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Biomedical subjects

K Atarashi

Publications and source records attributed to K Atarashi.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effects of treatment with captopril on exercise tolerance and plasma catecholamines in elderly hypertensives.

We examined the effects of antihypertensive therapy with captopril, an angiotensin converting enzyme inhibitor, on exercise tolerance and humoral factors in 19 elderly patients (greater than 60 years old) with essential hypertension. Captopril (37.5-75 mg/day) was administered for 8 weeks. Fourteen of the 19 patients in whom captopril was effective took a treadmill exercise test according to Kattus' protocol. Exercise tolerance was increased in all patients (from 13.1 +/- 1.3 to 16.5 +/- 1.0 min, P less than 0.01). Captopril attenuated the rise in blood pressure during the exercise test but did not affect the heart rate. Resting values of plasma adrenaline decreased by 47% and noradrenaline by 17%, with no significant changes in plasma renin activity (PRA) or aldosterone. The change in mean blood pressure showed an inverse relationship to pretreatment plasma noradrenaline (r = -0.73, P less than 0.01). The results show that captopril is effective in the treatment of hypertensive elderly patients, and suggest that the sympathetic nervous system is involved in the mechanism of the antihypertensive response to captopril therapy.

Aged↗
PubMed1989

Effect of atrial natriuretic factor on renin and aldosterone.

Atrial natriuretic factor (ANF) inhibits basal and stimulated aldosterone production in vitro and in vivo. Infusions of ANF have been reported to inhibit renin release in several species, including humans. A 4-h infusion of ANF into 12 patients with mild hypertension reduced plasma aldosterone at 2 and 4 h, with a rebound increase 2 h after the end of the infusion. Plasma renin activity also showed a mild but significant reduction at 2 h with a rebound increase at 6 h. The effect of ANF on renin release in vitro is controversial. Using a superfusion system of rat renal cortical slices and of dispersed juxtaglomerular (JG) cells, we found that ANF did not affect basal or isoproterenol-stimulated renin release by the kidney slices or dispersed JG cells. These studies suggest that ANF does not inhibit renin release by a direct effect on the JG cells and that the inhibition of renin release found in vivo studies may be mediated through a macula densa mechanism. Since calcium plays an important role in aldosterone secretion, we investigated the effect of ANF on calcium fluxes in rat adrenal glomerulosa cells. ANF did not affect either calcium influx or calcium efflux in rat adrenal glomerulosa cells. These studies suggest that the inhibitory effect of ANF on aldosterone production is distal to the calcium messenger system.

Aldosterone↗
PubMed1988

Endothelin: a new inhibitor of renin release.

Endothelin is a recently-discovered vasoconstrictor peptide which is produced by endothelium and acts on vascular smooth muscle cells. At present its actions on other organs or cells are unknown. We studied the effect of endothelin on renin release in a dynamic superfusion system of dispersed rat juxtaglomerular (JG) cells. Endothelin in concentrations of 10(-11) M or more inhibited renin release dose-dependently and this inhibitory action vanished in the absence of extracellular Ca. It is suggested that endothelin is an inhibitory regulator of renin secretion from JG cells and its action is Ca-dependent.

Animals↗
PubMed1988

The effect of atrial natriuretic peptide on acid-base balance in rats with chronic renal failure.

We explored the effects of 12-hour infusion of atrial natriuretic peptide (alpha-rANP:rat, 1-28) on arterial acid-base balance, using 5/6 nephrectomized rats with chronic renal failure. Before the infusion, nephrectomized rats had a higher mean arterial blood pressure, greater urine volume, and lower creatinine clearance than the normal controls, but they did not show a significant difference in arterial hydrogen ion concentration (pH), plasma bicarbonate concentration (HCO3-), partial pressure of carbon dioxide (PCO2), plasma base excess (BE), or plasma ANP concentration. alpha-rANP infusion produced a continuous blood pressure reduction in both nephrectomized and control rats. Urine volume and urinary sodium and potassium excretion tended to increase at 2-hour infusion, but not at 12-hour infusion. In the controls alpha-rANP significantly increased pH from 7.47 to 7.50, and decreased PCO2 by 14%. In contrast, in nephrectomized rats alpha-rANP significantly decreased pH from 7.48 to 7.44, HCO3- by 13%, and BE from -0.07 to -3.22 meq/l. Rats with chronic renal failure had greater reduction in HCO3- than the controls (p less than 0.05). There was no difference in plasma ANP level between the two groups. Thus, it is indicated that the long-term infusion of alpha-rANP reduces pH in rats with chronic renal failure, thereby adversely affecting the acid-base balance.

Acid-Base Equilibrium↗
PubMed1988

Dopamine and aldosterone in adrenal glomerulosa cells in spontaneously hypertensive rats.

To investigate the possible significance of dopamine in aldosterone production, the adrenal zona glomerulosa was examined for the presence of dopamine and aldosterone in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) aged 10 weeks. Aldosterone and dopamine were measured in the adrenal capsular portions (mostly zona glomerulosa) by radio-immunoassay and high-performance liquid chromatography, respectively. Dopamine was found in the adrenal zona glomerulosa, with a significantly higher level in SHR than in WKY, whereas the content of aldosterone was significantly lower in SHR than in WKY. Furthermore, there was a significant negative relationship between the content of dopamine and that of aldosterone. These results suggest that the inhibitory effect of dopamine on aldosterone production may be mediated within the adrenal zona glomerulosa and that an increased dopamine content in the adrenal zona glomerulosa may contribute to the decreased aldosterone content in SHR.

Adrenal Glands↗
PubMed1988

Effects of intracerebroventricular infusion of aldosterone on blood pressure and sodium and potassium concentrations in cerebral spinal fluid in rats.

The central effects of aldosterone on blood pressure and sodium (Na) and potassium (K) concentrations in cerebral spinal fluid (CSF) were examined by chronic intracerebroventricular (ICV) infusion of aldosterone. The rats were infused for 14 days with either ICV artificial CSF, ICV aldosterone or aldosterone subcutaneously using miniosmotic pumps. ICV aldosterone increased blood pressure and lowered the K concentration in CSF. The Na concentration in CSF tended to increase, although not significantly. No significant changes in concentrations of serum Na and K, plasma renin, aldosterone, norepinephrine or ANP were observed. These results suggest that aldosterone induces blood pressure elevation through a central action, and that a change in Na or K concentration in CSF may be involved.

Aldosterone↗
PubMed1987

Relationship between the renin-aldosterone system and atrial natriuretic polypeptide in rats.

In order to examine the relationship between the renin-aldosterone system and atrial natriuretic polypeptide (ANP), we investigated the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on the plasma concentrations of renin (PRC) and aldosterone (PAC), as well as the effects of captopril pretreatment on the natriuresis and blood pressure reduction induced by alpha-hANP in rats. Although alpha-hANP infused into conscious rats at 0.67 microgram min-1 kg-1 markedly increased the urinary excretion of sodium and decreased mean arterial pressure, its infusion did not change PRC; however, it significantly lowered PAC. Frusemide infusion at 20.8 micrograms min-1 kg-1 induced natriuresis comparable with that of alpha-hANP and it elevated both PRC and PAC, but mean arterial pressure was not altered. Pretreatment of rats with captopril did not have any significant influence on the acute natriuretic and hypotensive effects of alpha-hANP. Although the inhibitory effect of ANP on the renin-aldosterone system may be involved in the chronic modulation of body fluid volume and blood pressure, this effect does not seem to be directly involved in the acute natriuretic and hypotensive effects of the peptide.

Aldosterone↗
PubMed1987

Evidence for lack of a role of cGMP in effect of alpha-hANP on aldosterone inhibition.

To investigate the role of guanosine 3',5'-cyclic monophosphate (cGMP) in the inhibitory effect on aldosterone production of alpha-human atrial natriuretic polypeptide (alpha-hANP) we first compared the effects of the peptide with those of sodium nitroprusside (SNP) on the production of aldosterone and cGMP in dispersed adrenal capsular cells of rats, second, examined the effects of derivatives of cGMP on the production of aldosterone, and, third, studied the influence of potassium on the effects of alpha-hANP on the production of aldosterone and cGMP. alpha-hANP at concentrations of 3 X 10(-8) to 3 X 10(-7) M decreased the production of aldosterone in a dose-dependent manner, while markedly increasing the production of cGMP. On the other hand, although SNP at concentrations of 10(-5) to 10(-3) M increased the production of cGMP in a dose-dependent manner, it caused no significant changes in the production of aldosterone. Neither dibutyryl cGMP nor 8-bromo-cGMP affected the production of aldosterone in the adrenal cells. Although the aldosterone-inhibitory effect of alpha-hANP was lost in the potassium-free medium, the cGMP-stimulatory effect of the peptide was not altered by adding potassium to the incubation medium at concentrations of 0-5 meq/l. These results suggest that cGMP plays a minor role in the inhibitory effect of alpha-hANP on the production of aldosterone and that the production of cGMP stimulated by the peptide is not directly involved in the decrease in aldosterone production in adrenal capsular cells of rats.

Aldosterone↗
PubMed1986

Blood pressure, renal and endocrine responses to alpha-human atrial natriuretic polypeptide in healthy volunteers.

Intravenous infusion of graded doses of alpha-human atrial natriuretic polypeptide (alpha-hANP) resulted in a dose-dependent decrease in blood pressure and an increase in heart rate in 11 healthy male volunteers. However, there were no significant changes in urine output or in the urinary excretion rate of sodium. Glomerular filtration rate did not change, while renal blood flow decreased, leading to significant increases in filtration fraction and renal vascular resistance. Although plasma renin activity (PRA) and plasma concentration of norepinephrine (PNE) increased during infusion of alpha-hANP (both p less than 0.001), plasma concentrations of aldosterone (PA) and cortisol (PC) decreased (both p less than 0.001). Plasma concentration of arginine vasopressin (PAVP) did not change during the infusion, but greatly increased after cessation of the infusion. The hematocrit increased slightly, but significantly, during the infusion. These results show that, although alpha-hANP has a potent hypotensive action and inhibits the secretion of aldosterone, cortisol, and probably arginine vasopressin, it does not dilate renal vessels in normotensive persons, and likely increases vascular permeability. The lack of consistent diuretic and natriuretic responses to alpha-hANP may be related to the predominance of the hypotensive effect over the renal effects of the peptide in normotensive persons, or a diurnal change may have served to obscure such a response.

Adult↗
PubMed1985

Effect of indomethacin on the adrenal renin response to nephrectomy in the rat.

The role of prostaglandins in the control of adrenal renin in vivo was evaluated in nephrectomized rats. Nephrectomy increased adrenal renin from 13.2 +/- 1.37 ng angiotensin I/mg protein/hr to 166.5 +/- 17.3 ng angiotensin I/mg protein/hr. Indomethacin treatment significantly suppressed the adrenal renin response to nephrectomy. (47.8 +/- 5.22 ng angiotensin I/mg protein/hr). Adrenal aldosterone was also suppressed by indomethacin. Adrenal prostaglandin E2 increased after nephrectomy and decreased after indomethacin. Plasma corticosterone and serum potassium did not change after indomethacin. These data indicate that inhibition of prostaglandin synthesis by indomethacin partially blocks the adrenal renin response to nephrectomy, suggesting that prostaglandins may play a role in the adrenal response to nephrectomy.

Adrenal Glands↗
PubMed1985

Effect of atrial peptides on aldosterone production.

This study examines the effects of the synthetic atrial peptides (atriopeptin I, II, and III) on aldosterone and corticosterone production by rat adrenal cell suspensions. Furthermore, we studied the effect of atriopeptin II infusion on the plasma aldosterone response to angiotensin II in the rat in vivo. Atriopeptin I, II, and III decreased aldosterone release from zona glomerulosa cells in a dose-dependent fashion. 10 pM atriopeptin II inhibited basal aldosterone release significantly (P less than 0.01), and 10 nM atriopeptin II or III lowered it by 79%. Atriopeptin II decreased the sensitivity of the glomerulosa cells to adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin II had no effect on basal or ACTH-stimulated corticosterone release by fasciculata-medullary cells. In vivo infusions of angiotensin II with or without simultaneous infusions of atriopeptin II showed that atriopeptin II significantly inhibited the aldosterone response to angiotensin II. This inhibition by atriopeptin II was independent of any effect on plasma renin activity, serum potassium, or ACTH. These data raise the possibility that the atrial natriuretic peptides may affect sodium excretion by the kidney, not only directly, but also indirectly through the inhibition of aldosterone production.

Adrenal Glands↗
PubMed1985

An immunohistochemical study of renal vascular lesions in hypertensive patients.

This study examined the immunohistochemical findings in renal arterioles from biopsy specimens, and related the findings to those of light and electron microscopy. The renal biopsy specimens were obtained from 57 normotensive patients with primary glomerular diseases or idiopathic hematuria, 14 hypertensive patients with associated primary glomerular diseases, 4 patients with essential hypertension and 1 with primary aldosteronism. The tissue slices for the immunohistochemical study were processed with FITC-labelled rabbit antihuman immunoglobulin antisera. Deposits of IgM were detected on the renal arterioles in 16 of the hypertensive patients (84%), but in only 7 of the normotensive patients (12%). The difference in incidence was significant (p less than 0.005). C3 was almost always deposited in the renal arterioles regardless of whether the patient was hypertensive or normotensive. IgG, IgA or fibrinogen were demonstrated only in a few cases, and albumin in no cases. When sections stained with horseradish peroxidase-conjugated anti-IgM antibody were compared under a light microscope with the adjacent PAS-stained sections, it was demonstrated that IgM was deposited only in the portions of the arteriolar walls which showed hyalinotic changes. Electron microscopic examination demonstrated that electron-dense deposits in the subendothelial or intercellular spaces of arteriolar walls were more frequent in the hypertensive patients (11 of 14 cases, 79%) than in the normotensive patients (5 of 18 cases, 28%, p less than 0.05). The deposits appeared to be similar to those which are often found in the glomeruli of patients with glomerulonephritis and which are considered to be immune complexes. These findings suggest that some immunologic mechanism mediated by IgM antibody might be a factor in the development of hypertensive vascular lesions.

Adolescent↗
PubMed1984

Inhibition of aldosterone production by an atrial extract.

Crude extracts of rat atria reduced the basal amount of aldosterone released from rat zona glomerulosa cells and partially inhibited aldosterone stimulation by adrenocorticotropic hormone and angiotensin II. The destruction of this activity by trypsin suggests that the active factor is a peptide, possibly atrial natriuretic factor. These data suggest that atrial natriuretic factor affects sodium excretion by the kidneys both directly and through the inhibition of aldosterone production.

Adrenocorticotropic Hormone↗
PubMed1984

Inhibition of aldosterone production by atrial natriuretic factor.

Extracts of rat atrial muscle lowered basal aldosterone release from rat adrenal glomerulosa cell suspensions, and partially inhibited the stimulation of aldosterone release by adrenocorticotropic hormone (ACTH) and angiotensin II. Atriopeptin I, an atrial peptide with natriuretic, diuretic and smooth muscle relaxant activities, significantly decreased basal aldosterone release at 1 pM concentrations. Also, atriopeptin I decreased the sensitivity of the glomerulosa cells to adrenocorticotropin and angiotensin II. These data suggest that peptides contained in mammalian atria affect sodium excretion not only by a direct effect on the kidney, but also indirectly through inhibition of aldosterone production.

Adrenal Glands↗
PubMed1983

Plasma levels of 6-keto-prostaglandin F1 alpha in normotensive subjects and patients with essential hypertension.

To assess the pathophysiological role of prostacyclin in essential hypertension, plasma levels of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable, nonenzymatic metabolite of prostacyclin, were assayed in 25 patients with essential hypertension and 25 age-matched normotensive subjects. Supine plasma levels of 6-keto-PGF1 alpha were 270 +/- 14 (SE) in normotensive subjects and 203 +/- 14 pg/ml in the patients with essential hypertension. The difference was statistically significant (p less than 0.001). There was a significant negative correlation between plasma levels of 6-keto-PGF1 alpha and systolic blood pressure (r = 0.44, P less than 0.002), diastolic blood pressure (r = 0.55, p less than 0.001), or mean blood pressure (r = 0.56, p less than 0.001) in the pooled subjects. The same relationship was found in the hypertensive patients. There was no definite relationship either between plasma levels of 6-keto-PGF1 alpha and plasma renin activity (PRA) in the supine position, or between changes in plasma levels of 6-keto-PGF1 alpha and changes in PRA after 60 min of upright posture. These results indicate that circulating prostacyclin is reduced in patients with essential hypertension as compared to normotensive subjects. This reduction of plasma prostacyclin may participate, in part, in the maintenance of blood pressure elevation in patients with essential hypertension. It is also suggested that upright posture is not sufficient to elevate circulating prostacyclin.

6-Ketoprostaglandin F1 alpha↗