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Biomedical subjects

M Seino

Publications and source records attributed to M Seino.

At least 127 records · Page 7Linked to original sources
PubMed1987

The mechanism of centrally mediated cardiovascular actions of the three structurally different calcium antagonists, verapamil, diltiazem and nicardipine, in rats.

Centrally mediated cardiovascular effects of the three structurally different calcium antagonists (Ca-antagonists), i.e., verapamil, diltiazem and nicardipine, were studied in rats. In conscious rats, when administered intracerebroventricularly (i.c.v.) in doses of 0.3, 1 and 3 micrograms/kg/min for 30 min, all the three Ca-antagonists induced dose-dependent increases in mean arterial pressure (MAP) and pulse rate (PR), whereas nicardipine administered intravenously (i.v.) caused a decrease in MAP and an increase in PR. In anesthetized rats all the three Ca-antagonists in a dose of 3 micrograms/kg/min for 60 min i.c.v. significantly potentiated the hypotensive and bradycardic effects of i.c.v. clonidine. Nicardipine, in a dose of 0.3 microgram/kg/min for 60 min i.c.v., attenuated the hypotensive and bradycardic effects of i.c.v. clonidine or B-HT 920, an alpha 2-adrenoceptor agonist, in anesthetized rats, whereas it did not modify the cardiovascular effect of i.c.v. angiotensin II or gamma-aminobutylic acid in conscious rats. Nicardipine, in a dose of 0.3 microgram/kg/min for 60 min i.v., did not modulate the hypotensive and bradycardic effects of i.c.v. clonidine. 3-Isobutyl-l-methylxanthine (IBMX), a cyclic AMP phosphodiesterase inhibitor, in a dose of 3 micrograms/kg/min for 60 min i.c.v., also attenuated the hypotensive and bradycardic effects of i.c.v. clonidine. Potentiation by the three i.c.v. Ca-antagonists of the hypotensive and bradycardic effects of clonidine would be explainable if their inhibitory effect on Ca-influx is exerted at presynaptic nerve terminals but not at postsynaptic. The mechanisms of the cardiovascular effect of i.c.v. Ca-antagonists still remain to be elucidated but may be independent of a central alpha 2-adrenoceptor mechanism. Dihydropyridine Ca-antagonists like nicardipine are also potent inhibitor of cyclic AMP phosphodiesterase. Since IBMX mimicked the effect of nicardipine, the effect of a low dose of i.c.v. nicardipine in attenuating the hypotensive and bradycardic effects of i.c.v. clonidine may be mediated by inhibition of cyclic AMP phosphodiesterase in the central nervous system.

Animals↗
PubMed1987

The effects of atrial natriuretic peptide on renal function and the renin-aldosterone system in anesthetized rabbits.

To determine the effects of alpha-human atrial natriuretic peptide (ANP) on renal function and the renin-aldosterone system in anesthetized rabbits, ANP (0.05 micrograms/kg/min) or 5% dextrose solution in vehicle control was infused intravenously. The infusion of ANP resulted in a significant decrease in mean arterial pressure with an increase in renal blood flow (RBF). ANP also produced significant increases in urine volume and urinary sodium excretion. ANP tended to increase glomerular filtration rate, filtered sodium load and net tubular reabsorption of sodium. However, there were no significant differences in these parameters compared with control group. Fractional sodium excretion was increased significantly by ANP. Plasma renin activity (PRA) was suppressed only at 30 min after the infusion of ANP, while a significant fall in plasma aldosterone concentration (PAC) lasted even in the recovery period. These results indicate that ANP produces a diuresis and natriuresis through the increased RBF in anesthetized rabbits. It is also suggested that ANP suppresses PAC independent of the inhibition of PRA.

Aldosterone↗
PubMed1986

Functional partial epilepsies in childhood.

Out of the 314 children with partial epilepsies below the age of 15 who had been followed for more than 5 years, 122 children with functional partial epilepsies (FPE) were the subjects of this study. The specific modality of interictal EEG findings reminiscent of that of the Rolandic spikes (Dalla Bernardina, 1982, 1984) was compared between functional and organic partial epilepsies. The results were: 1) One hundred and twenty-two patients were found to have FPE out of a total of 314 patients (39%). 2) Fifty-five patients were diagnosed as typical benign epilepsy of children with centro-temporal EEG foci (BECCT) of the 122 functional cases (45%). The remaining 67 patients who defied the diagnostic criteria of BECCT were; 9 cases with frontal EEG focus (7%), 11 cases with central and/or midtemporal EEG foci (9%), 10 cases with occipital EEG focus (8%) and 14 cases with multiple foci (11%). 3) Unfavorable seizure control was observed in cases with frontal foci (44%) and with multiple EEG foci (64%) compared with those whose EEG focus was located in the centro-midtemporal area, (including BECCT; 98%) and in the occipital region (80%). 4) It was noteworthy that the recurrent interictal spikes similar to those of the Rolandic spikes (Dalla Bernardina) were found in more than 50% of the patients not only with functional but with organic partial epilepsies. Our results, at least at the present time, appear to indicate that the recurrent spikes never did signify the benignancy of the seizure prognosis. The importance of differential diagnosis of BECCT from FPE was specifically stressed.

Brain↗
PubMed1986

Role of the renal kinin-prostaglandin system in diltiazem-induced natriuresis.

Intravenous infusion of the Ca2+ entry blocker diltiazem (10 micrograms . kg-1 . min-1 for 30 min) induced an increase in urinary excretion of sodium (UNaV) from 209 +/- 42 to 922 +/- 311 mueq without significant alterations in renal hemodynamics in anesthetized rabbits. Urinary excretion of kinin (UkinV) and prostaglandin E (UPGEV) were also increased by diltiazem, from 14.3 +/- 2.5 to 25.9 +/- 4.8 ng and 1.33 +/- 0.20 to 2.44 +/- 0.34 ng, respectively. Moreover, there was a significant correlation between UkinV and UNaV (r = 0.81, P less than 0.05). A significant relationship between UPGEV and UNaV (r = 0.83, P less than 0.05) was also observed. However, no correlation between urinary excretion of kallikrein (UkallV) and UNaV was found after infusion of diltiazem. Further, to examine a possible contribution of renal kinins and prostaglandins in diltiazem-induced natriuresis, aprotinin (50,000 KIU/kg bolus + 1,000 KIU . kg-1 . min-1 infusion) and indomethacin (8 mg/kg) were used. Aprotinin pretreatment attenuated diltiazem-induced natriuresis, accompanied by suppression of UkallV, UkinV, and UPGEV. However, indomethacin pretreatment did not affect this drug-induced natriuresis, although UPGEV was significantly decreased. Furthermore, under the indomethacin pretreatment, a significant increase in UkinV was produced by diltiazem. These results suggest that renal kinins rather than renal prostaglandin E, at least in part, play a role in diltiazem-induced natriuresis.

Animals↗
PubMed1986

Effect of age on the renin-angiotensin-aldosterone system in normal subjects: simultaneous measurement of active and inactive renin, renin substrate, and aldosterone in plasma.

To investigate the effect of aging on the renin-angiotensin-aldosterone system, plasma renin substrate concentrations (PRSC); plasma total, active, and inactive renin concentrations (TRC, ARC, and IRC); PRA; and plasma aldosterone concentrations (PAC) were measured simultaneously in 60 normal subjects, 18-84 yr old. PRSC was measured by the addition of excess human renal renin. ARC and TRC after trypsin activation were measured by adding sheep renin substrate; IRC was calculated by subtracting ARC from TRC. The active renin ratio was calculated as follows: ARC/TRC X 100%. PRA and PAC were measured by RIA. There were no significant changes in PRSC, TRC, IRC, and PRA to PAC ratio with aging. Both ARC and active renin ratio fell significantly with aging (r = 0.46 and P less than 0.01; and r = 0.54 and P less than 0.01, respectively). PRA and PAC also tended to decrease with aging (r = 0.35 and P less than 0.01; and r = 0.59 and P less than 0.01, respectively). A significant positive correlation was found between PRA and ARC (r = 0.72; P less than 0.001). PRA was also correlated with PAC. In conclusion, the age-related decrease in PRA is not due to the change in PRSC, but is mainly due to the fall in ARC. Decreased conversion of inactive to active renin might be responsible in part for the reduced ARC in the elderly.

Adolescent↗
PubMed1986

The changes in active and inactive renin induced by various maneuvers in hypertensive patients.

The changes in active and inactive renin after captopril (n = 29) or furosemide administration (n = 10) were studied in hypertensive patients. Furthermore, after percutaneous transluminal angioplasty (PTA) in 3 cases of renovascular hypertension (RVH), and after nephrectomy in a case of juxtaglomerular cell tumor, the time course of the changes in these two types of renin was investigated. Inactive renin was activated by trypsin treatment. Plasma renin concentration was measured by using an excess of sheep substrate. In patients with essential hypertension or primary aldosteronism, inactive renin was unchanged, irrespective of response in active renin, after the administration of captopril and furosemide. In patients with RVH, inactive renin was markedly decreased by furosemide but unchanged by captopril, in spite of significant increase in active renin. After PTA and nephrectomy, inactive renin decreased slower than active renin. These data support the idea that in patients with RVH, the increase in active renin by furosemide is at least partly due to the activation of inactive renin. It is also suggested that the increase in active renin by captopril is mainly due to the promoted release of active renin from the kidney. Furthermore, it seems likely that the metabolic clearance of inactive renin is slower than that in active renin.

Administration, Oral↗
PubMed1986

Hypotensive and natriuretic effects of nifedipine in essential hypertension. Role of renal kallikrein-kinin-prostaglandin and renin-angiotensin-aldosterone systems.

To assess the role of renal kallikrein-kinin-prostaglandin and renin-angiotensin-aldosterone systems in the diuretic and natriuretic actions of nifedipine, a calcium-channel blocker, 20 mg of nifedipine was administered orally to 15 patients with essential hypertension. Nifedipine promptly induced a hypotensive effect and an increase in pulse rate. Urine volume, urinary sodium excretion, and creatinine clearance were significantly increased after the administration of nifedipine by 63.5%, 48.5% and 12.4%, respectively. Urinary excretion of kallikrein and prostaglandin E were also significantly increased after the administration of nifedipine by 29.4% and 50.0%, respectively. The change in urinary kallikrein excretion was significantly correlated with that in urine volume (r = 0.70, p less than 0.01) or that in urinary sodium excretion (r = 0.86, p less than 0.01). In addition, the change in urinary prostaglandin E excretion was also significantly correlated with that in urine volume (r = 0.72, p less than 0.01) or that in urinary sodium excretion (r = 0.53, p less than 0.05). Plasma aldosterone concentration did not change despite of the marked increase in plasma renin activity, and plasma aldosterone concentration/plasma renin activity ratio decreased after the administration of nifedipine. These results suggest that the augmented renal kallikrein-kinin-prostaglandin system and the suppressed secretion of aldosterone may be associated with the diuretic and natiuretic action of nifedipine and may contribute to the reduction in blood pressure that is caused mainly by its vasodilatory action.

Adult↗
PubMed1985

Episodic psychotic states in temporal lobe epilepsy: an investigation on their physiopathogenesis.

The discussion here is about the direct relationship of epileptic seizures to episodic psychotic states. The episodic psychotic states were divided into three groups: interictal, ictal and postictal. In each group, one representative case was described and the neurophysiological pathogenesis discussed according to a recent research, mainly depth-electrode findings. It is believed that: interictal psychotic state--limbic paroxysmal discharges play an important role in its pathogenesis, according to the theory of Geschwindt and others; ictal psychotic state--repetitive auras develop to the psychotic state, and aura continua itself can be described as a psychotic state; and postictal psychotic state--the increased limbic discharges might be responsible for the psychotic state. The common neurophysiological cause in all the three groups is due to the increased epileptic discharges in the limbic system. It is concluded that the episodic psychotic states in temporal lobe epilepsies are possibly of an epileptic nature in themselves.

Adolescent↗
PubMed1985

Active, inactive and total renin concentrations in plasma of hypertensive patients.

To assess the role of inactive renin in hypertensive patients, active, inactive and total renin concentrations (ARC, IRC and TRC) were measured in 37 patients with hypertension of various etiologies. Inactive renin was activated by trypsin and renin concentration was measured using an excess of sheep substrate. Mean values of ARC, IRC, TRC and active renin ratio (AR ratio = ARC/TRC) were higher in 6 cases of renovascular hypertension, and lower in 6 cases of primary aldosteronism and 1 case of idiopathic hyperaldosteronism, when compared with 59 cases of normal subjects. Between ARC and IRC, a slightly positive correlation was observed. Moreover, between ARC and TRC as well as between ARC and AR ratio, close positive correlations were observed. Exceptionally, in a case of juxtaglomerular cell tumor, AR ratio was low in spite of the extremely high value of ARC. Our data suggest that the increase in circulating active renin is due to both the enhancement of the release of renin from the kidney and the increase in the activation of inactive renin, and vice versa.

Adolescent↗
PubMed1984

Sex and age-related differences in the urinary excretion of TXB2 in normal human subjects: a possible pathophysiological role of TXA2 in the aged kidney.

Urinary excretion of thromboxane B2 (TXB2), a stable metabolite of TXA2, was measured by radioimmunoassay in 58 normal subjects (17 males and 41 females) aged from 19 to 98 years. The basal level of urinary TXB2 in normal subjects was 100 +/- 6.7 ng/day (mean +/- SEM). In young males, contamination of urine specimens with seminal fluid, which is known to contain large amounts of prostaglandin E, did not change the level of urinary TXB2. Urinary excretion of TXB2 was significantly higher in male subjects than in female (124 +/- 12.6 vs 90 +/- 7.4 ng/day, p less than 0.05). There was no significant age-related difference in 24-h urinary excretion of TXB2 in normal subjects. However, when urinary excretion of TXB2 was expressed as a function of urinary creatinine excretion, it was significantly higher in the elderly (60-93 years old) than in the younger subjects (19-59 years old)(141 +/- 15.7 vs 99 +/- 7.7 ng/g creatinine, p less than 0.02). Renal TXA2 may have a pathophysiological role in the functional impairment of the kidney in elderly people.

Adult↗
PubMed1984

Effects of nifedipine on renal vascular responses to vasoactive agents in rabbits.

The present study was designed to investigate the effects of the Ca-antagonist, nifedipine, on receptor-mediated renal vascular responses to vasoconstrictors (angiotensin II, norepinephrine and vasopressin) and vasodilators (bradykinin and prostaglandin E2). Renal blood flow was estimated by noncannulating electromagnetic flowmetry in anesthetized rabbits. Vasoactive substances were infused directly into the renal artery. After the intravenous administration of nifedipine (50 micrograms/kg), decreases in renal blood flow in response to angiotensin II infused at rates of 2.5, 5 and 10 ng/kg/min were attenuated by 64% (p less than 0.01), 45% (p less than 0.05) and 42% (p less than 0.05), respectively. Decreases in renal blood flow in response to vasopressin infused at rates of 10, 20 and 50 mU/kg/min were also attenuated by nifedipine, 50% (p less than 0.05), 57% (p less than 0.05) and 38% (p less than 0.05), respectively. However, renal vasoconstrictor responses to norepinephrine (25, 50 and 100 ng/kg/min) did not change significantly after the administration of nifedipine. Increases in renal blood flow induced by the intrarenal infusion of bradykinin (2.5, 5 and 10 ng/kg/min) and prostaglandin E2 (20, 50 and 100 ng/kg/min) were not affected by nifedipine. These results suggest that receptor-mediated vasoconstrictor responses of the renal vascular bed to angiotensin II and vasopressin are produced mainly by Ca++ influx but that of norepinephrine is not. Furthermore, it is confirmed that the renal vasodilator effect of bradykinin and prostaglandin E2 is not altered by nifedipine in anesthetized rabbits.

Angiotensin II↗
PubMed1984

Renal kallikrein-kinin system and the depressor effect of angiotensin converting enzyme inhibitors MK 421, SA 446, and captopril in rats.

Responses in urinary kallikrein and kinin excretion and systolic blood pressure to MK 421, SA 446 or captopril were studied in normotensive rats fed on a regular or a low sodium diet to assess the role of renal kallikrein-kinin system in their hypotensive effect. MK 421, SA 446 or captopril were infused at a rate of 6 mg/kg/day by osmotic minipump implanted intraperitoneally for up to 6 days. The magnitude of fall in systolic blood pressure was greater on a low sodium diet when compared to on a regular diet, whereas the pattern of the fall was similar on both diets. The magnitude of falls in plasma angiotensin II and aldosterone concentration induced by MK 421, SA 446 and captopril was not significantly different between both regular and low sodium diets. Urinary kallikrein and kinin excretion and sodium excretion were increased during infusion of MK 421, SA 446 or captopril on a low sodium diet, however any significant changes were not found in each of them on a regular diet. The present results suggest that on a low sodium diet the augmented hypotensive response to angiotensin converting enzyme inhibitors in the rats might be due to the enhanced renal kallikrein-kinin system in addition to suppressed renin-angiotensin system.

3-Mercaptopropionic Acid↗