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Biomedical subjects

K Omata

Publications and source records attributed to K Omata.

At least 145 records · Page 8Linked to original sources
PubMed1986

Urinary excretion of TXB2 after angiotensin converting enzyme inhibition in hypertensive patients.

Urinary excretion of thromboxane B2 (TXB2), a stable metabolite of thromboxane A2 (TXA2), was measured by radioimmunoassay in 7 essential hypertensive patients before and after a converting enzyme inhibitor, SQ 14225, administration. When a single oral dose of SQ 14225 (50mg) was given to 7 patients with essential hypertension, urinary excretion of TXB2 was increased significantly (from 58.9 +/- 18.1 to 116.1 +/- 20.7 pg/min, mean +/- SE, P less than 0.02) with simultaneous increase in plasma renin activity, urine volume, urinary sodium, urinary potassium and urinary excretion of PGE (from 58.8 +/- 12.8 to 135.1 +/- 30.0 pg/min, mean +/- SE, P less than 0.05). These results indicate that SQ 14225 stimulates vasoconstricting TXA2 production as well as vasodilating PGE production.

Adult↗
PubMed1986

Effects of sodium and angiotensin II on urinary active and inactive kallikrein in rats.

To assess possible relationships between sodium balance, angiotensin II (ANG II), and renal active and inactive kallikrein, we studied the effects of sodium loading with 1% NaCl and chronic ANG II infusion (900 micrograms/kg per day) on the urinary excretion of total and active kallikrein for 6 days in conscious rats. We determined urinary total, active and inactive kallikrein by measuring kallikrein activity using a kininogenase assay before and after treatment with trypsin (200 micrograms/ml). Sodium loading produced a sustained increase in urinary total, active and inactive kallikrein excretion. Chronic infusion of ANG II induced a sustained increase in urinary total, active and inactive kallikrein excretion in rats on a regular diet. In rats loaded with sodium, however, ANG II did not induce any further changes in urinary kallikrein excretion. Thus, the present study suggests that both sodium loading and ANG II infusion might stimulate the synthesis of renal kallikrein. In addition, it is suggested that ANG II infusion might stimulate the synthesis of kallikrein, at least partly, via the same mechanism as sodium loading does.

Angiotensin II↗
PubMed1986

Effects of ouabain on blood pressure regulation in rats.

In order to test the hypothesis that a circulating inhibitor of the sodium-potassium ATPase pump may cause a concomitant rise in blood pressure and increased sodium excretion, we studied chronic effects of continuous infusion of ouabain, an inhibitor of sodium-potassium ATPase, for up to 6 days on systolic blood pressure and urinary sodium excretion in conscious rats. We also evaluated the effect of this substance in rats with hypertension induced by chronic infusion of norepinephrine. Continuous infusion of ouabain (1.2 mg/kg per day) into the jugular vein by an osmotic minipump did not induce any changes in systolic blood pressure and urinary sodium excretion in intact rats on regular diets. Furthermore it did not cause a change in systolic blood pressure in rats drinking 1% NaCl, and in unilaterally nephrectomized rats drinking 1% NaCl, when compared with vehicle-infused animals. When the same dose of ouabain was administered simultaneously with 1.8 mg/kg per day norepinephrine infused intraperitoneally by another osmotic minipump in conscious rats, systolic blood pressure rose on day 1 to only 129.3 +/- 2.8 mmHg compared with the rist to 145.0 +/- 2.0 mmHg when norepinephrine alone was infused (P less than 0.01). The antihypertensive effect of ouabain was sustained for the entire experimental period lasting for 6 days and was not associated with any changes in urinary sodium excretion. The administration of ouabain to rats made hypertensive by a 3-day infusion of norepinephrine, returned the blood pressure to control levels, and the antihypertensive effect was sustained throughout the experimental period lasting a further 3 days and was not associated with any changes in urinary sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
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 atrial natriuretic factor on angiotensin II-induced hypertension in rats.

To assess the physiological role of atrial natriuretic factors in blood pressure regulation, we studied the effect of chronic infusion of a synthetic atrial natriuretic factor of 25 amino acid residues (Arg 102-Tyr 126) in rats with angiotensin II-induced hypertension. Rats were studied while on a normal sodium diet or during sodium loading with 1% NaCl solution used as drinking water. Systolic blood pressure decreased slightly during combined infusion of synthetic atrial natriuretic factor, 150 micrograms/kg/day, and angiotensin II, 900 micrograms/kg/day. This effect was sustained for 3 days in rats receiving a regular sodium intake (p less than 0.01) and during sodium loading (p less than 0.01). Administration of synthetic atrial natriuretic factor to rats made hypertensive by a 3-day infusion of angiotensin II reduced blood pressure slightly, but not to control levels, and this effect was sustained for the remaining 3 days of the experiment in both dietary groups. These results indicate that a nonhypotensive dose of synthetic atrial natriuretic factor can modulate the vasopressor effect of angiotensin II. Thus, the attenuating effect may be involved in blood pressure regulation independently of sodium metabolism, although its actual physiological importance remains undetermined.

Angiotensin II↗
PubMed1986

Atrial natriuretic factor and cyclic guanosine 3',5'-monophosphate in vascular smooth muscle.

To elucidate the molecular mechanism of the vascular action of atrial natriuretic factor (ANF), we investigated the effects of synthetic ANF and sodium nitroprusside on the levels of intracellular cyclic nucleotides and prostacyclin (measured as its stable metabolite 6-keto-prostaglandin F1 alpha) in cultured vascular smooth muscle cells from rat mesenteric artery and, in some experiments, from rat renal artery. Both ANF and sodium nitroprusside increased intracellular cyclic guanosine 3',5'-monophosphate (cGMP) levels in a dose-dependent manner but did not affect cyclic adenosine 3',5'-monophosphate levels or 6-keto-prostaglandin F1 alpha synthesis. The stimulatory effect of ANF and sodium nitroprusside on cGMP levels were additive. Neither the deprivation of extracellular Ca2+ nor calcium entry blockers affected ANF-stimulated cGMP levels. Preincubation of ANF or sodium nitroprusside with kallikrein attenuated only the effect of ANF on cGMP levels. The effect of kallikrein was abolished by serine protease inhibitors. In contrast, the oxidant methylene blue inhibited the effect of sodium nitroprusside on cGMP levels, but not that of ANF. The stimulatory effect of ANF on cGMP levels was greater in cells from renal artery than in those from mesenteric artery. These results in cultured vascular smooth muscle cells further support the hypothesis that cGMP mediates the vasorelaxant action of ANF.

6-Ketoprostaglandin F1 alpha↗
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

Effects of acute water load, hypertonic saline infusion, and furosemide administration on atrial natriuretic peptide and vasopressin release in humans.

A new specific RIA for alpha-human atrial natriuretic hormone (alpha hANP) was used to determine whether changes in plasma volume elicited by acute water loading, hypertonic saline infusion, and furosemide administration caused changes in ANP release and resultant changes in renal and cardiovascular function in normal subjects. In addition, changes in plasma arginine vasopressin (AVP), PRA, and aldosterone concentrations were studied simultaneously. Mean plasma alpha hANP and AVP levels were 51.3 +/- 16.0 (+/- SE) and 3.1 +/- 0.6 pg/ml, respectively, in the basal state. Plasma alpha hANP rose to 77.8 +/- 27.6 in response to a 4.5% increase in plasma volume induced by water loading, increased further to 134.1 +/- 28.9 in response to a 23% volume increase induced by hypertonic saline, and fell to 70.2 +/- 15.8 pg/ml in response to a decrease in plasma volume after furosemide treatment (P less than 0.01-0.05). On the other hand, plasma AVP fell to 1.8 +/- 0.1 pg/ml after the water load, rose to 4.1 +/- 0.6 after hypertonic saline, and rose further to 5.8 +/- 0.8 pg/ml after furosemide (P less than 0.01-0.05). Water and hypertonic saline loading decreased PRA, but plasma aldosterone concentrations did not change; subsequent furosemide administration increased both (P less than 0.01-0.05). Arterial pressure and heart rate did not change significantly. Increases in urinary Na excretion and osmolar clearances were associated with a rise in plasma alpha hANP after water loading and hypertonic saline infusion (P less than 0.01-0.05), but changes in urine flow were mainly associated with alterations in AVP release. associated with alterations in AVP release.

Adult↗
PubMed1986

Antihypertensive effect of synthetic atrial natriuretic factor in vasopressin-infused rats.

To assess the pathophysiological role of atrial natriuretic factors in the regulation of blood pressure, we studied the effect of chronic infusion of a synthetic atrial natriuretic factor of 25 amino-acid residues on blood pressure and sodium-water excretion. Experimental subjects were rats with hypertension made by chronic infusion of vasopressin on regular intakes of sodium or on sodium loading with 1% NaCl as drinking water. When a subdepressor dose (150 micrograms/kg/day) of synthetic atrial natriuretic factor was delivered via an osmotic minipump into the jugular vein simultaneously with 7.2 U/kg/day of vasopressin infused intraperitoneally by another osmotic minipump, the expected elevation of systolic blood pressure was completely inhibited. This was not accompanied by any changes in urine volume and urinary sodium excretion. The antihypertensive effect was sustained throughout the experimental period lasting 3 days in rats on regular sodium intake (p less than 0.01) or on sodium loading with 1% NaCl as drinking water (p less than 0.01). These results indicate that a subdepressor dose of synthetic atrial natriuretic factor can modulate the vasopressor effect of vasopressin. Therefore it is suggested that an atrial natriuretic factor may be involved in the regulation of blood pressure via its antagonizing effect to vasopressin.

Animals↗
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

Chronic effect of a synthetic atrial natriuretic factor on the development of hypertension in young spontaneously hypertensive rats.

The chronic effect of a synthetic atrial natriuretic factor (ANF) of 25 amino acid residues on the development of hypertension in the 6-week-old spontaneously hypertensive rat (SHR) was assessed. The SHR, on regular diets or given 1% NaCl solution for drinking, were continuously infused with ANF (150 micrograms/kg per day) or vehicle (physiological saline) as controls for up to 14 days. The ANF attenuated transiently the development of hypertension in the sodium-loaded SHR, but the blood pressure returned to control levels by day 5. In SHR on regular diets ANF did not affect the development of hypertension. In addition, ANF did not induce any significant changes in urine volume, fluid intake, urinary sodium and potassium excretion, heart rate, heart weight or haematocrit in young SHR on either normal or increased sodium intake when compared with those in vehicle-infused SHR. These results suggest that ANF may exert some role via a vascular effect at the early stage of development of hypertension in young sodium-loaded SHR.

Animals↗
PubMed1986

[Clinico-pathological study of thyroid carcinomas detected by mass screening].

Ultrasound examination is a useful diagnostic procedure in mass screening for thyroid tumors. Between September 1983 and September 1985, we found many cases of nodular lesions in the thyroid, in which we frequently detected small carcinomas by echo-guided aspiration cytology. Nineteen thousand eight hundred twenty-four samples were examined, and echo-guided aspiration cytology was carried out in 1,169 persons, from which 115 positive cases were obtained. Seventy-four patients were operated upon, and 71 of them (96%) were found to have carcinomas, including 40 cases of small papillary carcinomas less than 10 mm in largest diameter. These small carcinomas were classified into four types histologically. Echogram patterns were different from each other and corresponded to histological types. Cytological figures of the small papillary carcinomas were also varied.

Adult↗
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↗
PubMed1986

Mechanism of antihypertensive effect of atenolol in patients with borderline hypertension during short-term treatment. A comprehensive study.

Short-term treatment with 1-(p-carbamoyl-methylphenoxy)-3-isopropylamino)-2-propanol (atenolol, Tenormin) (100 mg/d for 5 days) was conducted in 12 patients with labile essential hypertension. Before and at the end of the treatment, cardiohemodynamics, renal hemodynamic and excretory function, and renal pressor (renin-angiotensin-aldosterone) and depressor (renal kallikrein-kinin and prostaglandin) systems were examined. Atenolol decreased cardiac output (CO) without affecting total peripheral resistance. Atenolol also decreased plasma renin activity, plasma aldosterone concentration, urinary excretion of kallikrein-kinin, and urinary excretion of potassium whereas it increased plasma potassium concentration. Urinary excretion of prostaglandin E and sodium was not affected by atenolol. Glomerular filtration rate decreased, but renal plasma flow remained unchanged during the treatment by atenolol. A significant positive correlation was found between the changes in CO and in systolic blood pressure (SBP) while negative correlation was observed between the changes in total peripheral resistance and in SBP. A significant positive correlation was also noted between urinary kallikrein excretion and renal plasma flow. The change in urinary kinin excretion was conversely correlated to that in SBP. This study demonstrates that the hypotensive mechanism of atenolol is very complex. Decrease in CO and inhibition of renin-angiotensin-aldosterone system may mainly be responsible for hypotension. It is likely that potassium retaining action of atenolol partly contributes to its hypotensive action. It is also hypothetized that renal kallikrein-kinin system may play a role in modulating the hypotensive action of atenolol.

Adult↗
PubMed1985

Atrial natriuretic factor inhibits the hypertension induced by chronic infusion of norepinephrine in conscious rats.

To assess the physiological role of atrial natriuretic factors in the regulation of blood pressure and sodium-water excretion, we studied the chronic effects of continuous infusion of a synthetic atrial natriuretic factor of 25 amino acids for up to 3 days on systolic blood pressure, urine volume, and urinary excretion of sodium, prostaglandin E2 and kallikrein in conscious rats, and also evaluated the antihypertensive effect of this substance in rats with hypertension caused by chronic infusion of norepinephrine. Continuous infusion of atrial natriuretic factor (150 micrograms/kg per day) into the jugular vein via osmotic minipumps did not induce any changes in systolic blood pressure, urine volume, and urinary excretion of sodium, prostaglandin E2, and kallikrein for up to 3 days, compared with those in vehicle-infused rats. When the same dose of atrial natriuretic factor was administered simultaneously with 1.8 mg/kg per day of norepinephrine infused intraperitoneally by osmotic minipumps, the systolic blood pressure of conscious rats rose on day 1 to only 127.3 +/- 6.3 mm Hg compared with the rise to 146.3 +/- 1.6 mm Hg when norepinephrine alone was infused (P less than 0.05). The antihypertensive effect of atrial natriuretic factor was sustained for 3 days in rats infused with norepinephrine. The administration of atrial natriuretic factor to rats made hypertensive by 3 days of infusion with norepinephrine alone returned the blood pressure to control levels, and the antihypertensive effect was sustained throughout the experimental period lasting for 3 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗