Biomedical subjects

M Ideishi

Publications and source records attributed to M Ideishi.

At least 37 records · Page 2Linked to original sources

PubMed1998

Mechanism of antiarrhythmic effects of class Ic drugs in paroxysmal atrial fibrillation in man.

While class Ic antiarrhythmic drugs are effective in treating patients with atrial fibrillation, their mechanism of action is poorly understood. We performed electrophysiological studies before and after their administration to 22 patients with paroxysmal atrial fibrillation. Atrial refractoriness, maximal interatrial conduction delay and the wavelength index were measured at two basic cycle lengths (600 or 400 ms). Both drugs studied increased atrial refractoriness and wavelength index. Flecainide reduced the maximal interatrial conduction delay, but pilsicainide did not. Each drug increased the wavelength index in a tachycardia-dependent manner. Class Ic drugs may reduce atrial vulnerability by increasing the wavelength of the reentrant circuit during periods of rapid heart rate.

Administration, Oral↗

PubMed1998

Differences in tissue angiotensin II-forming pathways by species and organs in vitro.

Angiotensin (Ang) II plays an important role in cardiovascular homeostasis, not only in the systemic circulation but also at the tissue level, and is involved in the remodeling of the heart and vasculature under pathological conditions. Although alternative Ang II-forming pathways are known to exist in various tissues, the details of such pathways remain unclear. The aim of this study was to examine tissue Ang II-forming activities and to identify the responsible enzyme in several organs (lung, heart, and aorta) in various species (human, hamster, rat, rabbit, dog, pig, and marmoset). Among the organs examined, the lung contained the highest Ang II-forming activity. The responsible enzyme for pulmonary Ang II formation was angiotensin I-converting enzyme (ACE) in all of the species except the human lung, in which a chymaselike enzyme was dominant. In the heart, the highest total Ang II-forming activity was observed in humans, and a chymaselike enzyme was dominant in all of the species except rabbit and pig. Aorta exhibited a relatively high total Ang II-forming activity, with a predominance of chymaselike activity in all of the species except rabbit and pig, in which ACE was dominant. Our results indicate that there were remarkable differences in Ang II-forming pathways among the species and organs we examined. To study the pathophysiological roles of ACE-independent Ang II formation, one should choose species and/or organs that have Ang II-forming pathways similar to those in humans.

Aged↗

PubMed1997

Amlodipine lowers blood pressure without increasing sympathetic activity or activating the renin-angiotensin system in patients with essential hypertension.

OBJECTIVE: Recent clinical studies suggest that the reflex increase in sympathetic nervous activity accompanying a reduction in blood pressure may contribute to the untoward effects of dihydropyridine calcium antagonists. The aim of this study was to examine whether plasma noradrenaline levels and renin activity are increased with the reduction of blood pressure during the initial phase of administration of the long-acting dihydropyridine calcium antagonist amlodipine. METHODS: The effects of amlodipine on ambulatory blood pressure and on diurnal variations in plasma noradrenaline and renin activity were examined 1, 4, and 7 days after the start of amlodipine administration in eight inpatients with essential hypertension. RESULTS: The 24-h mean systolic and diastolic blood pressure on day 7 was significantly lower than it was 1 day before the start of treatment. There was no change in the mean heart rate. The mean trough to peak ratios of systolic and diastolic blood pressure of seven patients were 61% and 71%, respectively. Diurnal patterns of plasma noradrenaline levels and renin activity 1, 4, and 7 days after the start of amlodipine administration were unchanged. CONCLUSION: The antihypertensive effects of amlodipine were of slow onset and long duration and were not accompanied by an increase in sympathetic activity or activation of the renin-angiotensin system.

Aged↗

PubMed1997

Purification and characterization of a kinin- and angiotensin II-forming enzyme in the dog heart.

OBJECTIVE: To purify and characterize a kinin-forming enzyme in the dog heart and to examine the ability of this enzyme to generate angiotensin (Ang) II from Ang I. METHODS: The enzyme was isolated from heart homogenate using a diethylaminoethyl-Sepharose column, an aprotinin affinity column and a wheat germ lectin-Sepharose 6MB column. Kininogenase activity was assessed with a kinin radioimmunoassay after samples had been incubated with bovine low-molecular-mass kininogen at 37 degrees C for 1 h. Ang I-converting activity was assessed by the quantitation of Ang II formed by incubation of the sample with Ang I at 37 degrees C for 3 h, using high performance liquid chromatography. The enzyme was subjected to 12.5% sodium dodecyl sulphate-polyacrylamide gel electrophoresis, stained by Coomassie brilliant blue and transferred electrically to a membrane with glycoprotein staining. RESULTS: The purified enzyme is a glycoprotein with an apparent relative molecular mass of 65 kDa by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. Its kininogenase activity was approximately 20 micrograms bradykinin/h per mg protein at an optimal pH of 8.0. The enzyme also converted Ang I to Ang II at an optimal pH of 6.5. Its specific activity was approximately 2 micrograms Ang II/h per mg protein. Both activities were inhibited by aprotinin, a tissue kallikrein inhibitor. Western blot analysis using polyclonal antibody against this enzyme demonstrated that this enzyme exists both in the myocardium and in the coronary artery. CONCLUSIONS: The present study showed that the kinin-forming enzyme in the dog heart is a kallikrein-like enzyme that is different from cathepsin D, cathepsin G and chymase. It is also able to Ang I to Ang II. This enzyme might play a role in regulating myocardial perfusion, mainly by generating kinins and in part by forming Ang II.

Angiotensin II↗

PubMed1996

Molecular cloning of a novel rat salt-tolerant protein by functional complementation in yeast.

To elucidate the genetic basis of salt-sensitivity in mammalian hypertension, we isolated six rat complementary DNAs by functional complementation in yeast. These genes were able to substitute for the salt-tolerant activity of HALI which confers salt tolerance by modulating the cation transport system in yeast. We identified these genes as beta-globin, lambda-crystallin, androgen-regulated protein, mitochondrial cytochrome b, a homologue of infant brain cDNA, and a novel gene, called salt-tolerant protein (STP). STP contains 1964 bp nucleotides and an open reading frame which encodes 496 amino acid residues. Northern blot analysis showed that STP mRNA is expressed in various rat tissues.

ATPases Associated with Diverse Cellular Activitie↗

PubMed1996

Role of endogenous ouabain-like substance during graded exercise in hypertensive individuals.

Changes in plasma endogenous ouabain-like substance (EOLS) and plasma noradrenaline, along with changes in blood pressure (BP), heart rate, and blood lactate concentration, were investigated in hypertensive individuals during strenuous exercise testing. Thirteen (4 men and 9 women) middle-aged (34-63 years, mean 50 +/- 2 years) patients with mild essential hypertension underwent graded multistage submaximal exercise testing on a cycle ergometer. The workload in each exercise test was increased depending on the individual's physical fitness until they reached 75-80% of the predicted age-adjusted maximal heart rate prescribed by the American College of Sports Medicine. Systolic (S) BP rose by 67 +/- 9 mm Hg (P < 0.001), mean (M) BP by 28 +/- 3 mm Hg (P < 0.001), diastolic (D) BP by 9 +/- 2 mm Hg (P < 0.005) and heart rate by 79 +/- 6 beats/min (P < 0.001) after submaximal graded exercise. The blood lactate concentration and plasma noradrenaline increased significantly (+3.40 +/- 0.34 mmol/l and +895 +/- 94 pg/ml respectively, P < 0.001). Although the change in EOLS was not significant, it showed a strong positive correlation with the change in plasma noradrenaline (R = 0.760, P < 0.001). These results suggest that EOLS may participate in modifying sympathetic vasoconstriction during submaximal graded exercise.

Adult↗

PubMed1995

Human urinary kallikrein can generate angiotensin II from homologous renin substrates.

We previously proposed the "kinin-tensin system," a unique vasoregulatory system that can produce both angiotensin II and kinins. To verify whether tissue kallikrein is a part of this system in humans, we examined the ability of human urinary kallikrein (HUK) to generate angiotensin (ANG) II directly from homologous renin substrates such as purified human angiotensinogen (AOGEN) and authentic human tridecapeptide renin substrate (13 RS). HUK released ANG II not only from ANG I but also directly from both AOGEN and 13RS at an optimum pH of 7.0. The amount of generated ANG II from 7.5 nmol of each of the three substrates at pH 7.0 was as follows: ANG I, 292.7 +/- 67.2; 13 RS, 1951.7 +/- 239.6; AOGEN, 2.2 +/- 0.3 (pmol/3h, n = 3 mean +/- SE). HUK cleaved Phe-His and His-Leu bonds in 13 RS, and Tyr-Ile and Phe-His bonds in ANG I. These results suggest that HUK is a part of the "kinintensin system", i.e., HUK can not only release kinins, but can also generate ANG II mainly through ANG I conversion and from AOGEN, the latter being a minor source of ANG II. Furthermore, HUK may play a role in regulating vascular tone under certain conditions in vivo.

Angiotensin I↗

PubMed1995

Plasma free and sulfoconjugated dopamine before and after a half-marathon.

To elucidate whether increased plasma levels of free dopamine (F-DA) after exercise are due to deconjugation of sulfoconjugated (S-) DA in plasma, we compared the changes in plasma F- and S- DA, as well as changes in both the S- and F- forms of epinephrine (E) and norepinephrine (NE), after running a half-marathon. Free catecholamines (F-CAs) were measured by automated high-performance liquid chromatography (HPLC). Total (F+S) CAs were determined using an efficient deconjugation method as follows; 1200 microliters plasma was incubated with 152 mU arylsulfatase (AS) for 30 min at pH 7.6. The plasma levels of F-CA (pg/ml) (mean +/- SEM) all increased significantly (p < 0.01) after the half-marathon; i.e., F-DA increased from 13.3 +/- 5.7 to 176.3 +/- 32.2; F-E from 58.0 +/- 12.3 to 764.3 +/- 136.4; F-NE from 246.6 +/- 15.2 to 3082.0 +/- 690.3. OF S-CAs, S-E (from 127.8 +/- 26.0 to 1218.2 +/- 190.8) and S-NE (from 717.1 +/- 61.6 to 5586.9 +/- 761.9) also increased, but, in contrast, among the S-CAs, only the increase in S-DA (from 5324.9 +/- 1967.3 to 7359.6 +/- 1627.9) was not statistically significant. Sulfoconjugation may play an important role in inactivating F-DA as well as F-NE and -E, that are released into plasma in response to vigorous exercise. Thus, plasma F-DA is unlikely to be derived through deconjugation of plasma S-DA.

Adult↗

PubMed1994

Angiotensin II formation by an alternative pathway during exercise in humans.

OBJECTIVE: We postulated a 'kinin-tensin system' in which angiotensin II (Ang II) is cleaved by one or more serine protease independent of renin or angiotensin converting enzyme (ACE). The aim was to determine whether this alternative Ang II-forming pathway by serine proteases participates in the rise in plasma levels of Ang II during exercise in humans. DESIGN AND METHODS: The study consisted of two double-blind crossover experiments. in experiment 1 six healthy volunteers who had been taking either placebo (group P) or the ACE inhibitor captopril (150 mg/day for 3 days; group C) performed a cycle ergometer graded exercise test at four different exercise intensities: stage 1, half of the intensity at the blood lactate threshold (WLT); stage 2, the intensity at WLT; stage 3, the intensity at 4 mmol/l blood lactate; and stage 4, an intensity between stage 3 and maximum intensity. In experiment 2 the same volunteers took captopril (150 mg/day for 3 days) and performed exercise at an intensity corresponding to 90% of the 4 mmol/l blood lactate intensity for 30 min during intravenous drip injection of a serine protease inhibitor, nafamostat [NAF; 0.2 mg/kg per h; NAF(+) group] or saline [NAF(-) group]. RESULTS: In experiment 1 plasma Ang II levels increased from at rest to after exercise in both groups P and C. Although there was a significant treatment effect, captopril did not significantly alter the exercise-induced changes in Ang II level. In experiment 2 the increase in Ang II level after 30 min exercise in the NAF(+) group was significantly lower than in the NAF(-) group. CONCLUSIONS: These results suggest the presence of an alternative Ang II-forming pathway independent of ACE, and that one or more NAF-sensitive serine protease is responsible, at least partly, for generating Ang II during exercise.

Adult↗

PubMed1994

Comparative effects of an angiotensin-converting enzyme inhibitor and an angiotensin II antagonist in Dahl rats.

The antihypertensive, cardioprotective, and renoprotective effects of a nonpeptide angiotensin II antagonist (AIIA, CV-11974) and an angiotensin-converting enzyme inhibitor (CEI, captopril) were compared in Dahl salt-sensitive rats. Six-week-old male rats received a high-salt diet (4% NaCl) and were divided into control, CEI, and AIIA groups. The CEI group received captopril (15 mg/kg/day) and the AIIA group received CV-11974 (0.72 mg/kg/day), an active metabolite of the AIIA TCV-116, for 4 weeks by continuous subcutaneous infusion. After 4 weeks, systolic blood pressure (SBP) was significantly lower in the treatment groups than in the control group. The heart weight/body weight ratio and urinary protein excretion were reduced in the treatment groups, and renal damage (glomerular sclerosis score) was reduced by approximately 50%. CV-11974 and captopril were comparable in reducing BP, cardiac hypertrophy, and renal damage, suggesting that the renin-angiotensin (R-A) system is involved in elevating BP and promoting cardiovascular damage, despite suppression of the R-A system in this model. The antihypertensive effect of CEI may be due primarily to inhibition of the action of angiotensin II, while other effects, e.g., potentiation of the kinin system, may be less important.

Angiotensin Receptor Antagonists↗

PubMed1994

Taurine amplifies renal kallikrein and prevents salt-induced hypertension in Dahl rats.

OBJECTIVE: To determine whether taurine reduces blood pressure by stimulating the renal kallikrein-kinin system. METHODS: The effects of taurine on blood pressure, urinary kallikrein activity and renal kallikrein gene expression were investigated in Dahl salt-sensitive (Dahl-S) rats. The specificity of the action of taurine was verified by comparison with the action of beta-alanine, a carboxylic analogue of taurine. The effect of co-administration of the specific bradykinin B2 receptor antagonist Hoe 140 was also examined. RESULTS: Administration of taurine (3% in drinking water) for 4 weeks retarded the development of salt (4% sodium chloride diet)-induced hypertension. Systolic blood pressure at the end of the experiment was significantly higher in control rats than in taurine-treated rats. Urinary sodium excretion was not decreased by the reduction in blood pressure. The heart weight:body weight ratio was significantly lower, and urinary volume and kallikrein excretion were significantly higher, in taurine-treated rats. Renal kallikrein gene expression at weeks 1 and 4 was higher in taurine-treated rats. Systolic blood pressure 3 and 4 weeks after the administration of beta-alanine was slightly, but not significantly, lower than that of untreated rats on a high-salt diet, and was accompanied by a significantly lower body weight. Urinary kallikrein excretion decreased with a high-salt diet regardless of beta-alanine administration. Continuous systemic administration of Hoe 140 did not cause any significant alteration in blood pressure in Dahl-S rats that received taurine with a high-salt diet. Taurine also showed a renoprotective effect, as judged by a reduction in proteinuria. CONCLUSION: These results suggest that taurine is an effective antihypertensive agent for salt-induced hypertension. Although taurine activated renal kallikrein, further studies are required to confirm the participation of activated kallikrein in the antihypertensive, cardioprotective and renoprotective effects of taurine.

Animals↗

PubMed1994

Urinary kallikrein activity is increased during the first few weeks of exercise training in essential hypertension.

OBJECTIVE: To determine whether the renal kallikrein-kinin and dopamine systems participate in lowering blood pressure during mild exercise in hypertensives. DESIGN: After a general clinical observation period of 4 weeks, 27 essential hypertensives were divided into two groups. The exercise group underwent blood lactate threshold exercise, using a cycle ergometer for 60 min three times a week for 10 weeks. The non-exercise group was observed at the outpatient clinic. Blood pressure and humoral parameters were measured at weeks 0, 1, 2, 4 and 10 in both groups. METHODS: Blood pressure was measured indirectly with an automatic blood pressure recorder. Twenty-four-hour urinary kallikrein activity (by kininogenase assay), total or free dopamine and total noradrenaline (by high-performance liquid chromatography) were also measured. RESULTS: In the non-exercise group blood pressure and humoral parameters did not change. In the exercise group the change in resting blood pressure between weeks 0 and 10 was statistically significant. The change in 24-h urinary kallikrein activity of the exercise group was significantly greater than that of the non-exercise group between weeks 0 and 1 and weeks 0 and 2. Moreover, the change in systolic blood pressure (SBP) between weeks 0 and 2 was negatively correlated with the change in urinary kallikrein activity between weeks 0 and 2, the change in total dopamine between weeks 0 and 2 was negatively correlated with the change in diastolic blood pressure in the same period, and the change in SBP between weeks 0 and 10 was positively correlated with the change in total noradrenaline in the same period in the exercise group. Subjects with a relatively high baseline urinary kallikrein activity had a significantly greater change in SBP between weeks 0 and 10 than subjects with a relatively low baseline activity. CONCLUSIONS: The renal kallikrein-kinin and dopamine systems may participate in lowering blood pressure during the first few weeks of exercise training. The subsequent reduction of sympathetic activity may be involved in maintaining the lowered blood pressure. Mild exercise is more effective in reducing blood pressure in hypertensives who have a relatively high basal renal kallikrein-kinin system activity.

Adult↗

PubMed1993

Beneficial effects of a serine protease inhibitor in peripheral vascular disease.

Kallikrein, a serine protease known to generate bradykinin (a vasodilating peptide) in alkaline conditions, also generates angiotensin II (a vasoconstricting peptide) in weak acidic conditions. Based on this previous observation, the present study was performed to determine whether ischemic muscle tissue, in which the regional pH must decrease, produces angiotensin II by kallikrein or a similar enzyme, and whether nafamostat (NAF), a serine protease inhibitor, improves local hemodynamics under ischemic conditions caused by exercise in patients with ischemic peripheral vascular disease. NAF was administered intravenously to 20 patients with peripheral vascular disease. Lower-limb thermograms and blood flow were measured before and after exercise. Femoral venous blood of affected limbs was obtained to measure viscosity and humoral variables (i.e., pH, lactate, angiotensin II and bradykinin). Walking distance and subjective symptoms were also recorded. As a control, the same patients repeated this test with saline infusion on a separate day. NAF significantly increased maximal walking distance, improved subjective symptoms during exercise, and attenuated exercise-induced venous lactate and blood viscosity increases, and pH reduction. The blood viscosity increase correlated with the lactate increase. Pretreatment with NAF also resulted in a higher lower-limb skin temperature, and a greater increase of blood flow in the lower limbs after exercise than did pretreatment with saline. The results suggest that kallikrein-like serine protease may exacerbate ischemic symptoms. Changes in plasma bradykinin and angiotensin II in the femoral vein were not detectable, probably because of the lower levels of these peptides in the peripheral circulation.

Aged↗

PubMed1993

Role of locally formed angiotensin II and bradykinin in the reduction of myocardial infarct size in dogs.

OBJECTIVE: The aim was to investigate the role of local formation of angiotensin II and bradykinin in the reduction of myocardial infarct size. METHODS: Bilaterally nephrectomised male mongrel dogs were used. Effects were compared of pretreatment with three inhibitors of angiotensin II forming enzyme-captopril (an angiotensin converting enzyme inhibitor), nafamostat (a serine protease inhibitor), and chymostatin (a cysteine protease inhibitor)--on left anterior descending coronary artery occlusion. Haemodynamic variables were monitored and blood was collected from the anterior interventricular vein and the aorta. Angiotensin I, angiotensin II, and bradykinin were measured by radioimmunoassay. After 90 min of occlusion, infarct sizes were determined by a macroscopic enzyme technique. RESULTS: Angiotensin II release into the anterior interventricular vein increased from 0.03(SEM 1.19) pg.min-1 (before coronary occlusion) to 4.64(1.37) pg.min-1 (n = 14, p < 0.05), while angiotensin I release and plasma renin activity remained unchanged. The increase in angiotensin II release was inhibited by nafamostat and chymostatin, but not by captopril. Bradykinin release increased from -3.18(2.72) (before coronary occlusion) to 34.7(12.3) pg.min-1 (n = 14 p < 0.05) by 30 min after occlusion. This increase was augmented by captopril, from 4.10(2.86) before occlusion to 97.8(39.6) pg.min-1 at 5 min after occlusion (n = 12, p < 0.05), but not by nafamostat or chymostatin. Infarct size was smaller (p < 0.05) in the captopril group than in the control group. CONCLUSIONS: Angiotensin II is locally produced in the ischaemic heart by both serine protease(s) and chymostatin inhibitable protease(s), but not by angiotensin converting enzyme. From the reduction in myocardial infarct size produced by angiotensin converting enzyme inhibition, it seems that bradykinin accumulation may play a more important role than the suppression of angiotensin II formation.

Angiotensin II↗

PubMed1993

Crossover comparison between the depressor effects of low and high work-rate exercise in mild hypertension.

1. The relationship between work-rate and the antihypertensive effect of exercise in hypertensives, and the mechanism of that effect, were investigated by a crossover clinical trial. 2. Ten mild hypertensives were randomly divided into two groups. One group performed low work-rate exercise (LWE) on a cycle ergometer for 10 weeks (blood lactate threshold; approximately 50% of maximum oxygen consumption [Vo2max]). After a 10 week interval without exercise training, these subjects were then switched to a high work-rate exercise (HWE) regimen (4 mmol/L of blood lactate; approximately 75% of Vo2max) for another 10 weeks. In the other group, the order of exercise training was reversed. Since two patients withdrew from the protocol during HWE periods, statistical analysis was performed on the data from the remaining eight patients. There were no order effects observed in any of the data from the two groups. 3. During both LWE and HWE, resting blood pressure (BP) fell significantly after the initiation of exercise therapy (P < 0.05). Furthermore, the overall effects of 10 weeks of LWE and HWE on BP were not significantly different. 4. The work-rate at the lactate threshold, which reflects physical fitness, had increased significantly by 16 W (P < 0.01) after the LWE period and by 11 W (P < 0.01) after the HWE. 5. During the LWE period, changes in haemodynamic and humoral variables were not significant, except for a reduction in plasma norepinephrine at week 10 (P < 0.05). In the HWE period, changes in haemodynamic and humoral variables were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

[A case of idiopathic hyperaldosteronism diagnosed by adrenal imaging].

We report a case of idiopathic hyperaldosteronism (IHA) which was differentiated from an aldosterone producing adenoma by the adrenal imaging techniques with computed tomography (CT) and scintigraphy. In this patient, the high basal aldosterone level with the suppressed plasma renin activity typically indicated the diagnosis of primary aldosteronism. However, the differentiation from an aldosterone producing adenoma by responses of plasma aldosterone levels to upright posture, captopril or adrenocorticotropic hormone (ACTH) administration was not definitive. Abdominal CT revealed bilateral adrenal swelling. Adrenal scintillation scanning with 131I-iodocholesterol showed bilateral uptake even after the administration of dexamethasone. Blood sampling from the right adrenal vein was unsuccessful. Blood pressure and serum potassium levels remained unchanged during dexamethasone administration (2 mg/day) over ten days. After the administration of spironolactone and nisoldipine blood pressure and serum potassium levels were normalized. Adrenal imaging is considered to be very useful for the diagnosis of IHA.

Adrenal Glands↗

PubMed1993

Angiotensin II forming activity of vascular endothelial and smooth muscle cells.

To clarify the role of vascular endothelial cells (VEC) and smooth muscle cells (VSMC) in the generation of angiotensin (Ang) II, we measured the Ang II forming activity of these cells in culture using synthetic Ang I and tridecapeptide renin substrate (13RS). Angiotensin converting enzyme (ACE) activity was demonstrated in both types of cells, and the Ang I converting activity was highly sensitive to an ACE inhibitor. Both VEC and VSMC were able to generate Ang II from 13RS independently of ACE and renin. The activity was partially inhibited by chymostatin. It is suggested that Ang I could be converted to Ang II not only by VEC but also by VSMC. Both VEC and VSMC possess alternate Ang II forming pathways independent of ACE and renin.

Angiotensin II↗

PubMed1992

Active and inactive renin after exercise.

The effects of graded exercise on plasma concentrations of active and inactive renin were studied in seven healthy men. Exercise was performed on a cycle ergometer at four different exercise intensities (corresponding to 30%, 50%, 80% and 87% of VO2max) for 10 min each. Concentrations of active renin and total renin after activation by trypsin were measured by direct immunoradiometric assay. Non-trypsin-activated renin concentration (inactive) was obtained by subtraction. Active renin concentrations at 30%, 50%, 80% and 87% of VO2max were 1.2, 1.9, 3.1 and 4.6 times higher than the control concentration, respectively. Similar increases in plasma renin concentration, determined by conventional enzymatic assay, were observed at every stage. In contrast, changes in inactive renin concentration were not significant at any stage. Significant increases in noradrenaline concentration were found at every exercise stage, but adrenaline, aldosterone and lactate concentrations were significantly elevated only after exercise at 50%, 80% and 87% of VO2max. The similarity between the changes in concentration of active renin and noradrenaline would suggest that sympathetic nerve activity may have been responsible either for the release of active renin or for the conversion of inactive renin to its active form in the kidney.

Adult↗