Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood pressure, both venous and urinary catecholamines and plasma renin activity (PRA) were studied in 10 patients (6 men and 4 women, mean age 70 +/- 10 years) on the first three days after cerebral infarction. Blood pressure fell significantly (p less than 0.02) on the second and third day after stroke. There was a small but significant (p less than 0.01) decrease in plasma epinephrine concentration on the third day. The norepinephrine values remained constant on the three days. The PRA showed a significant (p less than 0.01) rise on the third day. No significant correlation was detected between the course of the blood pressure and the plasma catecholamines or PRA. When blood pressure was correlated with the urinary catecholamines, however, a significant correlation with epinephrine (r = 0.45; p less than 0.05) and with norepinephrine (r = 0.44; p less than 0.05) was found. We conclude that the changes in blood pressure after stroke are at least partly mediated by the changes in catecholamine production.
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PMID:Blood pressure and both venous and urinary catecholamines after cerebral infarction. 328 45

We reported a case of neuroleptic malignant syndrome (NMS) associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 71-year-old woman, who had been diagnosed as hypertension and multiple cerebral infarction, was given sulpiride 150 mg daily for depressive state. Three days after started sulpiride, she developed fever, sweating, difficulty of movement and was admitted to the hospital. The white blood cell count rose to 16,300/mm3 and serum creatine kinase (CK) to 3,063 IU/L. Two days later CK rose to 20,050 IU/L regardless of stopping the drug, so she was transferred to our hospital for further investigation. On admission, it was the 6th day from the onset, she was mute and akinetic accompanied by muscle pain and rigidity in extremities. Serum CK was 1,831 IU/L, Na 122 mEq/L, osmolality 244 mOsm/kg, plasma antidiuretic hormone (ADH) level 6.5 pg/ml and urine Na was 101 mEq/L, osmolality 467 mOsm/kg. Renal and adrenal functions, plasma renin activity were normal. From the history, course and these data, diagnosis of NMS associated with SIADH was made. Intravenous sodium (130-200 mEq/day) and fluids (1,000-1,200 ml/day) were carefully infused. She became active, muscle pain disappeared and rigidity, akinesia decreased. CK, serum Na and osmolality gradually improved to normal. About the transient increase in ADH secretion, we considered that hypothalamic disturbance in NMS might induce leakage of stored ADH from neuroendocrine neurons in it.
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PMID:[Neuroleptic malignant syndrome associated with the syndrome of inappropriate secretion of antidiuretic hormone]. 778 Dec 36

Iganidipine, a new water-soluble calcium antagonist, was administered at a nonhypotensive dose (NHD) of 0.3 mg/kg/day, a moderate-hypotensive dose (MHD) of 1.0 mg/kg/day, and a sustained-hypotensive dose (SHD) of 3.0 mg/kg/day to Dahl salt-sensitive (Dahl-S) rats fed a high-salt diet for 8 weeks. The effects on survival, and on renal and cerebral injuries, were then examined. Iganidipine completely prevented hypertensive death at the SHD and tended to increase the survival at the NHD and MHD. Iganidipine reduced glomerulosclerosis and renal arterial and tubular injuries in a dose-dependent manner. Iganidipine at the SHD, but not NHD or MHD, improved plasma creatinine, serum urea nitrogen, and glomerular filtration rate. Iganidipine at all doses examined increased the urinary prostaglandin (PG) I2 and PGE2, but not PGF2alpha or thromboxane B2, and decreased plasma angiotensin II (AII) level and renin activity. The renal glomerular, tubular, and arterial injuries were significantly correlated with blood pressure (r = 0.56 to 0.80) and plasma AII level (r = 0.50 to 0.71) but not with urinary prostanoids. Iganidipine also reduced the incidence of cerebral infarction. The infarction area was slightly and significantly correlated with urinary PGI2 (r = 0.42) and PGE2 (r = 0.41) but not with blood pressure or plasma AII. In conclusion, iganidipine prevented renal and cerebral injuries in Dahl-S rats. In addition to the reduced blood pressure, the reduction of plasma AII and the increase of vasodilatory prostanoids may also partially contribute to the renal and cerebral protective effects of iganidipine.
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PMID:Preventive effect of iganidipine on renal and cerebral injuries in salt-induced hypertension. 927 81

This study was to investigate the relationship between circadian blood pressure (BP) variation and circadian variation of neurohumoral factors during the acute phase of stroke. We studied 17 patients with cerebral infarction in 16 and cerebral hemorrhage in one. We performed 24-hour ambulatory BP monitoring and examined plasma renin activity (PRA), catecholamine, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endothelin 1 (ET1) and prothrombin fragment 1+2 (PT F1+2) and urinary catecholamine. Our result showed that the circadian variation of BP, neurohumoral and coagulation factors were diminished. There were significant relationships between BP levels and plasma BNP levels, nocturnal urinary adrenalines and ET1s. There were also significant relationships between night/day ratio of BP and plasma ET1 level. In conclusion the abnormal patterns of circadian BP rhythm were frequently observed during the acute phase of stroke. The cause of this abnormality may result from the diminished circadian rhythms of neurohumoral factors.
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PMID:Circadian variation of blood pressure and neurohumoral factors during the acute phase of stroke. 1184 63

Malignant hypertension is a rare but serious syndrome complicating 1% of essential hypertension and causing neurological, renal and cardiac complications. Despite improved anti-hypertensive medication, the incidence of this condition fails to decline. In the first part of this review, we discuss transgenic rat models of malignant hypertension, generated by over-expressing renin, to illustrate the role of the renin-angiotensin system in the development of systemic hypertensive vascular remodelling and hypertension. In the second part, we focus on the cerebrovascular response to hypertension and discuss new data using a conditional, transgenic model of malignant hypertension, the inducible hypertensive rat (IHR). Cerebral infarction associates strongly with hypertension in man and the mechanisms by which hypertension predisposes to different types of stroke remains poorly understood. Rats have similar cerebrovascular anatomy and structure to humans and as such provide a good experimental tool. To date, such models lack controllability and blood-pressure matched controls. Using the IHR, we have manipulated dietary salt and water intake to generate a novel, controllable stroke phenotype. Hypertensive small-vessel stroke develops over a predictable time period, permitting the study of developing cerebrovascular lesions. Systemic end-organ injury and hypertension are not affected. Dissociation of the systemic and central vascular responses in this way, will allow for comparative study of animals with equivalent hypertension, genetic background and systemic features of hypertension with or without stroke.
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PMID:The role of the renin-angiotensin system in malignant vascular injury affecting the systemic and cerebral circulations. 1476 41

Epidemiological reports show that about half of all adults suffer from hypertension, and the incidence of diabetes mellitus, dyslipidemia and obesity is markedly increasing in Japan. Recent progress in gene determination has shown that lifestyle-related diseases, including hypertension, are multigenetic diseases. In particular, renin-angiotensin genes play an important role in the pathogenesis of hypertension. Upregulation of the transcription of angiotensinogen and angiotensin-converting enzyme genes increases blood pressure and cardiovascular organ damage through increased levels of angiotensin II. In this review, I first introduce the history of the recognition, understanding and the development of treatment for hypertension. Secondly, the basic relationship of the pathogenesis between hypertension and the new concept of metabolic syndrome will be shown, and the usefulness of angiotensin II receptor antagonist for hypertensive patients with obesity and/or metabolic syndrome. Finally, I will reveal the utility of gene diagnosis for acute myocardial infarction and cerebral infarction by detecting the polymorphism of renin-angiotensin genes. On the other hand, the positive correlation between blood pressure and body mass index is affected by the Gln27Glu genotype of the beta2-adrenoceptor gene. These studies investigating the gene-environmental relationship will contribute to the development of tailor-made medicine in the future.
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PMID:[Increasing menace of cardiovascular diseases in the era of obesity]. 1654 38

Cerebral ischaemia-reperfusion injury is associated with an inflammatory response, with contributions from leucocytes and microglia. Formation of free radicals and nitric oxide contributes to the development of cerebral infarction and of the neurological deficit that follows transient focal ischaemia. The circulating and cerebral renin-angiotensin systems contribute, via stimulation of the angiotensin II (Ang II) types 1 (AT1) and 2 receptors, to the initiation or progression of inflammatory processes, and blockade of AT1-receptors prevents irreversible tissue injury and improves outcome from stroke in animal experiments. Such cerebral protection can be achieved even when treatment is initiated hours after established reperfusion. Blockade of AT1-receptors also reduces the incidence of stroke and cardiovascular mortality associated with stroke in patients; however, the mechanisms underlying the prevention of stroke by AT1-receptor blockade in patients remain to be elucidated. In this review we summarize the existing experimental and clinical data demonstrating that the renin-angiotensin system contributes to the inflammation and subsequent irreversible injury after cerebral ischaemia-reperfusion. We conclude that AT1-receptor blockade reduces cerebral ischaemia-reperfusion injury in part by attenuating inflammatory processes.
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PMID:Angiotensin II type 1 receptors in cerebral ischaemia-reperfusion: initiation of inflammation. 1660 65

The present review examines various reports describing prevalence of primary aldosteronism (PA) among hypertensives and the screening method of PA to better understand the current concepts used for diagnosing and managing PA among clinicians as well as specialists. Here, we describe and compare the prevalence of PA in Japan, which is well known to induce various vascular complications due to hyperaldosteronemia, resulting in cerebral infarction, myocardial infarction and renal failure, with that in another Asian area, US, European countries, Australia and Africa. The incidence rates for PA among hypertensives were recently reported to be widely raged between 3.2% and 20%. Those discrepancies are due in part to the completely different characteristics of the starting subjects used for studying the prevalence. Moreover, the criteria for screening PA among hypertensives, including aldosterone-renin ratio (ARR), and confirmatory tests for definitely diagnosing PA, such as saline infusion test are varied. We had already reported that a diagnosis of PA was made in 61 (6%) of the 1,020 hypertensive patients during the past five years, from 1995 until 1999. In our study, only 18% of the patients showed a serum K level of 3.3 mEq/l or less. Thus, many clinicians seem to misdiagnose PA as essential hypertension, because of absence of hypokalemia. Finally, we describe highlight key evidence for optimal methods for screening and definitely diagnosing PA among hypertensive patients in order to avoid misjudgment before or after treating hypertensive patients.
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PMID:Prevalence of primary aldosteronism: should we screen for primary aldosteronism before treating hypertensive patients with medication? 1712 64

Accumulating evidence suggests that the angiotensin-(1-7) [Ang-(1-7)], is an active member of the brain renin-angiotensin system (RAS). We evaluated the possibility that intracerebroventricular (ICV, lateral ventricle) infusion of exogenous Ang-(1-7) could participate in the potentiation of bradykinin (BK) release and the kinin receptor expression in ischemic brain parenchyma after focal cerebral ischemia-reperfusion in rats. The middle cerebral artery occlusion (MCAO) and sham-operated models were prepared, continuously administrated with Ang-(1-7) or artificial cerebrospinal fluid (aCSF) by implanted Alzet osmotic minipumps into lateral cerebral ventricle after reperfusion in male Sprague-Dawley (SD) rats. Experimental animals were divided into sham-operated group (sham+aCSF), aCSF treatment group (MCAO+aCSF) and Ang-(1-7) treatment groups [MCAO+Ang-(1-7)] at low (1 pmol/0.5 microl/h), medium (100 pmol/0.5 microl/h) or high (10 nmol/0.5 microl/h) dose levels. Cerebral infarction resulted in a significant increase of BK formation from 3 h to 6 h compared with sham-operated group after reperfusion, whereas medium- and high-dose Ang-(1-7) infusion markedly enhanced BK levels from 6 h to 48 h after reperfusion. Medium- and high-dose Ang-(1-7) infusion markedly increased kinin B(2) receptor mRNA and protein expression, whereas only high-dose Ang-(1-7) infusion induced upregulating the expression of B(1) receptor. Low-dose Ang-(1-7) infusion did not modify both the kinin B(1) and B(2) receptor expression compared with aCSF treatment group after focal cerebral ischemia-reperfusion at each time point. The finding might indicate complex interactions between Ang-(1-7) and kallikrein-kinin system in the CNS after focal cerebral ischemia-reperfusion in rats.
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PMID:Effects of intracerebroventricular infusion of angiotensin-(1-7) on bradykinin formation and the kinin receptor expression after focal cerebral ischemia-reperfusion in rats. 1853 11

Cognitive impairment leading to dementia is associated with high prevalence of hypertension, decreased quality of life and poor prognosis. Aldosterone is known as a risk factor for cardiovascular and cerebrovascular diseases. In addition, mineral corticoid receptors are abundantly expressed in the hippocampus, which plays a pivotal role in cognitive function; however, it has not been determined whether plasma aldosterone level is associated with cognitive impairment in patients with hypertension. We enrolled 68 patients with essential hypertension and assessed their cardiovascular risk factors, including blood pressure, hyperlipidemia, diabetes mellitus, obesity, smoking, history of cerebral infarction, renal function, parameters of inflammation, oxidative stress and nitric oxide bioavailability, a parameter of cerebral blood flow and carotid plaque by ultrasound examination, plasma renin activity and plasma aldosterone concentration (PAC). The mini-mental state examination (MMSE) was used to evaluate cognitive function. The relevance of cardiovascular risk factors and MMSE score was statistically evaluated. Multiple regression analysis showed that age (P < 0.01), PAC (P < 0.01) and history of cerebral infarction (P < 0.05) were inversely and independently associated with MMSE score. Mineral corticoid receptor antagonists, including spironolactone and eplerenone, increased MMSE score in seven patients with hypertension, but not in the controls. In conclusion, increased PAC is associated with impaired cognitive function and mineral corticoid receptor blockade may protect against not only cardiovascular mortality, but also cognitive impairment in patients with hypertension.
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PMID:High plasma aldosterone concentration is a novel risk factor of cognitive impairment in patients with hypertension. 2086 41


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