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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of svate on platelet morphology and aggregation were studied and compare with Radix Salviae Miltiorrhizae. The results showed that svate remarkably inhibited platelet aggregation in patients with coronary heart disease and hypertension. Svate could increase plasma 6-keto-PGF1 alpha and decrease plasma TXB2. After treatment with svate, levels of platelet cAMP was increased. Svate enhanced platelet 5-HT and reduced plasma 5-HT. Electron microscopic study showed that the percentage of discoid and dendritic platelets were increased, while those of spread and aggregate platelets were decreased following svate therapy. It was found that svate is superior to Radix Salviae Miltiorrhizae in inhibition of platelet function. The results indicate that svate inhibits platelet aggregation and release through increasing prostacyclin generation in the vascular wall, raising platelet cAMP and inhibition of TXA2 production.
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PMID:[Effects of svate on platelet morphology and function in patients with coronary heart disease and hypertension]. 165 75

Both marked hypercholesterolemia and severe hypertension have been reported to be associated with an enhanced sensitivity of blood platelets to activating agents. To investigate a possible mutual synergistic effect of moderate hypercholesterolemia and mild hypertension on platelet reactivity, we studied in 29 patients the response to aggregating agents, ADP and collagen, and the intracellular cyclic AMP content and cytosolic Ca2+ concentration that participate, respectively, as inhibitory and stimulatory mediators in platelet responses. When compared to age- and blood pressure-matched patients with normal or slightly elevated plasma cholesterol, the patients with total platelet cholesterol higher than 6.4 mM were characterized by a decreased response to collagen and ADP (14.5 +/- 3.0 vs. 23.8 +/- 2.0 a.u. and 17.7 +/- 4.5 vs. 26.9 +/- 2.7 a.u., respectively), a tendency to a reduced cAMP content both in the basal state and after phosphodiesterase inhibition by Ro-15 2041 (2.83 +/- 0.18 vs. 3.26 +/- 0.22 mumol/10(8) cells and 4.57 +/- 0.29 vs. 5.38 +/- 0.36 mumol/10(8) cells, respectively), and no change in cytosolic Ca2+ concentration (190 +/- 11 vs. 203 +/- 13 nM). After a chronic treatment with nitrendipine (20 mg/day for 6 months), blood pressure, platelet [Ca2+]i and cAMP content decreased in the patients with normal or moderately elevated hypercholesterolemia (p less than 0.001, less than 0.001, and less than 0.05, respectively), but these effects were attenuated or absent in the patients with higher hypercholesterolemia. Plasma lipids and the platelet-aggregating response to ADP and collagen were unchanged by this long-term nitrendipine treatment in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercholesterolemia modulates the effects of nitrendipine on blood pressure and platelet function in essential hypertension. 172 3

In order to study the connection of diastolic activity of smooth muscles of blood vessels with development of hypertension, plasma cAMP, cGMP, TXB2, 6-K-PGF1 alpha, ANP, SP were determined with radioimmunoassay, of 173 hypertension patients with Liver Yang exuberance (LYE) 91 cases, and Yin deficiency and Yang exuberance (YDYE) 82 cases. In addition, 228 health subjects served as control. The results showed that the levels of cAMP, cGMP and TXB2 in both LYE and YDYE groups were higher than those in the control group, but the levels of ANP, SP and cAMP/cGMP ratio in LYE and YDYE groups were lower than those in the control. As to the level of 6-K-PGF1 alpha, no significant variance was found between these groups. After TCM-WM treatment, the levels of cAMP, cGMP and TXB2 in LYE and YDYE groups got down, as compared with those in the control, adversely the levels of ANP, SP and 6-K-PGF1 alpha in LYE and YDYE groups turned up significantly. However the cAMP/cGMP ratio had no remarkable change between these groups. The linear regression analyses between the diastolic pressure and ANP or SP both proved negative correlation (r = -0.36, P less than 0.05; r = -0.35, P less than 0.05). The findings indicated that the TCM-WM treatment was the most effective among the therapies employed in the study, and that this therapy affected the diastolic activity of smooth muscles by modulating the above factors existing in the nervous and endocrine systems of the patients with hypertension.
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PMID:[Experimental study on the treatment of hypertension with combined traditional Chinese and Western medicine]. 172 72

This article describes investigations of several aspects of the molecular biology of the human renin gene and the three-dimensional structure of renin and its precursor, prorenin. Because of the importance of the RAS in hypertension, heart failure, renal failure, and possibly other disorders such as atherosclerosis, it is critical to understand the detailed control of this system. This control involves regulation at the transcriptional level, folding of prorenin, sorting of prorenin to a regulated pathway where it is proteolytically cleaved to renin and released in response to secretogogues, constitutive release of uncleaved prorenin, and nonproteolytic activation of prorenin. Currently there is great interest not only in the control of renin in the kidney, the sole source of circulating renin, but also at extrarenal sites where RAS activity may regulate cardiovascular functions. The renin gene was found to be expressed significantly in the renal juxtaglomerular cells and several other cell types. Most tissue culture cells did not express the gene; exceptions were cultured SK-LMS-1 cells and cAMP-stimulated human lung fibroblasts. Cultured human uterine-placental cells expressed the human renin gene at levels higher than in other cell types assessed. Renin mRNA had the same start site in the placental cells as the kidney and was regulated by calcium ionophores and cAMP. Thus, these cells provide primary nontransformed human cells to study the homologous human promoter. Transfected renin promoters showed cell type-specific expression and cAMP responsiveness in these cells in constructs containing as few as 102 bp of 5'-flanking DNA. DNA upstream from this appears to contain an inhibitory element(s) that may have some tissue specificity in its distribution. The cAMP response is not due to cAMP induction of a transcription factor that secondarily affects the renin promoter. A novel element may be involved, since the promoter does not contain a CRE element that mediates many cAMP responses, and the cells do not appear to respond to another known cAMP-responsive transcription factor, AP-2. Studies with transfected vectors expressing a mutant cAMP-responsive protein kinase A regulatory subunit suggest that cAMP is not responsible for basal renin promoter activity in the placental cells. By contrast, cAMP induces in essence gene activation in WI26VA4 transformed human lung fibroblasts in which renin mRNA levels increase by up to 150-fold in response to forskolin. Thus, cAMP may activate renin gene expression under certain circumstances and tissue-specific renin gene expression may be directed by more than one mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Molecular biology of human renin and its gene. 174 21

Primary hyperparathyroidism (PHPT) is characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia. PTH acts by binding to cell surface receptors coupled to G proteins. Cyclic AMP is the classic second messenger of PTH action, but substantial evidence indicates that PTH also acts to stimulate formation of the dual second messengers, inositol trisphosphate and diacylglycerol, thereby mobilizing intracellular calcium. The physiologic actions of PTH include (1) an increase in extracellular fluid ionized calcium through direct actions on kidney and bone, the classic target organs for PTH, and (2) a decrease in extracellular fluid phosphate primarily through renal action. The pathophysiologic effects of PTH arise from (1) direct actions of PTH on bone and kidney, and possibly on nonclassic target organs, and (2) indirect effects of altered mineral homeostasis. PTH hypersecretion in PHPT can lead to bony demineralization, nephrolithiasis, and hypercalcemic crisis. PHPT may also be associated with mental disturbances, neuromuscular disease, hypertension, and glucose intolerance.
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PMID:Pathophysiology of primary hyperparathyroidism. 176 67

beta-Adrenergic blockers are less efficacious as monotherapy for the treatment of hypertension in blacks as compared with whites. Because beta-adrenergic stimulation and blockade differ between racial groups, biochemical differences in the beta-adrenergic pathway may exist. It is the intent of this report to show underlying similarities and differences, at least in part, in the beta-adrenergic pathway (e.g., baseline cAMP and protein concentrations) using the T-lymphocyte as the model system. A total of 20 (n = 10 black, n = 10 white) normotensive male volunteers were recruited, begun on a low-sodium diet to normalize serum catecholamines, and blood was collected for lymphocyte beta-receptor isotherm binding experiments and cAMP determination. There were no differences in Bmax, sites per cell, or kd. Basal cAMP concentrations were significantly higher in the black group (16.0 +/- 9.8 pmol/10(6) cells) compared with the white group (7.0 +/- 1.8 pmol/10(6) cells) (p less than 0.05). Protein levels from the lymphocyte suspension were also higher in the black group (1,081.0 +/- 367.7 micrograms/ml) compared with the white group (766.8 +/- 220.4 micrograms/ml) (p less than 0.05). Normalization of cAMP for protein yielded 83.2 +/- 55.4 fmol/micrograms protein in the black group and 56.6 +/- 29.8 fmol/micrograms protein in the white group (p = 0.11). Altered protein levels may be a confounding variable in studies of this type. Further work is necessary to identify the nature and significance of this protein elevation, its relationship to the adenylate cyclase system in lymphocytes, and the source of the cAMP elevation noted herein.
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PMID:Racial differences in baseline cyclic adenosine monophosphate concentrations per million T-lymphocytes and protein concentrations. 198 Mar 84

Recent advances in molecular biological techniques provide us with genetic approaches for studying the renin-angiotensin system. Renin and angiotensinogen cDNAs have been cloned in several species, and the sequences are highly conserved between the species. The 5'-flanking region of the human renin gene indicated putative regulatory sequences of glucocorticoid, estrogen, progesterone, and cAMP. The 5'-flanking region of the human angiotensinogen gene also had putative regulatory sequences of glucocorticoid, estrogen, acute phase protein, and cAMP. These structures may be related to the tissue specific expression of the renin and angiotensinogen genes. In this review, expression of rat renin and angiotensinogen genes in various tissues in the following conditions are described: a) different sodium intake in the liver, kidney, and brain; b) angiotensin II and converting enzyme inhibition in the liver, kidney and brain; c) renovascular hypertension in the kidney and liver; d) aging in the liver and kidney; e) adrenal steroids in the liver, kidney and brain; f) gonadotropin and testosterone in the testes, liver and kidney; g) triiodothyronine in the liver, kidney and brain; h) nephrectomy in the liver and brain; i) high potassium, angiotensin II, sodium intake and nephrectomy in the adrenal gland; j) transgenic animal. Our results suggest that the expression of the renin and angiotensinogen genes are regulated in a tissue-specific manner.
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PMID:[Expression of the renin and angiotensinogen genes]. 204 11

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the hormonal responsiveness of cultured renal papillary collecting tubule (RPCT) cells from SHR and Wistar-Kyoto rats (WKY) as control. Basal levels of PGE2 and cAMP were lower in 4-weeks-old SHR than in WKY, while PGE2 synthesis after stimulation with arachidonate, A23187 or bradykinin and the level of cAMP responded to vasopressin or exogenous PGE2 were similar in both strains. There was no difference in basal nor stimulated levels of cGMP between both strains. In 16-week-old rats, basal levels of cAMP, cGMP and PGE2 were significantly lower than in 4-week-old rats, but no differences were recognized between both strains. These results suggest that RPCT cells of SHR and WKY at the post-weaning period may differ in the metabolism of PGE2 and cAMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.
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PMID:[Responsiveness of cultured papillary collecting tubules to vasoactive hormones: comparison between spontaneously hypertensive rats and Wistar-Kyoto rats]. 206 16

Calcium channel blockers (CCBs), which are used clinically for treatment of angina and hypertension, are known to inhibit calcium influx into arterial smooth muscle cells and thereby decrease smooth muscle cell contraction. In addition, they prevent cholesteryl ester (CE) accumulation, the hallmark of human atherosclerosis, in arteries of cholesterol-fed animals by cellular mechanisms that remain undefined. To assess whether CCBs enhance CE hydrolysis and reduce CE accumulation in human arterial cells, we measured activities of the CE metabolic cycle in aortic tissues that were stripped of endothelial cells and adventitia from 35 patients undergoing coronary artery bypass surgery. Patients who were treated with either nifedipine or diltiazem (n = 23) for several months demonstrated a threefold increase in arterial CE hydrolytic activities compared with untreated patients. This difference was independent of serum cholesterol levels, age, or treatment with other medications. No effects were observed on CE synthetic activity. Cyclic AMP levels in the aortic tissue of patients treated with CCBs were also significantly elevated twofold to threefold. In addition, both free and esterified cholesterol were significantly reduced in aortic tissue from patients taking CCBs compared with untreated patients. These data are the first to show that CCBs can increase CE hydrolysis in human aortic tissue by increasing intracellular cyclic AMP with resultant decrease in CE accumulation. Collectively, these findings support the hypothesis that CCBs can act as antiatherosclerotic agents in human tissue by mobilizing stored CE in the arterial wall.
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PMID:Calcium channel blockers enhance cholesteryl ester hydrolysis and decrease total cholesterol accumulation in human aortic tissue. 215 60

To study the effects of prolonged oral calcium loading on the development of hypertension in spontaneously hypertensive rats (SHR), 48 male animals (age 9 weeks) were divided into four groups according to the treatment: control, calcium, deoxycorticosterone (DOC) and calcium/DOC. Both calcium groups received 1.5% calcium chloride solution ad libitum as their drinking fluid. The animals in the DOC groups were treated with a mineralocorticoid, deoxycorticosterone trimethylacetate 25 mg kg-1 s.c. once a week. Systolic blood pressure (BP) was measured twice a week during the 4-week study period. Calcium loading alone lowered BP (p less than 0.01) after four weeks. Combined with DOC treatment, calcium administration had no significant effect on BP. Calcium loading increased the total plasma calcium concentration in the calcium group (p less than 0.05). Urinary excretions of sodium and potassium were augmented in both groups receiving calcium compared to DOC group. DOC treatment alone increased the excretion of calcium (P less than 0.05). Calcium supplementation decreased the plasma phosphate concentration in both groups (calcium p less than 0.05; calcium/DOC p less than 0.01) as well as the excretion phosphate (p less than 0.005) compared to control. The urinary excretion of cAMP remained unaffected by the calcium treatment. The present results indicate that mineralocorticoid treatment can prevent the BP-lowering effect of calcium in SHR. The mechanism of this action remains unclear, but it does not seem to depend on electrolyte or phosphate balance. The investigation of this action of DOC may provide a means for further exploration of the mechanisms by which increased calcium intake lowers BP in SHR.
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PMID:Deoxycorticosterone prevents the blood pressure-lowering effect of calcium in spontaneously hypertensive rats. 215 18


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