Search PubMed⌕ Search

Biomedical subjects

K Omata

Publications and source records attributed to K Omata.

At least 127 records · Page 7Linked to original sources
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

Effect of atrial natriuretic factor on renin release in isolated afferent arterioles.

This study was designed to examine the effect of alpha-human atrial natriuretic polypeptide (alpha-hANP) on renin release in the absence of tubules, glomeruli and macula densa. Rabbit afferent arterioles were microdissected and incubated for two consecutive, 20 minute periods. Hourly renin release rate from a single arteriole was calculated. Basal renin release rate was 0.97 +/- 0.13 ng AI.hr-1.Af-1/hr (X +/- SEM, N = 18) and remained stable throughout the incubations. When afferent arterioles were exposed to alpha-hANP (0.01, 0.1 or 1 microM), renin release rate did not change significantly. Isoproterenol (5 microM) increased renin release rate from 0.92 +/- 0.28 to 1.50 +/- 0.46 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). After pretreatment of afferent arterioles with alpha-hANP (1 microM), isoproterenol still increased renin release rate from 0.98 +/- 0.24 to 1.64 +/- 0.37 ng AI.hr-1.Af-1/hr (N = 7, P less than 0.01). The increases in renin release rate induced by isoproterenol were not different between the two groups. Pretreatment of rabbits with furosemide for two days before experiments resulted in greater basal renin release rates from microdissected afferent arterioles (1.70 +/- 0.35 ng AI.hr-1.Af-1/hr, N = 14). However, exposure to alpha-hANP (1 microM) did not alter this elevated renin release rate. It is concluded that atrial natriuretic factor may not have a direct action on juxtaglomerular cells.

Animals↗
PubMed1987

Renal kallikrein activity in spontaneously hypertensive rats.

To assess possible roles of the renal kallikrein-kinin system in the development of spontaneous hypertension, we determined daily excretion of urinary total and active kallikrein in 6-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats for up to 2 weeks. We also evaluated the effect of aprotinin, a reversible inhibitor of kallikrein and other serine proteases, on the development of hypertension in the 6-week-old SHR on ordinary intakes of sodium or on sodium loading with 1% NaCl for up to 2 weeks. Active kallikrein was determined by its kininogenase activity, and the generated kinins were radio-immunologically measured. Total kallikrein was also determined by measuring kininogenase activity after inactive kallikrein had been activated with trypsin (200 micrograms/ml). Urinary active kallikrein excretion was significantly reduced in 7-week-old SHR (1.5 +/- 0.2 microgram/day compared to 2.8 +/- 0.3 micrograms/day in WKY, P less than 0.05) and in 8-week-old SHR (1.6 +/- 0.2 microgram/day compared to 3.2 +/- 0.4 micrograms/day in WKY, P less than 0.01). Urinary total kallikrein excretion was also reduced in the 7- and 8-week-old SHR whereas the ratio of active to total kallikrein did not change. In addition, renal contents of total and active kallikrein were significantly lower in the 8-week-old SHR than in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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↗
PubMed1987

Long-term effects of aldosterone on kallikrein, prostaglandin E2 and sodium in rats.

To assess the long-term effects of mineralocorticoids on the regulation of the synthesis or release of kallikrein and prostaglandin E2 in the renal kallikrein-kinin-prostaglandin E system, we studied the effects of chronic infusion of aldosterone (50 micrograms/kg/day) on urinary excretion of total and active kallikrein, and prostaglandin E2 for 10 days in conscious rats on regular intakes of sodium and on sodium loading with 1% NaCl as a drinking water. Chronic infusion of aldosterone induced a prompt and transient decrease in the ratio of sodium to potassium and a sustained increase in urinary prostaglandin E2 excretion in rats on regular diets, whereas urinary total and active kallikrein excretion did not increase significantly until the 4th day of aldosterone infusion. In rats loaded with sodium, aldosterone did not induce any changes in urinary total and active kallikrein excretion, whereas it induced similar changes in the ratio of sodium to potassium and urinary prostaglandin E2 excretion to those in rats on regular diets. Thus, the present results suggest that aldosterone might stimulate the synthesis or release of renal prostaglandin E2 independent of sodium balance. Furthermore, it is also suggested that aldosterone might stimulate the synthesis or release of kallikrein, at least partly, via the same pathway as sodium loading does.

Aldosterone↗
PubMed1987

No evidence on significant roles of the prostaglandin-thromboxane and kallikrein-kinin system in the antihypertensive effect of MK 421 in rats made hypertensive by norepinephrine or vasopressin.

Inhibition of angiotensin converting enzyme by MK 421 (6 mg/kg/day ip) induced a significant increase in urinary kinin excretion in norepinephrine-infused rats (1.8 mg/kg/day ip), whereas it had no effect on urinary prostaglandin E2 excretion. In contrast, MK 421 did not induced any significant changes in urinary kinin and prostaglandin E2 excretion in vasopressin-infused rats (7.2 U/kg/day ip). The simultaneous administration of indomethacin (10 mg/kg/day sc), OKY 046 (12 mg/kg/day sc) or aprotinin (100,000 units/kg/day sc) did not affect the antihypertensive effect of MK 421 in rats made hypertensive by chronic infusion of norepinephrine or vasopressin. The present results suggest that the hypotensive effect of MK 421 may depend on a reduced sensitivity of the vasculature to vasoconstrictor substances. In addition, it is also suggested that neither the prostaglandin-thromboxane or kallikrein-kinin systems are essential for the antihypertensive effect of MK 421 in these models of hypertension.

Animals↗
PubMed1987

Effects of angiotensin converting enzyme inhibitors MK 421, SA 446 and captopril on renal prostaglandin E and kinins in conscious normotensive rats.

Angiotensin converting enzyme inhibition by MK 421, SA 446 or captopril (6 mg/kg/day ip) for up to 6 days induced significant fall in systolic blood pressure and plasma angiotensin II concentration. The hypotensive effect was greater in sodium depleted rats than in sodium repleted rats. The hypotensive effect was also accompanied by increased excretion of urinary prostaglandin E2, however the levels of urinary prostaglandin E2 in sodium repleted rats were not different from those in sodium depleted rats. Urinary kinin excretion was increased during infusion of MK 421, SA 446 or captopril in sodium depleted rats, whereas no significant change was found in sodium repleted rats. Thus the present results suggest that renal prostaglandin E system may not be essential for the hypotensive effect of these inhibitors. In addition, the greater hypotensive effect of these inhibitors in sodium depleted rats may be in part due to stimulated renal kinin system.

3-Mercaptopropionic Acid↗
PubMed1987

Distribution of kininase activity along the rabbit nephron.

The distribution of kininases along microdissected nephron segments was studied. Single nephrons from collagenase treated rabbit kidney were microdissected and divided into following 9 segments: glomerulus; early proximal tubule; middle proximal tubule; late proximal tubule; cortical thick ascending limb; distal convoluted tubule; connecting tubule; cortical collecting tubule; medullary collecting tubule. Kininase activities in these nephron segments were measured with or without kininase II inhibitor. Kininase II and other peptidases were mainly localized in glomeruli and whole part of the proximal tubules.

Animals↗
PubMed1987

Role of endogenous angiotensin II and prostaglandins in the antihypertensive mechanism of angiotensin converting enzyme inhibitor in hypertension.

The role of endogenous angiotensin II and prostaglandins (PGs) in the antihypertensive effect of converting enzyme inhibitor, captopril, was studied in essential hypertension by the separate and the combined administration of captopril and indomethacin. Although plasma angiotensin II was similarly suppressed by the separate and the combined administration of captopril and indomethacin, captopril lowered and indomethacin increased the mean blood pressure. There were negative correlations between the changes in mean blood pressure and in urinary sodium excretion as well as in urinary PGE excretion. These results suggest that endogenous PGs may be implicated in the antihypertensive effect of captopril through the alteration of sodium balance.

Adult↗
PubMed1987

[Nuclear DNA content in small thyroid papillary carcinomas determined by microfluorometry].

Microfluorometric measurement of the DNA content of cell nuclei was performed on echo-guided aspiration specimens or imprints of operated fresh materials of fourty-one small thyroid papillary carcinomas of 10 mm or less in diameter and of six large ones more than 20 mm in diameter. The distribution patterns of the DNA content were classified into three groups: IIa, IIb and III. The DNA values in so-called sclerosing carcinomas mostly fell into Group-IIa, while ordinary papillary carcinomas were classified as Group-IIb and III. Our date suggests that the DNA microfluorometry of echo-guided aspiration specimens of small papillary carcinomas gives the index whether they will remain occult or not.

Adult↗
PubMed1986

Prostaglandins and sodium balance during the reversal of chronic two-kidney, one clip hypertension in rats.

To determine the role of endogenous prostaglandins and sodium balance in the maintenance of high blood pressure in chronic two-kidney, one clip hypertension in rats, we studied the effect of indomethacin infusion on the reversal of hypertension by unclipping. Indomethacin was infused after control measurements, and blood pressure was monitored continuously in conscious rats. Parallel control experiments and sham operations were also performed. Inhibition of prostaglandin synthesis did not affect the postoperative course of blood pressure after the unclipping operation despite the marked decrease of urinary prostaglandin E excretion. The decrease of blood pressure after unclipping was significantly correlated with plasma renin activity prior to unclipping. Sodium balance was not significantly different between the experimental groups. These data indicate no major participation of prostaglandins in the reversal of chronic two-kidney, one clip hypertension, and suggest that the renin angiotensin system participates, at least in part, in the maintenance of high blood pressure in this model of hypertension.

Animals↗