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Biomedical subjects

S Akabane

Publications and source records attributed to S Akabane.

At least 37 records · Page 2Linked to original sources
PubMed1990

A comparison of lisinopril with enalapril by monitoring plasma angiotensin II levels in humans.

The present study was designed to examine and compare the acute effects of lisinopril (20 mg) and enalapril (10 mg) after a single oral administration on the inhibition of the renin-angiotensin system (RAS) in eight normal subjects. Serum concentration of lisinopril and enalaprilat, an active metabolite of enalapril, reached the respective maximal levels at 6 and 4 hr after administration of the drugs. At 24 hr, the serum concentration of lisinopril was higher than that of enalapril; thus the rate of disappearance of lisinopril was retarded, in comparison to that of enalapril. The reduction of serum angiotensin I converting enzyme (ACE) activity was consistent with the pattern of increase of concentration of the drugs in the serum. However, with these two drugs, the concentration of plasma ANG II was decreased in a similar manner, and it returned to the pretreatment level within 24 hr. Thus, there was no significant difference in ANG II levels throughout the 24 hr-study between the lisinopril and enalapril treatment. The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. The measurement of ANG II provides useful informations for evaluating the efficacy of ACE inhibitors for the inhibition of circulatory RAS.

Administration, Oral↗
PubMed1989

Alterations in cerebrospinal fluid angiotensin II by sodium intake in patients with essential hypertension.

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 +/- 0.38 (SEM) to 1.83 +/- 0.43 fmol/ml (P less than 0.01) and of ANG III from 0.65 +/- 0.11 to 0.86 +/- 0.15 fmol/ml (P less than 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Adult↗
PubMed1989

Aspirin lowers blood pressure in patients with renovascular hypertension.

To clarify the role of renal prostanoid in hyperreninemia and high blood pressure in human renovascular hypertension, we measured prostaglandin E2 and renin activity in renal venous and abdominal aortic plasma before and after the intravenous administration of the cyclooxygenase inhibitor, aspirin DL-lysine. Subjects were six patients with unilateral renovascular hypertension and six with essential hypertension. In patients with renovascular hypertension, prostaglandin E2 concentration in renal venous plasma from the stenotic kidney was 9.25 +/- 1.48 pg/ml, which was significantly higher (p less than 0.01) than the concentration in the renal venous plasma from the normal kidney (4.97 +/- 1.02 pg/ml) or in the aortic plasma (2.59 +/- 0.15 pg/ml). Plasma renin activity was also higher in the renal vein of the stenotic kidney than in the other two sites. The stenotic side/normal side ratio of the renal venous prostaglandin E2 correlated significantly with a renin ratio greater than 1.5 (r = 0.8211, p less than 0.05). Intravenous injection of aspirin DL-lysine (18 mg/kg) 30 minutes later markedly suppressed prostaglandin E2 and renin levels at all sites and clearly lowered arterial blood pressure (mean: from 120 +/- 6 to 110 +/- 5 mm Hg, p less than 0.01). The reduction in blood pressure correlated significantly with the suppression of plasma renin activity in the aorta (p less than 0.05) and in the renal vein of the stenotic kidney (p less than 0.01). Conversely, in patients with essential hypertension, aspirin had little effect on renin levels and increased mean blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Cerebrospinal fluid angiotensin II in patients with essential hypertension.

We measured components of the cerebrospinal fluid renin-angiotensin system from patients with essential hypertension under different dietary sodium intakes. The cerebrospinal fluid concentration of angiotensin II (Ang II) from the patients on a normal-sodium diet was 1.36 +/- 0.41 fmol/ml (n = 5). Neither the inactive nor the active form of renin was detected by the enzymatic activity or by the immunoreactivity, whereas angiotensinogen was detected (38.6 +/- 3.1 pmol/ml, n = 5). The Ang II level remained unchanged even after incubation of the cerebrospinal fluid at 37 degrees C for 3 h. Further, when authentic Ang II was added to the cerebrospinal fluid followed by incubation for 3 h at 37 degrees C, more than 90% of the added Ang II remained unchanged. Thus, the cerebrospinal fluid Ang II level may be reflected by the activity of the brain Ang II-forming system, as it was not affected by the cerebrospinal fluid constituents. The circulating renin-angiotensin system was stimulated by sodium depletion, and the cerebrospinal fluid concentration of Ang II also increased significantly. Sodium depletion may stimulate the brain Ang-II forming system, as it does the circulating renin-angiotensin system.

Angiotensin II↗
PubMed1988

Renal actions of atrial natriuretic peptide on the postischemic kidney.

The objective of this study was to evaluate the renal actions of atrial natriuretic peptide (ANP) in the unilateral postischemic kidney of anesthetized dogs with a severe reduction in glomerular filtration rate. The dose of atrial natriuretic peptide (50 ng.kg-1.min-1) we gave did not alter the mean systemic arterial pressure, renal blood flow, and glomerular filtration rate in the normal kidney, as determined in foregoing studies. ANP was infused into the intrarenal artery continuously for 60 min after the release from 45 min of complete renal artery occlusion. In the vehicle-infused group, the glomerular filtration rate fell dramatically (6% of control), the renal blood flow decreased (60% of control), and the mean systemic arterial pressure tended to increase (136% of control). The urine flow rate and urinary excretion of sodium decreased significantly (25 and 25%, respectively) at 30 min after reflow in the postischemic period. Continuous renal artery infusion of ANP resulted in a marked increase in urine flow rate (246% of control) and the urinary excretion of sodium (286% of control). The administration of ANP led to an improvement in renal blood flow (99% of control) and glomerular filtration rate (40% of control), and attenuated the rise in mean systemic arterial pressure (109% of control), compared with findings in the vehicle-infused group. Plasma renin activity and prostaglandin E2 concentration in the renal venous blood were elevated after the release from complete renal artery occlusion in both groups. These results indicate that the vascular effects of ANP on the postischemic kidney were enhanced and that the peptide maintained the natriuretic effect.

Animals↗
PubMed1988

Alpha-form of atrial natriuretic peptide released from dog atrium during atrial distension.

To assess the released form of atrial natriuretic peptide (ANP) during atrial distension, we compared the form of ANP before and during atrial distension in anesthetized dogs, using radioimmunoassay combined with high performance liquid chromatography (HPLC). When increasing the left atrial pressure (LAP) from 2.2 +/- 0.9 mmHg to 9.4 +/- 1.3 mmHg, the plasma ANP concentration in the coronary sinus was increased by 190% over the control, during left atrial distension. The major form of the released ANP extracted in the blood sample obtained from the coronary sinus was alpha-form. However other unidentified immunoreactive peaks, preceding and following the main peak were also discernible. These results suggest that the major form of ANP released during left atrial distension was the alpha-form.

Animals↗
PubMed1988

Increases in renal angiotensin II content and tubular angiotensin II receptors in prehypertensive spontaneously hypertensive rats.

To examine the role of the intrarenal renin-angiotensin system in the development of hypertension in spontaneously hypertensive rats (SHR), we measured angiotensin II contents and tubular 125I-angiotensin II binding sites in the kidney of SHR and age-matched Wistar-Kyoto rats (WKY). In prehypertensive (4-week-old) SHR, not only the kidney angiotensin II content but also the angiotensin II receptor density in brush border membranes were significantly higher than in the WKY. In contrast, angiotensin II levels in the 20-week-old SHR kidneys were significantly lower than in the WKY. Acceleration of the intrarenal renin-angiotensin system and the increased density of tubular angiotensin II receptors in young SHR may therefore play an important role in the development of high blood pressure in SHR.

Angiotensin II↗
PubMed1987

Release of atrial natriuretic polypeptide by graded right atrial distension in anesthetized dogs.

In order to verify the contribution of right atrial pressure to atrial natriuretic polypeptides (ANP) release, we measured plasma levels of immunoreactive (ir)-ANP when graded rise of right atrial pressure was executed in anesthetized dogs. Increasing right atrial pressure (RAP) from 2.7 +/- 0.6 to 9.0 +/- 0.7 mmHg, plasma levels of ir-ANP in aorta tended to increase by 33% but not significantly (p greater than 0.05). However, when RAP was increased from 9.0 +/- 0.7 to 17.0 +/- 1.1 mmHg, ir-ANP levels in aorta were significantly (p less than 0.05) increased by 132% of control within 5 min from the start of RAP elevation. The RAP elevation produced a sustained increase in plasma levels of ir-ANP. There was a positive correlation between right atrial pressure and plasma levels of ir-ANP. The plasma levels of ir-ANP were similar between aorta and pulmonary artery. These results demonstrate that increasing atrial pressure is closely correlated with ANP release and ANP is not greatly metabolized by pulmonary circulation.

Animals↗
PubMed1987

Diuretic response of a second infusion of atrial natriuretic polypeptide into anesthetized dogs.

We examined the diuretic effects of a second infusion of atrial natriuretic polypeptide (ANP). Intrarenal infusion of ANP (50 ng X kg-1 X min-1) for 30 min to anesthetized dogs had no significant effect on mean arterial blood pressure (MABP), renal blood flow (RBF) and glomerular filtration rate (GFR), whereas there was an increase in urine flow (V) and urinary excretion of sodium (UNaV) from 7.5 +/- 1.5 to 34.1 +/- 9.4 microliters/g X min, from 0.97 +/- 0.20 to 4.38 +/- 1.32 microEq/g X min, respectively. When the same dose of ANP was infused 1 h after the first administration, V and UNaV were increased from 12.4 +/- 1.8 to 62.5 +/- 18.8 microliters/g X min, from 1.72 +/- 0.57 to 7.18 +/- 2.68 microEq/g X min, respectively. A second infusion of ANP caused a greater absolute increase in UNaV than did the first infusion but proportionally the increase in UNaV with the second ANP infusion was much the same. The present study shows that acute ANP infusion has no tachyphylaxis on the natriuretic response. These data will aid in establishing a bioassay for natriuretic response in vivo, thereby leading to elucidation of the physiological action of ANP.

Animals↗
PubMed1987

Distribution of alpha 1- and alpha 2-adrenoceptors in brush border and basolateral membranes from rat kidney cortical tubules.

To examine the localization of alpha-adrenoceptors within the kidney tubule, binding experiments with 125I-HEAT and 3H-yohimbine were performed using cortical homogenates, basolateral membranes (BLM) and brush border membranes (BBM). Bmax values for 125I-HEAT or 3H-yohimbine binding were 2.3- or 2.0-fold that of the homogenate in BBM and 8.2- or 10.7-fold in BLM, respectively. Kd values for 125I-HEAT or 3H-yohimbine were not significantly different between BBM and BLM. These results indicate that both types of alpha-adrenoceptors seem to be localized largely in the BLM.

Animals↗
PubMed1987

A sensitive method for precise measurement of endogenous angiotensins I, II&III in human plasma.

We measured endogenous angiotensins (ANGs) I, II&III using a system of extraction by Sep-Pak column followed by high performance liquid chromatography (HPLC) combined with radioimmunoassay (RIA). An excellent separation of ANGs was obtained by HPLC. The recovery of ANGs I, II&III was 80-84%, when these authentic peptides were added to 6 ml of plasma. The coefficient of variation of the ANGs was 0.04-0.09 for intra-assay and 0.08-0.13 for inter-assay, thereby indicating a good reproducibility. Plasma ANGs I, II&III measured by this method in 5 normal volunteers were 51,4.5 and 1.2 pg/ml. In the presence of captopril, ANGs II&III decreased by 84% and 77%, respectively, while ANG I increased 5.1 times. This method is therefore useful to assess the precise levels of plasma ANGs.

Angiotensin I↗
PubMed1986

Characterization of alpha 1- and alpha 2-adrenoceptors directly associated with basolateral membranes from rat kidney proximal tubules.

We have used 2-(beta-(3-125iodo-4-hydroxyphenyl)-ethylaminoethyl)-tetr alo ne ([125I]HEAT or BE2254), an alpha 1-selective antagonist, and [3H]yohimbine, an alpha 2-selective antagonist, to demonstrate and characterize binding sites in basolateral membranes from rat kidney cortex. Parathyroid hormone (PTH) stimulated the adenylate cyclase activity of the basolateral membranes, whereas thyrocalcitonin, arginine vasopressin (AVP) and isoproterenol did not. Therefore, the basolateral membranes were probably derived from the proximal tubules. The specific binding of [125I]HEAT and [3H]yohimbine to basolateral membranes was rapid, reversible, saturable and of high affinity. The maximum densities of alpha 1- and alpha 2-receptors were 364 and 1130 fmoles/mg protein, indicating that the ratio of alpha 1- to alpha 2-adrenoceptors was about 1:3. The specific binding of [125I]HEAT and [3H]yohimbine to the basolateral membranes was displaced by various adrenergic agents in a manner that suggests that the labeled sites probably represent alpha 1- and alpha 2-adrenoceptors respectively. These results suggest that the binding sites of [125I]HEAT and [3H]yohimbine, which appear to be alpha 1- and alpha 2-adrenoceptors, exist in the basolateral membranes of the proximal tubules.

Animals↗
PubMed1986

Additive effects of atrial natriuretic polypeptide and of renal vasodilating agents in the anesthetized dog.

In order to examine the contribution of an increase in renal papillary plasma flow to the mechanism of natriuresis by atrial natriuretic polypeptide (ANP), we compared the natriuretic effects of ANP administered into the renal artery of the dog together with secretin or acetylcholine (ACh). At an equivalent renal vasodilating dose, ACh increased urinary excretion of sodium (UNaV) to 212 +/- 36% of the control associated with a decrease in urine osmolality (62 +/- 6%), whereas secretin did not change UNaV (113 +/- 12%) or urine osmolality (101 +/- 14%). This result was compatible with the view that ACh causes natriuresis mainly by increasing papillary plasma flow. Combined administration of ANP with secretin caused a marked increase in UNaV to 407 +/- 55%, in association with a decrease in urine osmolality to 55 +/- 9%, suggesting that ANP may cause natriuresis by a mechanism similar to that of ACh. Combined administration of ANP with ACh further increased UNaV to 323 +/- 67% and decreased urine osmolality to 50 +/- 6%. These observations suggest that ANP and ACh share common but not identical mechanisms of natriuretic action since ANP caused additional natriuresis during ACh infusion. These findings, however, do not necessarily exclude the possibility that ANP also inhibits renal sodium reabsorption by a direct action.

Acetylcholine↗
PubMed1986

Plasma atrial natriuretic polypeptide and polyuria during paroxysmal tachycardia in Wolff-Parkinson-White syndrome patients.

The human atrial natriuretic polypeptide (hANP) concentration in plasma was measured during paroxysmal supraventricular tachycardia provoked in 2 patients with Wolff-Parkinson-White syndrome. A 10- to 20-fold increase in plasma hANP concentration was observed during the tachycardia: from 12 to 291 pg/ml in 1 case and from 14 to 174 pg/ml in the other. Although polyuria was associated with the tachycardia, urinary sodium excretion as well as urinary osmolality were decreased. The urinary arginine vasopressin was appreciably decreased during the tachycardia. These results suggest that hANP released by paroxysmal tachycardia might not act as a natriuretic factor in this range of plasma concentration. Polyuria during paroxysmal tachycardia was attributed mainly to the inhibition of arginine vasopressin release.

Adult↗
PubMed1986

Is renin secreted by exocytotic mechanism through mature renin granules from juxtaglomerular cells?

Mature renin granules were isolated by the combination of discontinuous and continuous Percoll density gradient centrifugation. Stored renin in the renin granules was found to consist of isoelectrically seven different forms. The seven different isoelectric points (pIs) were 5.6, 5.35, 5.2, 5.0, 4.8, 4.6 and 4.4. Approximately 70% of the stored renin as the total enzymatic activities from all isoelectric peaks was found in a peak which pI corresponded to be 5.35. Renin secreted from isolated glomeruli was also focused into seven peaks possessing identical values. However, the distribution pattern of renin peaks was quite different from that of stored renin. In the secreted renin, peaks of 5.35 (pI) and 5.2 (pI) showed high renin activity and each had approximately 30% of released renin as the total recovered. These results indicate multiple forms of renin are stored and secreted by rat kidney. As the distribution pattern of enzymatic activities in renin peaks between stored renin and secreted renin are different, it is probable that renin may not secreted through mature renin granules by exocytotic mechanism.

Animals↗
PubMed1986

Effect of plasma potassium on vascular response to pressor and depressor agents in dog kidney.

The effect of plasma potassium concentration on the vascular response to the pressor agent angiotensin II (ANG II) and to the depressor agent prostaglandin E2 (PGE2) was investigated in dog kidney. Renal vascular reactivity to the vasoactive agents was assessed from the change in renal blood flow (RBF) after infusion of the agent into the renal artery. Plasma potassium concentration was increased by intravenous infusion of potassium L-aspartate solution. The vascular response to ANG II was attenuated when plasma potassium was increased, i.e. percent decrease in RBF produced by ANG II (26.1 +/- 8.4%) during potassium infusion (plasma K+, 5.68 +/- 0.31 mEq/L) was significantly lower than those (35.8 +/- 9.8, 30.4 +/- 7.8%) obtained in the control period (plasma K+, 3.60 +/- 0.40 mEq/L) and in the postinfusion period (plasma K+, 4.70 +/- 0.42 mEq/L). On the other hand, the vascular response to PGE2 showed a tendency to be potentiated by elevation of plasma potassium concentration, i.e. percent increases in RBF produced by PGE2 were 44.9 +/- 10.5% in the control period (plasma K+, 3.47 +/- 0.25 mEq/L), 50.5 +/- 6.8% during potassium infusion (plasma K+, 5.45 +/- 0.25 mEq/L) and 44.9 +/- 7.2% in the recovery period (plasma K+, 4.55 +/- 0.21 mEq/L). These changes in the vascular response obtained by elevation of plasma potassium appear to act towards lowering blood pressure.

Angiotensin II↗
PubMed1985

Alterations in renal Na+K+ATPase activity and [3H]ouabain binding in Goldblatt hypertensive rabbits.

To evaluate the role of renal Na+K+ATPase in the presence of Goldblatt hypertension, the enzyme activity and [3H]ouabain binding were examined in cortical and medullary homogenates from two-kidney, one clip (2K1C), one-kidney, one clip (1K1C), unilaterally nephrectomized and normal rabbits. Four weeks after the surgery, systolic blood pressures (SBPs) of 2K1C and 1K1C rabbits were increased significantly to 128 +/- 3 and 129 +/- 2 mmHg, respectively. In contrast, SBPs in the normal controls and unilateral nephrectomized (1K) animals were 83 +/- 2 and 86 +/- 3 mmHg, respectively. In the 2K1C rabbits, atrophy (91%) occurred in the kidney on the ischaemic side and hypertrophy (110%) occurred in the contralateral kidney. Na+K+ATPase activity and number of [3H]ouabain binding sites were reduced in the homogenates of the ischaemic kidney of 2K1C rabbits. In the 1K1C rabbits, marked hypertrophy of the kidney (155%) occurred, and the activity of Na+K+ATPase and the number of [3H]ouabain binding sites increased slightly in the cortex and medulla, compared with the normal controls. 5'-Nucleotidase, a plasma membrane marker enzyme, remained unchanged in both groups of hypertensive rabbits. Dissociation constant (KD) values for [3H]ouabain binding did not differ significantly in the renal homogenates of of 2K1C and 1K1C, compared with findings in the normal controls. The inhibitory activity of plasma was measured by studying [3H]ouabain binding to Na+K+ATPase of renal tubular basolateral membrane vesicles purified by Percoll gradient. The inhibition was more pronounced with plasma from 2K1C, 1K1C and 1K rabbits than from the control animals. Our findings suggest that in the Goldblatt hypertensive model, changes in Na+K+ATPase activity were due to alterations in glomerular filtration rate (GFR).

Animals↗