Search PubMed⌕ Search

Biomedical subjects

K Yasunari

Publications and source records attributed to K Yasunari.

120 records · Page 7Linked to original sources
PubMed1987

Central alpha 2-adrenergic stimulation increases neurointermediate lobe immunoreactive beta-endorphin in spontaneously hypertensive rats.

A possible influence of the central alpha 2-adrenergic system on beta-endorphin was examined in rat anterior pituitary, neurointermediate lobe, and plasma. The concentration of beta-endorphin in anterior pituitary, neurointermediate lobe, and plasma was determined by radioimmunoassay 15 minutes after subcutaneous injection of clonidine in 14-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Clonidine reduced the concentration of the plasma beta-endorphinlike immunoreactivity in SHR and to a lesser extent in WKY. No significant changes in the concentration of beta-endorphinlike immunoreactivity were observed in anterior pituitary. Clonidine increased the concentration of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR in a dose-related manner but did not affect the concentration in WKY. Administration of yohimbine (1 mg/kg) completely blocked the clonidine-induced increase of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR, while prazosin (1 mg/kg) had no effect. These data suggest that the central alpha 2-adrenergic activation increases the neurointermediate lobe concentration of beta-endorphinlike immunoreactivity in SHR by suppressing beta-endorphin release from the neurointermediate lobe into the circulation.

Animals↗
PubMed1987

Effect of chronic treatment with angiotensin I converting enzyme inhibitors on circulating atrial natriuretic polypeptide in spontaneously hypertensive rats.

We have recently shown that circulating atrial natriuretic polypeptide (ANP) in adult spontaneously hypertensive rats (SHR) is higher than that in age-matched Wistar-Kyoto rats (WKY). The present experiment was designed to examine the possible effects of chronic treatment with angiotensin I converting enzyme inhibitors (ACEI) on plasma ANP levels in SHR. Captopril and enalapril lowered blood pressure and reduced relative ventricular weight in SHR but not to the level of WKY. Plasma ANP levels were decreased by captopril and enalapril compared with untreated SHR. These results suggest that the ANP release may be suppressed in ACEI-treated SHR compared with untreated SHR. We speculate that a reduction of cardiac overload by ACEI may in part explain the decline of circulating ANP.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Cytoplasmic free [Ca2+] is not increased in the platelets of deoxycorticosterone-salt and spontaneously hypertensive rats.

The cytoplasmic free calcium concentration ([Ca2+]i) in the platelets of spontaneously hypertensive rats (SHR), Wistar-Kyoto rats (WKY), deoxycorticosterone-salt hypertensive rats (DOC) and normotensive Sprague-Dawley rats (SD) was measured with the fluorescent dye, quin-2-tetra-acetoxymethyl ester. No significant difference in platelet [Ca2+]i was found between SHR and WKY or between DOC and SD rats. No correlations were found between systolic blood pressure and [Ca2+]i. These results suggest that the elevation of platelet [Ca2+]i does not necessarily accompany hypertension in rats.

Animals↗
PubMed1986

Decreased water and potassium content in erythrocytes in essential hypertension.

The water content in erythrocytes of subjects with borderline or established essential hypertension was measured by using gas-liquid chromatography and was found to be lower than that in normotensive controls (p less than 0.01). The water content in erythrocytes of normal controls (n = 14), borderline hypertensive subjects (n = 18), and established essential hypertensive subjects (n = 23) was (mean +/- SE) 71.0 +/- 0.2%, 69.9 +/- 0.2%, and 69.3 +/- 0.1% (vol/vol), respectively. A definite negative correlation was found between water content of erythrocytes and mean arterial pressure in normotensive and hypertensive subjects (n = 60, r = -0.59, p less than 0.001). Although there was no statistically significant between-group difference in the sodium content, the potassium content of erythrocytes from subjects with essential hypertension was significantly lower than that of normotensive controls (0.205 +/- 0.003 vs 0.222 +/- 0.004 mumol/mg dry red blood cells; p less than 0.01). There was no between-group correlation of sodium and water content in erythrocytes, but the potassium content correlated with the water content (n = 46, r = 0.49, p less than 0.001).

Blood Pressure↗
PubMed1985

Central alpha-activation by clonidine reduces plasma level of beta-endorphin in patients with essential hypertension.

Whether peripheral beta-endorphin contributes to the antihypertensive action of clonidine was examined by measuring plasma levels of beta-endorphin-like immunoreactivity (beta EpLI) after acute administration of clonidine in patients with essential hypertension. Administration of clonidine (0.225 mg) in one dose significantly lowered blood pressure, decreased heart rate and reduced the plasma level of beta EpLI and ACTH, while the placebo had no effect on blood pressure, heart rate or plasma level of beta EpLI suggesting that peripheral beta-endorphin does not play a major role in the antihypertensive action of acute clonidine administration.

Adrenocorticotropic Hormone↗
PubMed1985

Significance of the measurement of urinary alanine aminopeptidase and N-acetyl-beta-D-glucosaminidase activity in evaluating patients with essential hypertension.

To examine the relationship between the urinary levels of alanine aminopeptidase (AAP) or N-acetyl-beta-D-glucosaminidase (NAG) and the advance of essential hypertension, we measured the urinary levels of these enzymes in 20 normotensive controls, 8 subjects with borderline hypertension and 40 subjects with WHO stage I and stage II essential hypertension. The urinary level of NAG in stage II hypertensives was higher than that in the normotensives, and borderline or stage I hypertensives (p less than 0.01). Systolic blood pressure and the urinary level of NAG was positively correlated in hypertensives (rs = 0.43, p less than 0.01). The urinary level of NAG was correlated inversely with renal blood flow (rs = -0.61, p less than 0.01). The urinary level of AAP in stage II hypertensives was also higher than that in the normotensives (p less than 0.01) or stage I hypertension (p less than 0.01), but the urinary AAP level was not significantly correlated with systolic blood pressure or renal blood flow in hypertension.

Acetylglucosaminidase↗
PubMedDate not supplied

Erythrocyte water content in spontaneously hypertensive rats and DOCA-salt hypertensive rats.

Intra-erythrocyte water, sodium and potassium contents were measured in spontaneously hypertensive rats (SHR) and deoxycorticosterone acetate (DOCA)-salt rats. In 12 week old SHR, the intra-erythrocyte water content was slightly but significantly lower than that in age-matched Wistar-Kyoto (WKY) rats. SHR also exhibited a significantly lower intra-erythrocyte potassium content, but sodium content tended to be elevated. Although sodium content was not correlated with the water content, potassium content was. In DOCA-salt hypertensive rats, the intra-erythrocyte sodium content was higher than that in age-matched normotensive Sprague-Dawley rats by about 33%, but the water and potassium contents were similar. There were no significant correlations between these parameters. These findings provide no evidence of water retention in erythrocytes from DOCA-salt rat or SHR even though intra-erythrocyte sodium content was increased.

Animals↗
PubMedDate not supplied

Release mechanism of endothelin-1 and big endothelin-1 after stimulation with thrombin in cultured porcine endothelial cells.

Cultured porcine endothelial cells (EC) released immunoreactive endothelin-1 (ir-endothelin-1) and big endothelin-1 (ir-big endothelin-1) into the medium in a time-dependent way. Reverse-phase high-pressure liquid chromatography coupled with radioimmunoassay showed that the major component of ir-endothelin-1 corresponded to standard endothelin-1 (1-21) and that the major component of ir-big endothelin-1 corresponded to standard big endothelin-1 (porcine 1-39). This release was strongly inhibited by cycloheximide and was, therefore, related to de novo protein synthesis. The release of greater amounts was stimulated by thrombin. The protein kinase C (PKC) inhibitors from two chemical classes, H7 and staurosporine, inhibited release following such stimulation in a relatively dose-dependent way. Neither H7 nor staurosporine affected the basal release of both endothelin-1 and big endothelin-1. Phorbol myristate acetate, which activates PKC and the Ca2+ ionophore A23187, stimulated the release of ir-endothelin-1 and ir-big endothelin-1 in a dose-dependent way, respectively. In addition, the combination of both compounds had a synergistic effect. An inactive enantiomer of phorbol ester, 4 alpha-phorbol-12,13-didecanoate had no effect on the release of ir-endothelin-1 and ir-big endothelin-1. These results suggest that cultured EC release endothelin-1 and big endothelin-1 simultaneously, and that thrombin stimulates this release by a mechanism that probably involves intracellular Ca2+ mobilization and the activation of PKC.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗