Biomedical subjects

K Atarashi

Publications and source records attributed to K Atarashi.

62 records · Page 4Linked to original sources

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-PGF 1 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↗

PubMed1983

Effects of high salt intake on hemodynamic responses to isometric exercise in normotensive subjects and in patients with essential hypertension.

Hemodynamic responses to isometric exercise were compared between 9 normotensive subjects (NT) and 16 patients with essential hypertension (EH) before and during high salt intake. The subjects were hospitalized and placed on a diet containing 6g of salt per day. Baseline hemodynamic studies were carried out on supine subjects before and 3 min after isometric exercise (30% of the maximal voluntary handgrip). Plasma concentration of norepinephrine (PNE) was also measured. Brachial arterial pressure was directly recorded and cardiac output (CO) was measured by the dye-dilution technique using a cuvette. The hemodynamic studies were repeated on the 5th day of a high salt diet (16g of salt per day). Retention of sodium was calculated on a daily basis by measuring the actual intake of sodium and 24-hour urinary excretion of sodium. Pressor responses to isometric exercise were significantly greater in the EH than in the NT group. Patterns of hemodynamic responses were different in the 2 groups, i.e., the elevation of arterial pressure was maintained by an increase in CO in the NTs, while it was maintained by increases in CO and total peripheral vascular resistance (TPR) in the EHs. The increase in CO was significantly greater in the NT than in the EH group [15 +/- 3 (mean +/- SE) vs 7 +/- 1%, p less than 0.05]. Although the salt loading reduced heart rate similarly in both groups (-9.0 +/- 2.1, p less than 0.01, in the NTs and -11.9 +/- 2.9%, p less than 0.01, in the EHs), the high salt diet did not significantly alter mean arterial pressure (MAP), CO or TPR in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1983

Role of the aldosterone system in the salt-sensitivity of patients with benign essential hypertension.

This study compared responses of blood pressure, plasma concentrations of norepinephrine (PNE) and aldosterone (PA), plasma renin activity (PRA) and urinary excretion of aldosterone during a 5-day period of high salt intake in 11 untreated patients with essential hypertension and 11 age-matched normotensive control subjects. The hypertensive patients all had blood pressures that had been above 160 systolic and/or 90 mmHg diastolic before admission and had decreased to below 150/90 mmHg with only bed-rest and mild salt restriction (6 Gm per day). Sodium balance was also measured before and after high salt intake (16 Gm per day). The hypertensive patients showed both a significant reduction in blood pressure after hospitalization and a significant blood pressure elevation when salt intake was increased. In contrast, no obvious changes in blood pressure were observed in the normotensive subjects. Sodium retention and decreases in PNE and PRA during the high salt period were similar in both groups. However, the reduction in PA and urinary aldosterone excretion in response to excessive salt intake was less pronounced in the hypertensive patients than in the normotensive subjects. The ratio of percentage changes in PA to percentage changes in PRA after salt loading was significantly lower in the hypertensive patients than in the normotensive subjects. In addition, the changes in PA during salt loading were inversely proportional to changes in blood pressure (r = 0.66, p less than 0.01). Thus, it is suggested that the sensitivity of blood pressure to increased dietary salt intake in hypertensive patients may be related to altered aldosterone dynamics, and that the blunt responses of the PA and urinary excretion of aldosterone can be attributed to reduced sensitivity of the adrenal cortex to changes in circulating angiotensin.

Adolescent↗

PubMed1983

Adrenal renin: a possible regulator of aldosterone production.

We have confirmed the presence of adrenal renin and have shown that the concentration is much higher in the glomerulosa cells. The renin concentration of these cells is influenced by changes in sodium balance and after nephrectomy, while the renin of the fasciculata-medullary tissue is not. There is a positive correlation between adrenal renin and aldosterone concentration. The data suggest that adrenal renin may be a local hormone that plays a role in the regulation of aldosterone production.

Adrenal Glands↗

PubMed1982

Effects of norepinephrine infusion on systemic hemodynamics and plasma 6-keto-prostaglandin F1 alpha in normotensive subjects and patients with essential hypertension.

Altered prostacyclin metabolism may underlie essential hypertension. In this study, responses of plasma 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha: a stable metabolite of prostacyclin) to infused norepinephrine (NE) were compared in 14 normotensive subjects (NT) and 20 untreated patients with essential hypertension (EH). In addition, changes in systemic hemodynamics following NE-infusion were compared with changes in plasma 6-keto-PGF1 alpha. The subjects were all hospitalized and placed on a diet containing 6-8 g of salt per day. Blood pressure was recorded directly through the brachial artery, cardiac output (CO) was determined with the dye-dilution technique using cuvette and total peripheral vascular resistance (TPR) was calculated before and 60 min after NE-infusion. Arterial plasma 6-keto-PGF1 alpha was also determined before and after NE-infusion. The rate of NE-infusion was adjusted to elevate mean arterial pressure (MAP) by 10-15%. Plasma 6-keto-PGF1 alpha was radioimmunoassayed. Elevation of MAP was 13.0 +/- 1.2 (SE) in NTs and 11.7 +/- 1.4% in EHs. After NE-infusion, CO and TPR both significantly increased in NTs, while only CO increased significantly in EHs. Changes in CO and TPR were both significantly different between the two groups (p less than 0.01). Initial plasma 6-keto-PGF1 alpha was reduced in EHs as compared with NTs (174 +/- 15 vs 295 +/- 41 pg/ml, p less than 0.02). However, during NE-infusion, the increase in plasma 6-keto-PGF1 alpha was greater in EHs than in NTs (p less than 0.01). There was a significant negative correlation between changes in TPR and plasma PG (r = -0.36, p less than 0.05). The results indicate that responses of systemic hemodynamics and plasma 6-keto-PGF1 alpha to infused NE are different in the NT and EH groups, and that the absence of changes in TPR in EHs may be related to a marked increase in circulating prostacyclin. These findings, together with the reduced initial levels of plasma 6-keto-PGF1 alpha in EHs, probably represent altered prostacyclin metabolism in essential hypertension.

6-Ketoprostaglandin F1 alpha↗

PubMed1981

[The effects of the angiotensin converting enzyme inhibitor, captopril, on catecholamine concentrations in rat plasma, heart, brain and kidneys (author's transl)].

Two studies were designed to examine the effect of the angiotensin converting enzyme inhibitor, captopril, on the sympathetic nervous system. In the first study, blood pressure (BP), heart rate (HR), and norepinephrine (NE) concentrations in the heart were measured in rats which had been given the agent orally in tap water (0.5 mg/ml) for 2, 9, 19, 29, and 58 days. BP and HR were measured using a tail-microphone to which a tachometer to record HR was connected in the unanesthetized and unrestricted condition. Heart NE was extracted with perchrolic acid and measured with the THI method on a high pressure liquid chromatography. The same study was also done in the control rats. The BP of the rats which had been given captopril for 9 days or more was significantly lower than in the control rats, while HR was not different between the two groups of rats. The ratio of heart weight/body weight was significantly lower in the captopril rats than in the control rats 58 days after the captopril administration. The ratio was significantly correlated with BP in these captopril and control rats (r = 0.59, p less than 0.01). In contrast to the control rats, the NE concentrations in the heart gradually increased in the captopril rats, thus being significantly higher in the latter than in the former after 29 and 58 days of captopril administration (p less than 0.01 for both observations). In addition, the lower the BP was, the higher the NE concentrations in the heart was in all the rats (r = 0.52, p less than 0.001). In the second study, BP, HR, and NE concentrations in plasma, heart, brain and the left kidney were measured in rats which had been on captopril for 2 and 29 days. Renal renin content (RRC) was also measured in the right kidney. In this study, BP and HR were recorded through a carotid catheter which had been inserted 4 hrs previously under light ether anesthesia. BP was significantly lower and NE concentrations in the heart was higher in the captopril rats than in the control rats after 29 days of captopril administration. There was a significant negative correlation between BP and NE concentrations in the heart in the captopril and the control rats (r = -0.88, p less than 0.001). No difference in HR was found between the 2 groups. NE concentrations in plasma, brain and kidney showed no significant differences between the captopril and the control rats in either of the stages of sacrifice. RRC was markedly reduced in the rats with 2 days of captopril, while it increased in the rats with 29 days of captopril. However, the RRC had no definite relationship with the NE concentrations in plasma or that in the kidney. The results show that chronic administration of captopril reduces the heart weight in normotensive rats. This effect points on the one hand to a decrease in "cardiac after-load" and on the other to changes of humoral factors such as plasma angiotensin II induced by captopril...

Angiotensin-Converting Enzyme Inhibitors↗

PubMedDate not supplied

Elevated plasma catecholamines in hypertensives with primary glomerular diseases.

Supine plasma concentration of norepinephrine (PNE), epinephrine (PE), and aldosterone (PA), plasma renin activity (PRA), and blood volume (BV) were measured in 25 normotensive and 11 hypertensive patients with biopsy-proven glomerulonephritis who had serum creatinine concentrations of less than 1.6 mg/dl, and in 20 normotensive control subjects. PNE and PE were measured according to the trihydroxyindol method using high pressure liquid chromatography. Renal clearances of p-aminohippurate (CPAH) and endogenous creatinine (Ccr) were also determined. Age, BV, and 24-hour urinary excretion of sodium were not significantly different in the three groups. Although all the measured variables were comparable between the control subjects and the normotensive nephritic patients, blood pressure, PNE, PE, PRA, and PA were significantly higher and CPAH and Ccr were significantly lower in the hypertensive nephritic patients than in the normotensive nephritic patients or the control subjects. In the pooled nephritic patients, mean blood pressure was significantly correlated with PNE (r = 0.76, p less than 0.001), PE (r = 0.34, p less than 0.05), PRA (r = 0.33, p less than 0.05), PA (r = 0.40, p less than 0.05) and CPAH (r = -0.51, p less than 0.01). Highly significant positive correlation was also observed between PNE and systolic pressure (r = 0.63, p less than 0.001) or diastolic blood pressure (r = 0.78, p less than 0.001). The results suggest that deterioration of renal function is an important factor in the development of hypertension even in non-azotemic patients with glomerulonephritis, and that increased activities of the sympathetic nervous system and the renin-aldosterone system participate, in part, in elevating blood pressure in the hypertensive nephritic patients. Mechanisms involved in the elevation of plasma concentrations of catecholamines and renal effects on the plasma catecholamines remain to be elucidated.

Adult↗

PubMedDate not supplied

Effect of changes in sodium or potassium balance, and nephrectomy, on adrenal renin and aldosterone concentrations.

An active form of renin was confirmed in the adrenal gland of rats. It had a molecular weight of 40,000, generated angiotensin I (AI) from natural renin substrate at pH 7.4, and was found at concentrations 30 to 60 times higher than plasma renin in rats on a normal diet. Changes in sodium diet induced changes in adrenal capsular renin concentration (high Na 2.21 +/- 0.34, normal Na 4.34 +/- 0.53, low Na 13.19 +/- 1.67 ng AI/mg protein/hr). A high potassium diet also increased adrenal capsular renin from 5.27 +/- 0.53 to 39.78 +/- 5.68 ng AI/mg protein/hr, while plasma renin concentration decreased from 7.28 +/- 0.63 in the normal diet to 5.05 +/- 0.60 on the high potassium diet. Neither diet altered the concentration of renin in the fasciculata-medullary portion of the adrenal gland. Nephrectomy markedly increased the renin concentration in the adrenal capsules without any effect on the decapsular cells (20 hours after nephrectomy, 71.5 +/- 10.6 ng AI/mg protein/hr). Sodium loading or dexamethasone treatment prior to nephrectomy blunted the rise in adrenal renin (nephrectomy + dexamethasone = 27.64 +/- 4.33 ng AI/mg protein/hr; nephrectomy + NaCl = 38.70 +/- 5.82 ng AI/mg protein/hr). In all experiments, there was a positive correlation between adrenal renin and adrenal aldosterone concentrations, but the experiments did not rule out the possibility that this positive correlation was due to two independent variables changing in the same direction and not causally related. In conclusion, adrenal renin may be a local hormone, involved in the regulation of aldosterone production.

Adrenal Glands↗