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Query: UMLS:C0085580 (essential hypertension)
14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma renin activity and the relationship of renin activity and sodium excretion were analyzed in 50 untreated essential hypertensives classified according to their erythrocyte Na+ transport abnormalities. Renin activity was inappropriately high in 7 patients with increased activity of Na+,Li+ countertransport, inappropriately low in 12 patients with decreased activity of Na+,K+,Cl- cotransport and normal in 31 patients without either Na+ transport abnormalities. These results suggest that there are correspondences between the activity of the renin-angiotensin system and the main Na+ transport abnormalities present in erythrocytes of patients with essential hypertension.
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PMID:Correspondences between the activity of the renin-angiotensin system and the erythrocyte Na+ transport abnormalities in hypertension. 219 Jun 10

To block the renin-substrate reaction by immunological tools is a long-standing dream. Since 1951 active immunization and the passive transfer of antirenin antisera have been successfully carried out in different species and in different experimental models of hypertension and normotension. These studies indicated that renin is a powerful immunogenic protein, capable of breaking down self-tolerance in different species. In this initial period the most significant results were obtained with hog renin. Passive transfer of antisera raised against hog renin or active immunization with hog renin was able to decrease blood pressure in renovascular or essential hypertension in dogs. Renin was semipurified and injected without adjuvant, however, since there was no method for determining plasma renin activity. Recently, complete purification of murine and human renin has allowed an extension of this approach, using the passive transfer of antirenin polyclonal antisera or monoclonal antibodies. Active immunization against pure human renin was successful in normotensive marmosets. This immunization with a nearly homologous renin in a primate model induced a significant decrease in blood pressure, associated with a complete disappearance of plasma renin activity. Unfortunately this powerful immunization was associated with an autoimmune disease that is specific for the kidney, related to self-recognition of the production site of renin by antibodies and lymphocytes. Similar results were reported with the use of mouse submandibular gland renin as an immunogen in spontaneously hypertensive rats (SHR). This manipulation decreased blood pressure in SHR to a level near that of normotensive Wistar-Kyoto control rats. However, again the animals showed a severe autoimmune disease of the kidney.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunological approach to blockade of the renin-substrate reaction. 266 16

Renin plays a major role in the control of blood pressure and water and electrolyte metabolism and it is clear that blocking of this system is particularly effective in the treatment of essential hypertension and heart failure. A large number of converting enzyme inhibitors have been synthesized. Converting enzyme inhibitors are remarkably active in heart failure and they reduce microalbuminuria and possibly maintain glomerular function. Blocking of the renin-angiotensin system by converting enzyme inhibitors is not accompanied by hypotension or reflex stimulation of the sympathetic nervous system. Converting enzyme inhibitors represent a major therapeutic advance in the field of cardiovascular and renal disease but the long-term effects of decreased angiotensin II levels are unknown. There are other ways to inhibit the renin-angiotensin system. The recent discovery of orally-active non-peptide angiotensin II antagonists opens a range of fascinating prospects. Another approach consists in inhibiting the reaction of renin on angiotensinogen, which is remarkably selective. Although it is too early to know whether these new approaches will be less active, more active or as active as current converting enzyme inhibitors, they may constitute a progress in relation to currently available treatments.
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PMID:New therapeutic prospects of renin-angiotensin system inhibition. 269 Nov 25

Authors studied effect of captopril on serum kininogen and prekallikrein concentrations, as well as on plasma renin activity (PRA) in patients with primary hypertension. The control group consisted of 18 healthy persons, 5 patients were in I, 12 in II and 8 in III WHO class. Monotherapy with 150 mg per day of captopril had been performed for 3 weeks. Patients were 3 times examined: 1--before therapy, 2--after 24 hours of treatment, 3--after 3 weeks of captopril therapy. It was proved, that captopril lowers arterial pressure with coexisting PRA increase and induces changes in kinins system such as: decrease of kininogen+ concentration and increase of serum prekallikrein level in comparison with their pretreatment values. Maximum PRA increase and blood pressure decrease were observed after 24 hours of captopril administration, whereas changes in kinins system were taking place during the whole observation period. Presented studies indicate that antihypertensive action of captopril is related to Renin-Angiotensin-Aldosterone System as well as to plasma kinins one.
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PMID:[Effect of captopril on various components of the kinin system and plasma renin activity in patients with idiopathic arterial hypertension]. 269 82

We have identified a subgroup of patients with aldosterone-producing adenoma (APA) who are responsive to angiotensin. Thus, a fall in plasma aldosterone (PA) during saline infusion may cause confusion with low-renin essential hypertension. Responsiveness of PA to angiotensin infusion and to upright posture may cause confusion with bilateral hyperplasia. Renin levels were not as completely suppressed in this angiotensin-responsive subgroup, leading to speculation that non-tumorous adrenal glomerulosa might also be less suppressed and might respond to angiotensin. This is unlikely, since angiotensin infusion soon after removal of the adenoma produced aldosterone levels of less than 10% of those achieved preoperatively. A biosynthetic peculiarity of the tumours is more likely, since urinary 18-oxo-cortisol levels were normal in this subgroup (as in bilateral hyperplasia) and raised in the more typical angiotensin-unresponsive subgroup (as in glucocorticoid-suppressible hyperaldosteronism). Since angiotensin-responsive tumours respond just as well to surgery as angiotensin-unresponsive tumours, it is important not to misdiagnose this subgroup as bilateral hyperplasia or low-renin essential hypertension.
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PMID:Angiotensin-responsive aldosterone-producing adenoma masquerades as idiopathic hyperaldosteronism (IHA: adrenal hyperplasia) or low-renin essential hypertension. 283 71

The genetic basis of primary hypertension is not known. Renin is important in blood pressure and volume control and a HindIII restriction fragment length polymorphism (RFLP) is present within the human renin gene locus. To examine whether there is a relationship between this RFLP and primary hypertension, DNA and renin analyses were performed on leukocytes and plasma from hypertensive and normotensive individuals. In hypertensives the frequencies of alleles for the HindIII RFLP were found to be 0.55 and 0.45, compared with 0.60 and 0.40 in the total population of 231 subjects examined, a difference that was not statistically significant. There also appeared to be no significant difference in renin activity in plasma for hypertensive patients of each genotype, nor in their pre- or post-treatment blood pressures. We thus conclude that, within the limits of the present study, the suspected genetic abnormalities associated with primary hypertension in man do not appear to be related to a HindIII RFLP in the renin gene.
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PMID:Frequency in hypertensives of alleles for a RFLP associated with the renin gene. 289 88

Isradipine (Sandoz PN 200-110), a new dihydropyridine calcium channel antagonist, was evaluated in a randomized, double-blind, placebo-controlled trial for antihypertensive efficacy in 24 patients with essential hypertension. Two groups were studied: one received placebo throughout the entire study (n = 12) and the other received isradipine (n = 12), 2.5 mg b.i.d., for the first week, 5 mg b.i.d. the second week, and 10 mg b.i.d. the third week after an initial 3-week baseline placebo period. Blood pressure was measured approximately 3 hours after dosing. Isradipine, at a total daily dose of 10 mg, lowered average supine diastolic blood pressure 11.8 mm Hg, with only a 3.5 mm Hg decrease in systolic blood pressure compared with baseline. At a total daily dose of 20 mg, average supine diastolic blood pressure decreased 14.8 mm Hg and supine systolic blood pressure declined 13.9 mm Hg; both were significantly decreased compared with placebo or baseline. Heart rate was increased only minimally by isradipine. Renin level activity was increased slightly by isradipine. No serious adverse clinical or laboratory experiences were noted. Isradipine appears to be effective in lowering blood pressure without reflex tachycardia.
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PMID:Antihypertensive activity of isradipine in humans: a new dihydropyridine calcium channel antagonist. 294 7

Aldosterone concentration and renin activity in the blood from the ulnar, inferior cava veins at the level of the 12th thoracic vertebra, the left and right renal veins were studied in 60 patients with arterial hypertension by means of a radioimmunoassay kit (France). The patients were divided into 4 groups: with primary and idiopathic hyperaldosteronism, renal-parenchymatous and essential arterial hypertension. A significant increase in aldosterone concentration in the blood from the ulnar vein was detected in all the groups, especially in primary and idiopathic hyperaldosteronism. Hyperaldosteronism in the patients with renal-parenchymatous and essential arterial hypertension was regarded as secondary in a stable and malignant course of arterial hypertension. The diagnosis of primary and idiopathic hyperaldosteronism was also confirmed by low blood renin activity. Renin activity in the peripheral venous blood was considerably elevated in renal-parenchymatous arterial hypertension and was within normal in essential hypertension. Aldosterone concentration in the blood from the vena cava inferior and renal veins was 1.6-2-fold as high on the affected side as on the contralateral one.
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PMID:[Radioimmunologic determination of aldosterone and renin in the blood in the diagnosis of different forms of arterial hypertension]. 330 85

Forty hypertensive patients were studied to examine the assumption that the angiotensin pressor dose reflects endogenous renin activity. Peripheral renin activity was assayed by the method of Boucher et al.(4) Sensitivity to the infusion of synthetic angiotensin II was determined as suggested by Kaplan and Silah.(1)Sixteen patients with essential hypertension with normal renal angiography required 3.8 ng. angiotensin/kg./min. to raise the diastolic pressure 20 mm. Hg. All but one were sensitive to angiotensin infusion of less than 5 ng./kg./min. Renin activity was normal in all except in one sensitive subject. Angiotensin infusion response and mean renin activity in 13 patients with essential hypertension with abnormal renal angiography were similar to that of the first group. The pressor dose in 11 renovascular hypertensives was 9.8 ng./kg./min. All but three had elevated plasma renin activity.OUR RESULTS SUGGEST THAT: (1) the angiotensin infusion test is suitable for differentiating patients with true renovascular hypertension from those with essential hypertension with or without associated renal artery disease; (2) the angiotensin pressor dose correlates with the level of peripheral venous renin activity (p < 0.01).
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PMID:The angiotensin infusion test and peripheral venous renin activity. 429 Aug 36

Renin profiling stimulated research into the pathophysiology of essential hypertension and influenced the development of antihypertensive treatment strategies. Patients with a high renin value and usually younger age respond better to drugs that interfere with the renin-angiotensin system, that is, beta blockers or converting enzyme inhibitors. Patients with a low renin value and often older age respond better to calcium entry blockers or diuretics. Patients with normal renin levels exhibit mixed but, on average, equal responses to these types of drugs. A pathophysiology-oriented antihypertensive treatment strategy is proposed in which beta blockers or converting enzyme inhibitors are used as one and calcium entry blockers--in the place of diuretics when possible--as the other baseline drug, and this approach may provide a cardiac-protective effect.
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PMID:Renin profiling to select antihypertensive baseline drugs. Renin inhibitors for high-renin and calcium entry blockers for low-renin patients. 614 11


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