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

The short term regulation of the activity of the Na,K-pump (Na+,K(+)-ATPase) is just beginning to be understood. By using single microdissected proximal tubule segments (PCT) (permeabilized in order to clamp Na entry), it was possible to study regulation of Na+,K(+)-ATPase activity in its own environment and in a well defined cell population. The Na+,K(+)-ATPase activity can be regulated over a short term via guanidine triphosphate (GTP) dependent regulatory proteins. However the guanidine proteins are not directly coupled to the Na,K-pump and the mechanism involves the activation of complex intracellular signalling system. Locally produced dopamine induces a dose dependent inhibition of Na+,K+ ATPase activity. This inhibition is mediated by a complex mechanism that requires the activation of both membrane dopamine receptors, DA-1 and DA-2. It involves the activation of a pertussis toxin sensitive GTP-binding protein and activation of protein kinase C. A DA-2 agonist only inhibits Na+,K(+)-ATPase activity when it is incubated together with dibutyryl cAMP or Forskolin. We have therefore concluded that an increase in cellular cAMP levels plays a permissive role for DA-2 inhibition of Na+,K(+)-ATPase activity. A fully differentiated cell is required for dopamine inhibition of Na+,K(+)-ATPase activity. An abnormal regulation of proximal tubule Na+,K(+)-ATPase activity might be of importance in the pathogenesis of certain types of hypertension.
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PMID:Short-term regulation of Na+,K(+)-ATPase activity by dopamine. 216 34

By using the differential diagnosis of traditional Chinese medicine to determine the types of hypertension, using the diagnosis of western medicine (WM) to determine the phases of hypertension, 61 inpatients of Liver Yang exuberance type hypertension were randomly divided into Qigong group and WM group. The patients in the Qigong group were treated with both Qigong and antihypertensive drugs at low dosage, but those in the WM group were treated with the drugs alone. Several laboratory tests concerning sympathetico-adrenomedullary functions were conducted twice respectively at 1st and 9th week after hospitalization of the patients. The results indicated that the Qigong group after treatment of 9 weeks had more cases with normal sympathetico-adrenomedullary functions than it had before the treatment, and that their urinary CA, E, NE decreased, MHPG-SO4 increased, plasma cAMP and cGMP got down, but cAMP/cGMP ratio got up. It suggested that Qigong could modulate the sympathetico-adrenomedullary functions of patients with Liver Yang exuberance type hypertension.
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PMID:[Effect of qigong on sympathetico-adrenomedullary function in patients with liver yang exuberance hypertension]. 216 14

Pathological induced changes in beta-adrenoceptor function occur in diseases such as asthma and hypertension. The mechanism(s) of this dysfunction is at present unclear. In the present study, the effect of lymphokines on beta-adrenoceptor agonist induced cAMP production in peripheral blood mononuclear cells (PBMC) is investigated. Pre-incubation of PBMC during 20 h with interleukin-2 (IL-2, 100 u ml-1) and granulocyte/macrophage-colony stimulating factor (GM-CSF, 100 u ml-1) significantly decreases beta-adrenoceptor agonist induced cAMP production by 35 +/- 8% and 37 +/- 11% respectively. IL-3 and IL-4 do not affect beta-adrenoceptor agonist induced cAMP production in PBMC. It can be concluded that IL-2 and GM-CSF, mediators derived from T-lymphocytes, can induce beta-adrenoceptor dysfunction in PBMC.
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PMID:Effect of lymphokines on beta-adrenoceptor function of human peripheral blood mononuclear cells. 217 22

The correlation between serum calcium (S-Ca), plasma parathyroid hormone (P-PTH) and hypertension was determined in a population-based, cross-sectional study of carefully treated hypertensives (n = 391; diastolic blood pressure 90.2 mmHg; 57 years) compared with normotensive controls (n = 328; diastolic blood pressure 82.1 mmHg; 57 years). Levels of urinary cyclic-adenosinemonophosphate (U-cAMP), but not of plasma cAMP (P-cAMP), were higher (P less than 0.001) in hypertensives than in controls. This was the case regardless of the type of drug treatment and the blood pressure level that was reached. U-cAMP correlated with adrenaline in multivariate analyses. S-Ca levels were higher (P less than 0.001) and S-Mg levels were lower (P less than 0.001) in hypertensives than in controls. This was not explained by thiazide treatment. Thus, despite 'adequate' blood pressure reduction, substantial differences in S-Ca, S-Mg and U-cAMP still exist between hypertensives and normotensive controls.
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PMID:High urinary cAMP in hypertensives despite careful drug treatment--an epidemiological study from the Dalby population. 217 69

Prostacyclin (PGI2) is known to cause vasorelaxation and inhibit platelet aggregation by receptor-mediated mechanisms. While cyclic (c)AMP is known to act as a second messenger for platelet aggregation, vasorelaxation by hyperpolarization has been described only recently and may provide an explanation, in addition to stimulation of cAMP, for the PGI2 mechanism of action on blood vessels. When PGI2 is infused into healthy volunteers it reduces blood pressure only at infusion rates that also cause significant side effects, primarily nausea, emesis, flushing, diphoresis and restlessness. In hypertensive patients blood pressure responses are complex and are influenced to some extent by secretion. PGI2 stimulates renin secretion by a direct effect on the juxtaglomerular apparatus, and also has an indirect effect by activating the sympathetic nervous system. Thus it is useless as an antihypertensive agent even apart from its debilitating side effects. Vascular PGI2 is synthesized endogenously by both the endothelial cells and the muscularis of arteries. While the endothelial cells undoubtedly synthesize larger amounts of PGI2, the muscularis comprises a much larger tissue mass so that the overall synthesis is about equally distributed between the endothelial and muscle cells. In patients with pregnancy-induced hypertension and some patients with essential hypertension, endogenous synthesis of PGI2 has been evaluated by measuring 2,3-dinor-6-keto-PGF1 alpha and has proved to be defective. Some drugs (cicletanine, thiazides, propranolol) have been shown to stimulate PGI2 synthesis, and inhibition of cyclooxygenase has been shown to abolish their antihypertensive effects. Whether stimulation of PGI2 synthesis affects the antihypertensive efficacy of these drugs is not yet known.
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PMID:Prostacyclin in hypertension. 225 88

To investigate whether altered renal medullary prostaglandin (PG) synthesis is involved in the development of hypertension in spontaneously hypertensive rats (SHR), we compared the capacity of PGE2 synthesis in cultured renal papillary collecting tubule cells from young (4-week-old) and aged (16-week-old) SHR and control Wistar-Kyoto rats (WKY). Basal levels of PGE2 synthesis were lower in young SHR cells than in WKY cells (p less than 0.001). Arachidonic acid-stimulated PGE2 synthesis, however, had a slight tendency to be higher in SHR cells than in WKY cells. Bradykinin- and A23187-stimulated PGE2 synthesis were similar in both strains. Basal levels of cyclic AMP were also lower in young SHR cells than in WKY cells (p less than 0.001), but the cAMP response to exogenous PGE2 was equal between the strains. In papillary collecting tubule cells from aged rats, basal levels of PGE2 and cyclic AMP as corrected for cellular protein were significantly lower than those in young rats, but there was no difference between the strains. Urinary excretion of PGE2 and thromboxane B2 was equal in aged SHR and WKY. These results suggest that papillary collecting tubule of young SHR and WKY may differ in the metabolism of PGE2 and cyclic AMP. This difference may be attributed to the possible defect in arachidonate availability in SHR.
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PMID:PGE2 synthesis in cultured renal papillary collecting tubule cells from young and aged spontaneously hypertensive rats. 248 50

In recent years abnormalities of calcium metabolism have been described in human hypertension. In this study, the relationships between indices of calcium metabolism and the renin-aldosterone system were studied in 39 subjects with untreated essential hypertension. No significant associations were found between the major determinants of calcium metabolism (plasma ionised calcium, parathyroid hormone and 1,25(OH)2-vitamin D) and the renin-aldosterone system. Serum magnesium was, however, positively correlated to plasma renin activity (PRA) (r = 0.38, P less than 0.05) while both 24 h urinary excretion of calcium and cAMP were found to be correlated to both PRA and urinary aldosterone in a positive way (r = 0.39-0.42, P less than 0.01 and r = 0.33-0.57, P less than 0.01, respectively). In this study there was no other evidence of any major influence of the renin-aldosterone status on the calcium balance in human hypertension. The urinary leak of calcium might be determined by the action of the renin-aldosterone system.
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PMID:An association between mineral metabolism and the renin-aldosterone system in human hypertension. 254 51

Various abnormalities in platelet metabolism, including increased sensitivity to several aggregating agents, have been described in essential hypertension. Platelet response is controlled by Ca2+ and cyclic AMP-dependent mechanisms (stimulatory and inhibitory, respectively) which oppose one another. In the present study, the cyclic AMP contents of unstimulated platelets were measured by radio-immunoassay and observed to be lower in hypertensive than in normotensive subjects, either in the basal state or after prostaglandin E1 (PGE1) stimulation. In the presence of 7-bromo-1,5,dihydro-3,6-dimethylimidazo [2,1-b] quinazolin-2(3H)-one (Ro 15-2041), a specific inhibitor of phosphodiesterase, the increases in cyclic AMP content were similar in platelets from both groups, indicating that this enzyme was not responsible for the alterations in cyclic AMP metabolism observed in hypertension. Low external Ca2+ reduced basal and PGE1-stimulated cyclic AMP content in both normotensive and hypertensive groups but cyclic AMP levels remained lower in hypertensive patients than in normotensive subjects, indicating that Ca2+ influx is not responsible for this altered metabolism of cyclic AMP in hypertension. These data suggest that the reduced platelet cAMP content may participate in the hyperreactivity to various aggregating agents previously reported to accompany essential hypertension.
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PMID:Platelet cyclic AMP in essential hypertension. 255 May 42

Essential hypertension is accompanied by several modifications to platelet metabolism suggesting hyper-reactivity to various aggregating agents. As the platelet response is mediated by both cytosolic free calcium, which is stimulatory, and cyclic (c)AMP, which is inhibitory, this hyper-reactivity may be caused by a modification in cAMP metabolism. We therefore determined cAMP in unstimulated platelets from 19 patients with essential hypertension and 27 age-matched normotensive subjects, nine with and 19 without a family history of hypertension. The platelet cAMP content was reduced in the essential hypertensives and in the normotensives with a positive family history by 37.5% and 42%, respectively (P less than 0.001 for both). Platelet cAMP was inversely correlated with diastolic blood pressure (P = 0.036). After prostaglandin (PG) E1 stimulation, the platelet cAMP content remained lower in the patients with essential hypertension than in the normotensive subjects, whatever their hypertensive heredity. The rises in cAMP caused by inhibition of phosphodiesterase by 7-bromo-1,5-dihydro-3,6-dimethylimidazo-[2,1-b]quinazolin-2[ 3H]-one (Ro 15-2041) were similar in the three groups. These results indicate that cAMP, the platelet inhibitory messenger, is reduced in hypertensive patients and in their normotensive offspring and may affect the various platelet abnormalities previously described in this disease.
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PMID:Platelet cyclic AMP in essential hypertensive and normotensive offspring. 256 Nov 37

In order to study the nature of Liver Yang Exuberance Syndrome (LYES), and find new effective drug prescription to treat diseases with the syndrome, the authors chose 97 cases with LYES of hypertension, climacteric syndrome and hyperthyroidism. A clinical study was carried out on different diseases with the syndrome including the stagnancy of Liver Qi, excess of Liver Wind and rising of Liver Fire with a new prescription according to TCM theory. While another 83 cases with Yin Deficiency Yang Excess Syndrome (YDYES) of the same three diseases were employed as control group. The results showed that their total effective rates were 81.4% (in lowering blood pressure), 100% and 88.9% respectively. The marked effective rate of LYES of hypertension group was significantly higher than that of the control group (P less than 0.05), which showed the special characteristics of the TCM syndrome. Before and after treatment, the patients with LYES of the three diseases were examined in certain laboratory tests including function of autonomic nervous system, urinary MHPG-SO4, CA, plasma cAMP and TXB2, 6-keto-PGF1 alpha etc. The similar changes were found in different diseases with the same syndrome. The laboratory results of the cases got markedly improved with the improvement of their symptoms, which showed that these tests had active significance for comprehending the nature of LYES.
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PMID:[Clinical study on "liver yang exuberance syndrome"]. 276 20


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