PubMed Health⌕ Search

Biomedical subjects

O Mohara

Publications and source records attributed to O Mohara.

At least 19 recordsLinked to original sources
PubMed1996

A case of hypertrophic obstructive cardiomyopathy associated with autonomic nervous dysfunction.

Autonomic nervous dysfunction has recently been considered to be an etiological factor in syncope and sudden death in cases of hypertrophic cardiomyopathy. However, the precise mechanism is still unknown. A 73-year-old woman with obstructive hypertrophic cardiomyopathy was hospitalized with complaints of impaired consciousness; faintness 3 to 4 h after meals, lightheadedness while walking, and syncope during and after defecation and micturition. Faintness was induced by alimentary hypoglycemia related to gastrectomy performed 5 years previously. Lightheadedness and syncope were accounted for by autonomic nervous failure combined with an impairment of alpha 1-adrenoceptor in vasoconstriction and the carotid sinus hypersensitivity which accompanied preceding events such as abdominal pain, defecation and micturition, which could enhance the vagally-mediated baroreceptor reflex.

Aged↗
PubMed1994

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes.

A case of orthostatic and postexertional hypotension with ischemic electrocardiographic changes is reported. The etiology was considered to be the partial dysfunction of efferent sympathetic nerve endings. Peripheral adrenergic receptors (alpha and beta) were up-regulated, which might have caused pseudoischemic electrocardiographic changes and abnormal vasodilation after exercise.

Autonomic Nervous System Diseases↗
PubMed1992

[Lean hypertension].

Explore the source record for details and available documents.

Adrenal Gland Neoplasms↗
PubMed1991

Angiotensin II mediates hyperadrenergic activity evoked by sodium restriction in essential hypertension.

We examined the possible involvement of angiotensin II in the modulation of circulating norepinephrine produced by acute sodium restriction in essential hypertensive patients (n = 18). Sodium restriction potentiated plasma level of norepinephrine in parallel with an increased plasma renin activity (r = 0.81, F = 31.2, p less than 0.05 given by the percent changes). An intravenous infusion of sarcosine-1, isoleucine-8 angiotensin II produced a significant fall in mean arterial pressure (-6 +/- 2 mmHg, p less than 0.05) in patients on sodium restriction but not before sodium restriction, while the infusion of the antagonist produced a greater decrease (p less than 0.05) in plasma norepinephrine with sodium restriction (-158 +/- 23 pg/ml, p less than 0.05) when compared to that obtained before sodium restriction (-91 +/- 11 pg/ml, p less than 0.05). A single oral administration of an angiotensin I converting enzyme inhibitor, captopril caused a greater fall (p less than 0.01) in mean arterial pressure after sodium restriction (-32 +/- 3 mmHg, p less than 0.05) compared to that given before (-21 +/- 3 mmHg, p less than 0.05). However, sodium restriction did not affect the magnitude of reflex increase in plasma norepinephrine to hypotension evoked by captopril (from +88 +/- 16 pg/ml to +87 +/- 17 pg/ml; p greater than 0.05). It can be interpreted that acute sodium depletion results in a substantial contribution of angiotensin II to the expression of hyperadrenergic activity.

Adrenal Glands↗
PubMed1991

Captopril attenuates reflex adrenergic response in essential hypertension.

An attenuation of adrenergic activity during the inhibition of endogenous angiotensin II formation was evaluated by determining plasma norepinephrine concentration after a single oral administration of captopril compared to that after nifedipine in essential hypertension. Captopril produced a fall in mean arterial pressure (-24 +/- 2 mmHg, p less than 0.01) which magnitude was the same as that gained by nifedipine (-22 +/- 3 mmHg, p less than 0.01). Reflex tachycardia due to hypotension was produced (+13 +/- 1 beats/min, p less than 0.01) after nifedipine but not after captopril (-1 +/- 2 beats/min, p greater than 0.05). Although the enhancement of plasma renin activity induced by captopril (+1.54 +/- 0.56 ng/ml/hr, p less than 0.05) was similar (p greater than 0.05) to that by nifedipine (+1.44 +/- 0.47 ng/ml/hr, p less than 0.05), plasma norepinephrine concentration increased less (p less than 0.01) after captopril (+100 +/- 23 ng/ml, p less than 0.05) than after nifedipine (+283 +/- 51 ng/ml, p less than 0.05). Thus, the diminished adrenergic activity is a likely candidate for the abolished reflex tachycardia after the inhibition of angiotensin I converting enzyme activity by captopril in essential hypertension.

Administration, Oral↗
PubMed1988

Hemodynamic and neurohormonal changes in the development of DOC hypertension in the dog.

In this article we summarize studies of the hemodynamic and endocrine effects of desoxycorticosterone (DOC)-induced hypertension in dogs and also review new data of the action of this steroid on baroreceptors. The hemodynamic effect of subcutaneous injections of DOC to dogs, without supplementation of salt in their diet, consisted of increases in arterial pressure that were sustained for a 28-day observation period and associated with augmented cardiac output. At the early stage of the hypertensive response there was a rise in plasma Na+ concentration accompanied by increases in the plasma and cerebrospinal fluid (CSF) levels of vasopressin. The activity of the peripheral renin angiotensin system, as evaluated by the longitudinal changes in plasma renin activity and plasma immunoreactive angiotensin II (irAng-II), was markedly depressed in the hypertensive dogs. In contrast, the concentration of irAngII in the CSF did not change. Additional studies of the carotid occlusion reflex in anesthetized dogs revealed an enhanced buffering baroreceptor capacity in the early (less than day 10), but not the late (greater than day 28), stages of the hypertension. The abnormality in baroreflex function may be mediated by an effect of the steroid on an activity of brain angiotensin II that influences the inhibitory interaction between high and low pressure baroreceptors. The data acquired in these studies agree with the notion that excess mineralocorticoid production causes hypertension by mechanisms that influence the neurohormonal control of blood pressure by the central nervous system.

Angiotensin II↗
PubMed1988

Characteristics of hormonal and neurogenic mechanisms of deoxycorticosterone-induced hypertension.

We characterized the hemodynamic and endocrine changes associated with the evolution of steroid-induced hypertension in conscious, trained, instrumented dogs given intramuscular injections of deoxycorticosterone (DOC) pivalate on Days 1 (20 mg/kg) and 14 (10 mg/kg) of the study. Because hypertension could be produced in these dogs without salt loading and unilateral nephrectomy, the research afforded a novel opportunity to determine the primary effects of DOC excess on the renin-angiotensin and sympathetic nervous systems, and on vasopressin levels. Both before and during 28 days of DOC treatment, regular measurements of mean arterial pressure, heart rate, cardiac output, and total peripheral resistance were coupled with serial determinations of plasma and cerebrospinal fluid levels of angiotensin II, vasopressin, norepinephrine, and electrolytes. DOC induced a progressive rise in mean arterial pressure associated with increased cardiac output and no change in heart rate. These hemodynamic changes were accompanied by sustained decreases in plasma renin activity, and in plasma, but not cerebrospinal fluid, angiotensin II. In contrast, plasma and cerebrospinal fluid vasopressin rose transiently on the 7th and 14th days of the study, respectively. After anesthesia with morphine and chloralose, the hemodynamic response to occlusion of a sole innervated carotid artery was evaluated on the 5th week before and after cervical vagotomy. Compared to normal animals, dogs with DOC-induced hypertension showed a reduced pressor response to carotid occlusion associated with suppression of reflex tachycardia; vagotomy partially restored the pressor response to normal levels. The data suggest that DOC-induced hypertension changes central hormonal influences of cardiovascular function, and also alters cardiopulmonary baroreceptor reflex control of peripheral sympathetic nerve activity.

Angiotensin II↗
PubMed1987

The cause of death, risk factors and long-term prognosis of acute myocardial infarction.

Three hundred and eighty-six patients with acute myocardial infarction in the past 11 years between 1975 and 1985 were investigated retrospectively to clarify fatality, cause of death and long-term prognosis in relation to their risk factors and age. The average number of patients admitted in each year was 24.4 for the first 5 years and 44.0 cases per year in the last 5 years. The fatality decreased from 20.3% in the first 5 years to 15.7% in the last 5 years. A major cause of hospital death was cardiogenic shock and congestive heart failure. One hundred and thirty-six patients had coronary arteriography within 2 months after admission. They were divided into three groups; the young (less than or equal to 40 year old)-, middle (41-50 year old)-, and old (greater than or equal to 51-year old)-aged groups. Among the young-aged group, serum cholesterol levels at admission were significantly higher in patients with multi-vessel lesions than those in patients without multi-vessel lesions, while there were many heavy smokers who did not show a significant lesion of the coronary artery. These observations suggest that hypercholesterolemia may act as an important risk factor for coronary arteriosclerosis in young patients, and also that a heavy smoking may promote an initiation of myocardial infarction in young patients without severe coronary artery stenosis. The cumulative 5 and 10 year survival rate for all groups was 84% and 61%, respectively. Fifty-seven patients had reinfarctions, and thirty patients died. The survivors were younger and had a good tolerance to treadmill exercise test at discharge.

Age Factors↗
PubMed1985

Central actions of circulating angiotensin II on the sympathetic nervous system and blood pressure control.

The effects of intravertebral artery infusions of [Sar1, Ile8] and [Sar1, Thr8] angiotensin II on the central nervous system were studied in furosemide-treated dogs anesthetized with alpha-chloralose. Acute administration of furosemide led to a significant increase in plasma renin activity, plasma noradrenaline levels and heart rate, and also to a slight rise of blood pressure. In the furosemide-treated dogs, intravertebral artery infusion of either angiotensin II antagonist (250 ng/Kg/min, for 30 min) suppressed the furosemide-induced increases in plasma noradrenaline, heart rate and arterial blood pressure. The effects of [Sar1, Thr8] angiotensin II on the last two parameters were more pronounced than those of [Sar1, Ile8] angiotensin II. Intravenous infusion of the same dose of each antagonist had little influence on the furosemide-induced increases in arterial blood pressure, heart rate and plasma noradrenaline levels. These results suggest that the central actions of angiotensin II contribute to the regulation of blood pressure through the sympathetic nervous system.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1983

Changes in renal alpha 2-adrenoceptor in experimental hypertension in rats.

alpha 2-Adrenoceptors were studied in renal membrane fractions from spontaneously hypertensive (SHR), two-kidney, one clip hypertensive (2K, 1C HT) and DOCA-salt hypertensive (DOCA-salt HT) rats, using radioligand binding method. alpha 2-Adrenoceptor concentration in the kidney measured by [3H]yohimbine binding was significantly increased in SHR at 4 weeks old (41.5 +/- 2.8 fmol/mg protein, mean +/- SEM, p less than 0.01), 12 weeks old (54.9 +/- 2.5 fmol/mg protein, p less than 0.01) and 35 weeks old (59.8 +/- 3.4 fmol/mg protein, p less than 0.01) as compared with age-matched Wistar-Kyoto rats (WKY, 31.5 +/- 2.5, 40.9 +/- 1.8, 47.8 +/- 2.0 fmol/mg protein, respectively). There were no significant differences in binding affinity and 5'-nucleotidase activity (plasma membrane marker enzyme) between SHR and WKY at any age. In 2K, 1C HT rats, alpha 2-adrenoceptor concentration in the clipped kidney was higher than that of control rats, but alpha 2-adrenoceptor concentration in the unclipped kidney was unchanged. Binding affinity and 5'-nucleotidase activity showed no significant changes in renal hypertensive rats. In DOCA-salt HT rats, no significant change was found in concentration and affinity of renal alpha 2-adrenoceptor. The observed increase in renal alpha 2-adrenoceptor concentration in SHR may contribute to the pathogenesis and maintenance of hypertension through increased sodium and water reabsorption in the kidney.

Animals↗
PubMed1983

Changes in plasma norepinephrine after intravertebral artery infusion of saralasin in sodium depleted dogs.

This study was designed to investigate the central action of circulating angiotensin II on the regulation of blood pressure in sodium depleted states. The effects of intravertebral arterial infusion of angiotensin II and [Sar-1, Ala-8] angiotensin II (saralasin) on plasma norepinephrine (NE) were studied in alpha-chloralose anesthetized dogs. Intravertebral arterial infusion of angiotensin II (10 ng/kg/min) increased mean arterial pressure (MAP), heart rate (HR) and plasma NE. Plasma NE was decreased by intravertebral arterial infusion of saralasin (0.40 +/- 0.05 to 0.28 +/- 0.04 ng/ml, p less than 0.05) in normal dogs. The administration of furosemide produced significant increases in plasma NE (142.4 +/- 23.7%, p less than 0.01), plasma renin activity (PRA) (158.6 +/- 26.3%, p less than 0.01) and HR (32.3 +/- 6.0 beats/min, p less than 0.01). A slight rise in mean blood pressure (3.9 +/- 1.2 mmHg, p less than 0.05) was observed during the furosemide administration. Saralasin infused into the vertebral artery significantly suppressed the furosemide-induced increases in plasma NE, HR and PRA, and lowered mean arterial blood pressure. Intravenous infusion of the same dose of saralasin produced no changes in arterial blood pressure, HR and plasma NE. These results suggest that the central sympathetic potentiation induced by circulating angiotensin II may contribute to the regulation of blood pressure in sodium and volume depleted states produced by furosemide.

Aldosterone↗
PubMed1983

Contributions of central sympathetic neural activity to furosemide-induced increases in plasma renin activity and noradrenaline.

To evaluate the role of the central nervous system on the furosemide-induced increases in plasma noradrenaline (PNA), renin activity (PRA), and aldosterone concentration (PAC), central vasoactive sympathetic structures were inhibited by intravertebral artery infusion of colnidine. Intravertebral artery infusion of clonidine (0.06 microgram/Kg/min) significantly reduced basal PNA, heart rate, and arterial pressure, while both PRA and PAC were increased. Intravenous infusion of the same dose of clonidine caused no significant changes in PNA, PRA, and PAC. Intravertebral artery infusion of clonidine (0.02 or 0.1 microgram/Kg/min) significantly suppressed the furosemide-induced increases in PNA and heart rate, and induced a drop in arterial pressure. Although the furosemide-induced increase in PRA was suppressed by intravertebral artery infusion of clonidine, the furosemide-induced increase in PAC was not affected. These results suggest that the furosemide-induced increase in PNA may be mediated by the central sympathetic nervous system and that some of the furosemide-induced increase in PRA may be mediated by central sympathetic neural activation.

Aldosterone↗