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Biomedical subjects

K Omata

Publications and source records attributed to K Omata.

At least 109 records · Page 6Linked to original sources
PubMed1989

Atrial natriuretic polypeptide (ANP) as protective agent of renal ischemia.

The effect of atrial natriuretic polypeptide (ANP) on hemodynamics and renal function was evaluated after the reconstructive surgery of the left renal artery in a patient with renovascular hypertension secondary to Takayasu's arteritis. The reconstructive surgery was done using the femoral artery, since we were unable to obtain adequate vein segments to fit the renal artery. The femoral artery was reconstructed by her saphenous vein segments. After 30 min of the aortorenal bypass operation, alpha-human ANP (alpha-hANP) was infused intravenously for 10 min at a rate of 0.1 microgram/kg/min. Although total peripheral resistance was decreased by alpha-hANP infusion, blood pressure was not changed because of the increased cardiac output. Glomerular filtration rate was increased markedly with concomitant increase in urine volume and urinary excretions of sodium, potassium and phosphate. Fractional excretions of water and sodium were not changed, but fractional excretion of phosphate and potassium clearance were increased. Thus, the infusion of alpha-hANP markedly improved the renal function of the ischemic kidney by the reconstructive surgery of the renal artery, suggesting that alpha-hANP seems clinically applicable as a protective agent in renal ischemia at renovascular surgery as well as the renal transplantation.

Adult↗
PubMed1989

Effects of antihypertensive drugs on renal function and atrial natriuretic polypeptide in spontaneously hypertensive rats with renal ablation.

To determine whether pharmacological control of blood pressure could affect the renal function and levels of atrial natriuretic polypeptide (ANP) in spontaneously hypertensive rats (SHR) with renal ablation, and to ascertain the benefits of antihypertensive drugs, we studied effects of oral administration of captopril (50 mg/kg/day), an inhibitor of angiotensin converting enzyme, benidipine (3 mg/kg/day) and nilvadipine (10 mg/kg/day), newly developed blockers of calcium channel, and indapamide (10 mg/kg/day) for 14 days on systolic blood pressure, serum creatinine, blood urea nitrogen, and plasma ANP concentration in SHR subjected to surgical removal of the left kidney and infarction of two-thirds of the right kidney (5/6 nephrectomy) a week before. Three weeks after the surgery, systolic blood pressure (mmHg) in the untreated group was 253 +/- 9 (n = 10), in the captopril group 156 +/- 9 (n = 7, p less than 0.05), in the benidipine group 197 +/- 9 (n = 7, p less than 0.05), in the nilvadipine group 146 +/- 9 (n = 7, p less than 0.05) and in the indapamide group 206 +/- 5 (n = 7, p less than 0.05). Serum creatinine (mg/100 ml) was lower in the captopril group (0.58 +/- 0.02, n = 7, p less than 0.05) and in the benidipine group (0.50 +/- 0.03, n = 7, p less than 0.05) but not in the nilvadipine group and in the indapamide group 3 weeks after 5/6 nephrectomy compared to the untreated group. Blood urea nitrogen was also lower in the captopril group and in the benidipine group but not in the nilvadipine group and in the indapamide group. Plasma ANP concentration was significantly reduced by the treatment with captopril and benidipine but not with nilvadipine and indapamide. These results suggest that the reduction of blood pressure by the inhibition of angiotensin converting enzyme with captopril has the potential to ameliorate renal function of the SHR with remnant kidney, a model of chronic renal failure with hypertension, associated with the decreased concentration of plasma ANP. However, it remains to be determined whether the reduction of blood pressure by calcium channel blockers may be involved in the delayed progression of renal failure in this model since there were disparate effects on renal function and plasma ANP concentration with these two calcium channel blockers.

Animals↗
PubMed1989

Role of endogenous bradykinins in the acute depressor effect of angiotensin converting enzyme inhibitor captopril--assessed by a competitive antagonist of bradykinin.

To examine whether a hypotensive effect of converting enzyme inhibitor captopril was mediated partly by a potentiation of endogenous bradykinin, a newly synthesized competitive antagonist of bradykinin (B 4147) was used in anesthetized rats. The injection of B 4147 alone (50 and 100 micrograms) elicited significant increases in blood pressure. Although the administration of captopril (1 mg/kg, i.v.) caused a decrease in mean arterial pressure (MAP), the injection of the kinin antagonist (50 and 100 micrograms) after the captopril produced an increase in MAP by an average of 42 and 47% of the initial fall induced by captopril, respectively. The hypertensive effect of B 4147 was enhanced in magnitude and duration after the captopril. These results suggest that an accumulation of endogenous kinins by captopril contributes partly to the acute hypotensive effect of converting enzyme inhibitors in anesthetized rats.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1989

Interaction of atrial natriuretic peptide and amiloride on renal hemodynamics through renal kallikrein and kinins in anesthetized rabbits.

We investigated the interaction of atrial natriuretic peptide (ANP) and amiloride on renal function and the renal kallikrein-kinin system in anesthetized rabbits. The infusion of ANP alone (50 ng/kg/min) induced a natriuretic action with increments in renal blood flow (RBF) and creatinine clearance (Ccr). The infusion of ANP with amiloride (5 mg/kg + 0.04 mg/kg/min) produced a further increase in natriuresis despite the absence of an increase in RBF and Ccr induced by ANP alone. The urinary excretion of kallikrein and kinins was increased by the administration of ANP. However, the pretreatment with amiloride prevented the increase in the urinary excretion of kallikrein and kinins induced by ANP. These results suggest that the additive effect on sodium excretion might be attributable to changes in the tubular handling of sodium, although ANP did not modify the distal tubular function on sodium reabsorption. It is also suggested that the renal kallikrein-kinin system is not causally involved in the increased sodium excretion by ANP.

Amiloride↗
PubMed1989

Inhibitory effect of cicletanine on vascular smooth muscle cell proliferation.

We investigated the effect of cicletanine on vascular smooth muscle cell proliferation. In cultured vascular smooth muscle cells from rat mesenteric artery, cicletanine (10(-5) to 10(-4) M) increased prostacyclin synthesis (measured as 6-keto-PGF1 alpha by radioimmunoassay) dose-dependently. When added to cells in which mitogenesis was activated by 10% fetal bovine serum, cicletanine (3.3 x 10(-5) to 10(-4) M) inhibited [3H] thymidine incorporation up to 31% of the control level. Inhibitory effect of cicletanine on mitogenesis was also confirmed at 48 h by cell counts (control: 18965 +/- 629, cicletanine 10(-4) M: 14840 +/- 430, n = 6). The effect of cicletanine on platelet-derived growth factor (PDGF)-stimulated [3H] thymidine incorporation was not abolished by prostaglandin synthesis inhibition with aspirin, but the prostacyclin analogue OP-41483 (125-1000 ng/ml) inhibited it dose-dependently. Calcium entry blockers, nifedipine (3.3 x 10(-6) M) and diltiazem (10(-4) M), inhibited both [3H] thymidine incorporation and cell proliferation, while furosemide did not affect it. Cicletanine also inhibited PDGF-stimulated [3H] thymidine incorporation in cultured glomerular mesangial cells. We conclude that cicletanine stimulates prostacyclin synthesis and inhibits cell proliferation in cultured vascular smooth muscle cells, which may possibly be related to the intracellular calcium mobilization. Such a property might be contributory to the antihypertensive activity of cicletanine.

Animals↗
PubMed1988

Effects of methamphetamine upon circadian rhythms in multiple unit activity inside and outside the suprachiasmatic nucleus in the golden hamster (Mesocricetus auratus).

To investigate the circadian system of the golden hamster, multiple unit activity (MUA) was recorded inside and outside the suprachiasmatic nucleus (SCN). MUA inside the SCN showed a daily rhythm with a daytime peak during a 24 h light-dark cycle (LD, 12:12), whereas MUA outside the SCN revealed a nighttime peak. The phase reversal of MUA between inside and outside the SCN in the golden hamster was similar to the rat which is also a nocturnal rodent. MUA rhythms to the lighting cycle started to freerun after methamphetamine administration. This result indicates that methamphetamine may affect directly the neural circadian oscillator to induce behavioral change.

Action Potentials↗
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

Role of thromboxane A2 in the hypotensive effect of captopril in essential hypertension.

We have previously reported that captopril stimulates thromboxane A2 synthesis in patients with essential hypertension. In the present study, the hypotensive effects of captopril and OKY-046, a selective inhibitor of thromboxane A2 synthetase, were studied in nine patients with essential hypertension to determine whether thromboxane A2 is involved in the regulation of blood pressure. A single oral dose of OKY-046 (400 mg) decreased urinary thromboxane B2 (a stable metabolite of thromboxane A2) excretion significantly (from 113 +/- 19.0 to 51.0 +/- 6.1 pg/min; p less than 0.01) and increased urinary sodium excretion significantly (from 73.0 +/- 15.3 to 113.0 +/- 14.4 microEq/min; p less than 0.01), but no change was observed in mean arterial pressure. The administration of OKY-046 (600 mg/day) for 3 days induced a significant and sustained decrease in urinary thromboxane B2 excretion, but it did not affect the mean arterial pressure. Although captopril (50 mg) alone induced a significant increase in urinary thromboxane B2 excretion (from 91.4 +/- 11.0 to 297.3 +/- 30.8 pg/min; p less than 0.001) and a significant decrease in mean arterial pressure (from 97.0 +/- 4.7 to 88.1 +/- 5.1 mm Hg; p less than 0.01), captopril in combination with OKY-046 induced a decrease both in urinary thromboxane B2 excretion (from 70.8 +/- 12.3 to 54.2 +/- 14.7 pg/min; p less than 0.01) and in mean arterial pressure (from 105.1 +/- 3.8 to 84.2 +/- 3.6 mm Hg; p less than 0.01). Thus, the hypotensive effect of captopril was potentiated by OKY-046. OKY-046 did not affect the changes in plasma renin activity and plasma aldosterone concentration and blunted urinary prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion in response to captopril. These results indicate that thromboxane A2 counteracts the hypotensive effect of captopril in patients with essential hypertension.

Adult↗
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↗
PubMed1988

[A case of adrenal myelolipoma].

We report a case of surgically resected adrenal myelolipoma. Myelolipoma of the adrenal gland is a rare, benign and nonfunctioning tumor. The present patient represents the 57th reported clinical case of this tumor. It consists of fatty and hematopoietic tissue. It is asymptomatic and usually found only at autopsy incidentally. Ultrasonography, computed tomography and fine needle biopsy help in the preoperative diagnosis of adrenal myelolipoma. Especially fine needle biopsy is recommended when the diagnosis is doubtful.

Adrenal Gland Neoplasms↗
PubMed1987

Role of the prostaglandin-thromboxane system in the development and maintenance of spontaneous hypertension in the rat.

In spontaneously hypertensive rats (SHR) between the ages of 6 and 8 weeks before the development of established hypertension, repeated daily subcutaneous administration of indomethacin, an inhibitor of cyclo-oxygenase, at a dose of 5 mg/kg/day enhanced significantly the development of spontaneous hypertension, but repeated daily subcutaneous administration of OKY 046, an inhibitor of thromboxane (TX)A2 synthetase, at a dose of 12 mg/kg/day did not alter the development of spontaneous hypertension. In SHR between the ages of 15 and 18 weeks with established hypertension, indomethacin or OKY 046 did not alter the high blood pressure as compared with the injection of vehicle. In both young and adult SHR, indomethacin decreased significantly urinary prostaglandin (PG)E2 and TXB2 excretion but not PGE2. These results indicate that cyclo-oxygenase products other than TXA2 may play a protecting role in the development of spontaneous hypertension in the rat whereas their contribution to the maintenance of hypertension may be unlikely. In addition, it is suggested that TXA2 may not be involved in the development and maintenance of spontaneous hypertension in the rat.

Animals↗
PubMed1987

Interactions of renal prostaglandins, renin-angiotensin system and renal kallikrein-kinin system in human hypertension.

Dietary sodium deprivation lowered blood pressure in patients with essential hypertension, while indomethacin induced a rise in blood pressure with significant decreases in plasma angiotensin II concentration and urinary excretion of sodium and PGE. In contrast, captopril lowered blood pressure in them with significant decrease in plasma angiotensin II concentration and significant increase in urinary excretion of sodium and PGE. These data strongly indicate that the decreased PG generation in the nephron could elevate blood pressure by means of sodium retention caused by the reduced renal excretory function in spite of the decreased R-A system in human, suggesting the involvement of renal tubular PGE2 in the regulation of blood pressure.

Adult↗