin secretion with or without contralateral suppression, or only contralateral suppression of renin is highly suggestive of curable RVH.

Adult↗
PubMed1988

The effects of atrial natriuretic peptide and amiloride on renal haemodynamics and the renal kallikrein-kinin system.

Anaesthetized rabbits were used to examine the effects of amiloride (an inhibitor of a conductive sodium channel in the distal tubule) and atrial natriuretic peptide (ANP), both singly and in combination, on renal function and the renal kallikrein-kinin system. The administration of ANP (0.05 microgram/kg per min) produced a natriuresis with increases in renal blood flow and glomerular filtration rate. The administration of ANP superimposed on amiloride infusion (5 mg/kg + 0.04 mg/kg per min) showed an additive effect on the natriuresis, although the renal haemodynamic changes were now absent. The infusion of ANP alone increased the urinary excretion of kallikrein and kinins. Prior infusion of amiloride prevented the expected increases in the urinary excretion of kallikrein and kinins after infusion of ANP was superimposed. These results suggest that the observed renal haemodynamic changes could be mediated through renal kallikrein and kinins. The additive effect on sodium excretion might be elicited by the results of alterations in the tubular handling of sodium, although distal tubular function is not modified by ANP. It seems that the renal kallikrein-kinin system is not causally involved in the increased sodium excretion by ANP.

Amiloride↗
PubMed1987

Interaction of calcium ion and atrial natriuretic peptide on blood pressure, natriuresis and the renal kallikrein-kinin system in anesthetized rabbits.

To examine whether hemodynamic and natriuretic effects of alpha-human atrial natriuretic peptide (ANP) were modulated by calcium (Ca) ion, Ca entry blocker nifedipine (Nif) was administered prior to ANP infusion in anesthetized rabbits. We also examined the effect of Nif and ANP on the renal kallikrein-kinin system. Both Nif. (1.0 micrograms/kg/min) and ANP (50 ng/kg/min) increased urinary sodium excretion (UNaV) without change in renal hemodynamics, although mean arterial pressure (MAP) decreased. Fractional excretion of sodium (FENa) was also increased significantly by both Nif and ANP. Nif infusion alone decreased MAP, the additional infusion of ANP on Nif pretreatment induced a further decrease in MAP and caused an increase in UNaV and FENa without renal hemodynamics changes. The administration of ANP increased urinary excretion of kallikrein and kinin. The additional infusion of ANP on Nif pretreatment induced a further increase in urinary kallikrein and kinin. These results suggest that Ca ion does not participate in ANP-induced natriuresis. Renal kallikrein-kinin may partly involve in natriuresis induced by ANP.

Animals↗
PubMed1987

The effects of intravenous injection of alpha-human atrial natriuretic polypeptide on blood pressure, renal hemodynamics and urinary kinin excretion in anesthetized rabbits.

Studies were performed in anesthetized rabbits to examine the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on blood pressure, renal hemodynamics and urinary kinin excretion. Intravenous bolus injection of alpha-hANP at a dose of 5 micrograms resulted in a transient increase in renal blood flow from 26.6 +/- 2.2 to 33.7 +/- 2.2 ml/min (p less than 0.05) and a decrease in mean arterial pressure from 113 +/- 1.8 to 107 +/- 2.2 mmHg (p less than 0.01). The calculated renal vascular resistance decreased from 4.50 +/- 0.34 to 3.28 +/- 0.20 mmHg/ml/min (p less than 0.05). This vasodilatory effect of alpha-hANP was immediate and lasted for 30 min. These hemodynamic alterations were not associated with the changes in glomerular filtration rate estimated by creatinine clearance. Intravenous injection of alpha-hANP also produced marked increases in urine volume from 1.99 +/- 0.43 to 5.7 +/- 1.20 ml/10 min (p less than 0.01), urinary sodium from 42.2 +/- 7.6 to 243 +/- 54 mu Eq/10 min (p less than 0.01), urinary potassium from 37.5 +/- 5.5 to 74.8 +/- 10.3 mu Eq/10 min (p less than 0.01), and urinary kinin excretion from 3.44 +/- 0.49 to 5.26 +/- 0.82 ng/10 min (p less than 0.05). The observed natriuretic effect of alpha-hANP lasted only for 30 min, whereas diuretic and kaliuretic effects were sustained for 120 min. Hematocrit levels did not change significantly throughout the experiment. These results indicate that alpha-hANP is a potent vasodilator substance and that the natriuretic effect induced by the bolus injection of alpha-hANP is mediated mainly through its renal vasodilatory action. It is also suggested that the renal kinin, at least in part, contributes to the natriuretic effect of alpha-hANP.

Animals↗