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Biomedical subjects

T Okahara

Publications and source records attributed to T Okahara.

14 recordsLinked to original sources
PubMed1988

Renal effects of leukotrienes C4 and D4 in anesthetized dogs.

We investigated the effects of leukotrienes (LTs) C4 and D4 on renal function and hemodynamics of dogs. LTC4 (0.5 microgram/min, infused into the renal artery), but not LTD4 (1 microgram/min), caused an increase in renal blood flow, urine flow, urinary excretion of sodium and potassium, and rate of free water reabsorption, with a concomitant rise in systemic blood pressure. Intrarenal infusion of LTC4 under conditions of constant renal perfusion pressure induced no significant effect on renal blood flow or urine formation. Infusions or LTC4 and LTD4 into the renal artery induced no change in the release of prostaglandins, PGE2, PGF2 alpha, 6-keto-PGF1 alpha or thromboxane B2 into renal venous blood. From these findings, we concluded that the renal effects of LTC4 were secondary responses to a rise in systemic blood pressure.

Anesthesia↗
PubMed1987

Correlation between blood prostaglandins and blood pressure in chronic renal failure.

Plasma prostaglandins (PGs; PGE2, PGF2 alpha, 6-keto-PGF 1 alpha and TXB2) and plasma renin activity (PRA) were measured in 94 end-stage renal disease (ESRD) patients including 15 undialyzed, 74 maintenance-hemodialyzed and 5 anephric patients, and in 27 healthy controls. In the healthy controls, 6-keto-PGF 1 alpha inversely correlated with age, while TXB2 and the TXB2/6-keto-PGF 1 alpha ratio correlated with age. In the ESRD patients, 6-keto-PGF 1 alpha showed a tendency to decrease with age, and the TXB2/6-keto-PGF 1 alpha ratio significantly correlated with age. The undialyzed group showed significantly higher blood pressure and TXB2 but significantly lower 6-keto-PGF1 alpha compared to the other groups. In the dialyzed group, PGE2 and 6-keto-PGF1 alpha tended to be lower and TXB2 higher compared to the healthy control group. In the dialyzed group, 6-keto-PGF1 alpha correlated inversely with blood pressure independently from PRA. As for PGF2 alpha, it was higher in the undialyzed, dialyzed and anephric groups than in the healthy control group. These results suggested that PGs were involved in blood pressure abnormalities, and that PGI2 played an important role in controlling blood pressure in ESRD patients as one of the depressor factors.

Adult↗
PubMed1986

Effects of ouabain on autoregulation of renal blood flow in dogs.

Effects of ouabain on the autoregulation of renal blood flow (RBF) and renin release were examined in filtering and nonfiltering kidneys of anesthetized dogs. Autoregulation of RBF was observed in both kidneys; however, autoregulation in the nonfiltering kidney was comparatively less efficient. These findings indicate that both the myogenic mechanism via a sensor element in the afferent arteriole, a so-called baroreceptor, and the tubuloglomerular feedback mechanism via the macula densa are essential for complete autoregulation. In both the control and nonfiltering kidney, intrarenal arterial infusion of ouabain abolished the autoregulation of RBF and glomerular filtration rate, with no change in the renal vascular sensitivity to vasoactive substances or in renin release induced by pressure reduction. Since various vasoactive drugs elicited a normal vascular response, it appears that the site of action of ouabain was not the vascular contractile elements; at least, an impairment of autoregulation during ouabain infusion was apparently not due to a defect in these elements. These results suggest the possible existence of another mediator, a sensor element in the afferent arteriole that is affected by ouabain. Ouabain may abolish the autoregulation of RBF and renin release via a modification of this baroreceptor in the afferent arteriole as well as through inhibition of the macula densa.

Animals↗
PubMed1986

Plasma thromboxane and prostacyclin: comparison during normal pregnancy and pregnancy complicated by hypertension.

Plasma levels of thromboxane B2 (TXB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), stable metabolites of two prostanoids with opposing biological effects, TXA2 and prostacyclin, were measured by radioimmunoassay in normal pregnancy (controls) and pregnancy complicated by hypertension (PIH) from 32 to 36 (Period 1; P1) and from 36 to 40 (Period 2; P2) weeks of gestation. The plasma concentration of each compound in the control subjects was 265.6 +/- 58.4 (TXB2), 132.4 +/- 16.5 (6-keto-PGF1 alpha) for P1 (n = 10) and 142.6 +/- 11.8 (TXB2), 68.5 +/- 5.2 (6-keto-PGF1 alpha) for P2 (n = 10) respectively (pg/ml, mean +/- s.e). In the patients with PIH, TXB2 concentrations increased moderately for P1 (419.2 +/- 21.2; n = 7) and significantly (p less than 0.005) for P2 (452.8 +/- 31.0; n = 7) respectively (pg/ml, mean +/- s.e), while the plasma levels of 6-keto-PGF1 alpha revealed a slight to moderate decrease both for P1 (84.5 +/- 4.0; n = 7) and P2 (59.7 +/- 8.1; n = 7) respectively (pg/ml, mean +/- s.e). The physiological balance of TXB2 to 6-keto-PGF1 alpha was significantly greater (p less than 0.005) in the patients with PIH, where the TXB2/6-keto-PGF1 alpha ratio was 5.2 +/- 0.7 for P1 and 9.4 +/- 2.3 for P2 respectively (mean +/- s.e) compared with that of the controls, where it was 2.4 +/- 0.4 for P1 and 2.0 +/- 0.2 for P2 respectively (mean +/- s.e).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Comparison of plasma prostanoid levels in the human cord artery in normal and fetal distressed deliveries.

Prostaglandin E2 (PGE2), thromboxane B2 (TXB2; as a stable metabolite of TXA2), prostaglandin F2 alpha (PGF2 alpha) and 6-keto-PGF1 alpha (as a stable end product of prostacyclin) have been measured by using specific radioimmunoassay in the plasma of the cord artery immediately after delivery before the cord was clamped. Plasma prostanoid concentrations in normal deliveries (n = 8, as controls) were 24.8 +/- 2.6 (PGE2), 246.8 +/- 37.0 (TXB2), 122.2 +/- 13.3 (PGF2 alpha) and 82.1 +/- 7.7 (6-keto-PGF1 alpha) respectively (pg/ml, mean +/- s.e). On the other hand, in fetal distressed deliveries showing continuous bradycardia (n = 6), they increased significantly to 275.4 +/- 20.1 (PGE2), 948.6 +/- 102.5 (TXB2), 218.0 +/- 21.4 (PGF2 alpha) and 1498.6 +/- 298.4 (6-keto-PGF1 alpha) respectively (pg/ml, mean +/- s.e, p less than 0.005). However, both PGF2 alpha/PGE2 and TXB2/6-keto-PGF1 alpha ratios declined significantly from 4.70 +/- 0.33 to 0.68 +/- 0.05 and from 3.07 +/- 0.37 to 0.68 +/- 0.12 respectively (mean +/- s.e, p less than 0.005) in the fetal distressed group compared with those of the controls. From these results, it may be concluded that the cord artery, which is known as the patent source for the production of PGE2 and prostacyclin, did exert a sufficiently strong reaction to overcome the undesirable haemodynamic changes to maintain the fetal well-being in utero.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effects of a synthetic human atrial natriuretic polypeptide on regional blood flow in rats.

The effects of alpha-hANP on systemic hemodynamics and regional blood flow were examined in conscious WKY and SHR. An intravenous infusion of alpha-hANP (3 micrograms/kg per min) resulted in a rapid and marked fall of blood pressure and of total peripheral resistance but with no change in cardiac output in both strains. alpha-hANP decreased vascular resistance in most organs and there was a redistribution of renal blood flow. Thus, the acute hypotensive effect of alpha-hANP is probably related to a vasodilator action.

Animals↗
PubMed1979

Intrarenal role of renin-angiotensin system in the regulation of renal hemodynamics.

A reduction of renal arterial pressure in mongrel dogs to 70 mmHg resulted in marked increases in plasma renin activity and plasma levels of angiotensin I (AI) and angiotensin II (AII). Production of renin and AI but not AII in the kidney was observed. A reduction of renal arterial pressure also resulted in a redistribution of blood flow from the outer to inner cortex. An arterial infusion of AII (200 ng/min), however, failed to affect the intrarenal distribution of the blood flow. An intrarenal infusion of AII rather restored the normal pattern of the distribution of intrarenal blood flow altered by the pressure reduction. These results indicate that the renin-angiotensin system is probably not involved in the control of renal hemodynamics through the intrarenal formation of AII, and that the intrarenal hemodynamic changes caused by pressure reduction is due to the intrinsic differences in myogenic force in different cortical zones.

Angiotensin I↗
PubMed1977

Control of renin secretion.

The present study was designed to examine the interrelationship between the intrarenal vascular receptor and the sympathetic nerve, beta-adrenergic system, for renin secretion in the anesthetized dog. 1) A reduction in renal arterial pressure from a control pressure to 100 mmHg changed neither ther flow rates of all cortex zones nor renin secretion. Further reduction of renal arterial pressure to 75 mmHg resulted in a significant increase of renin secretion and a decrease of blood flow in the outer cortex. Intrarenal arterial infusion of norepinephrine at a control pressure increased a renin secretion. However, norepinephrine infusion at a reduced pressure suppressed the renin release with a recovery of the vascular resistance to the control level. These results suggest that the changes in the degree of blood flow and pressure in the renal afferent arterioles are not essential for the renin secretion,but renin secretion by the pressure reduction might be related to the autoregulatory capacity of afferent arterioles in the outer cortex. 2) At 5 min of hemorrhagic period (75 mmHg) arterial PRA elevated in control, and phenoxybenzamine and propranolol treated groups and any significant difference in responses was not observed among groups. However, at 60 min of hemorrhagic hypotensive period PRA in control and phenoxybenzamine treated groups further increased, but PRA in propranolol treated group was not alter from its 15 min value. These results indicated that the roles of vascular receptor and renal sympathetic nervous sytem in receptor and renal sympathetic nervous system in renin secretion might be separated, and that the renal sympathetic nervous system did not relate to the early response of renin release, but related to the late response. 3) Intrarenal arterial infusion of cAMP and DbcAMP resulted in a significant increase of renin release. In addition, CaC12 solution was infuesed into the renal artery and a significant rise in renal venous PRA was observed within 5 min of infusion. These data suggested that a beta-adrenergic receptor-adenyl cyclase-cAMP system was involved in the control of renin secretion, and that since the intracellular effect of cAMP was partly related to the change of intracellular Ca distribution, its change resulted in an increase in renin secretion.

Animals↗
PubMed1976

Relationship between intrarenal distribution of blood flow and renin secretion during ureteral occlusion.

The present study was undertaken to evaluate the relationship between renin secretion from the denervated kidney and intrarenal distribution of blood flow during reductions in renal perfusion pressure by partial constriction of the aorta with and without ureteral occlusion in the anesthetized dog. In addition, renin contents in different zones of the kidney were measured. A reduction in renal arterial pressure from normal pressure (125-135 mmHg) to 77 mm Hg resulted in significant increase in renin secretion and redistribution of cortical blood flow. A further reduction of renal arterial pressure to 51 mmHg produced a marked increase in renin secretion rate (RSR) without further changes in the intrarenal distribution pattern of blood flow. The pressure reductions during ureteral occlusion increased RSR without any change in the distribution pattern of blood flow, and a decrease in the amounts of extractable renin was found in the outer cortex of the experimental kidney. These findings suggest that renin release occurs mainly in the outer cortex, and this process may be stimulated when the mechanism of autoregulation fails as the perfusion presure approaches to the lower range of autoregulation in the outer cortex.

Animals↗
PubMedDate not supplied

Effect of SA-446, an angiotensin-converting enzyme inhibitor, on renal function in anesthetized dogs: special reference to arachidonic acid metabolites.

Intravenous infusion of SA-446 (1 mg/min) decreased systemic blood pressure and increased renal blood flow in anesthetized dogs. These changes were accompanied by a slight natriuretic response. During the infusion of this dose of SA-446, the pressor response to angiotensin I was abolished and the depressor response to bradykinin was markedly potentiated. Administration of indomethacin (13 mg/kg i.v.) suppressed natriuresis and, to some extent, the renal vasodilation caused by SA-446. Before and after administration of SA-446, four arachidonate metabolites, prostaglandin E2, prostaglandin F2 alpha, 6-keto-prostaglandin F1 alpha, and thromboxane B2, were determined in plasma and urine by radioimmunoassay. There were no remarkable changes in levels of prostaglandins and thromboxane B2 in arterial and renal venous plasma. The urinary excretion of the metabolites varied little, but thromboxane B2 excretion did significantly decrease. Thus, reduction in the biosynthesis of thromboxane B2 in the kidney may relate to the effects of SA-446 on renal hemodynamics and urine formation.

3-Mercaptopropionic Acid↗