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

The relationship between blood pressure (BP) and the renin-angiotensin-aldosterone system was studied in a stratified random sample (n=120) of 49-year-old men selected from a BP screening and covering a wide range of BPs. Only subjects not on antihypertensive treatment were included. None had malignant or secondary hypertension. Plasma renin activity, plasma concentrations of angiotensin II, aldosterone, sodium, potassium and noradrenaline and the 24-hour urinary excretions of sodium, cortisol and noradrenaline were determined. Of these variables, only p-aldosterone was significantly correlated wtih BP, both in the whole study group (R=0.22, p less than 0.02, n=119) and in the subjects with the highest BP range (R=0.36, p less than 0.02, n=30). Of the clinical groups compared, the hypertensive subjects had significantly higher mean p-aldosterone than the borderline and normotensive subjects. Multiple regression analysis showed that the 24-hour urinary excretion of noradrenaline was the factor most strongly correlated to p-aldosterone, suggesting that the sympathetic nervous system might stimulate aldosterone secretion. Our findings indicate that aldosterone may be of importance for the development and maintenance of essential hypertension.
 ...
PMID:Blood pressure in relation to the renin-angiotensin-aldosterone system. 705 60

Primary and secondary hypertension differ with regard to circadian blood pressure (BP) profiles. To evaluate the contribution of the renin-angiotensin system (RAS) to circadian BP regulation, we studied cardiovascular effects of the angiotensin II (AII) receptor antagonist losartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril in animal models of primary and secondary hypertension after morning and evening dosing. Systolic/diastolic BP (SBP/DBP) and heart rate (HR) were measured telemetrically in spontaneously hypertensive rats (SHR) and transgenic hypertensive rats (TGR[mRen-2]27). Losartan (0.3 to 30 mg/kg) or enalapril maleate (10 mg/kg) were injected intraperitoneally (i.p.) either at 0700 or 1900 h. Baseline SBP/DBP and HR showed significant circadian rhythmicity in both strains. The 24-h means in SBP/DBP were 190/127 mm Hg in SHR and 200/139 mm Hg in TGR. TGR showed a reversed circadian profile in BP, with peaks occurring during the daily resting period, whereas HR peaked at night. Losartan reduced BP dose dependently; reductions in TGR were significantly greater and obtained at 30-fold lower doses than in SHR. Maximum decreases induced by losartan were similar to those induced with enalapril 10 mg/kg. Both drugs reduced BP in TGR more effectively when applied at 0700 than at 1900 h, resulting in a normalized circadian BP profile. Our results demonstrate that the RAS is involved in both the pathomechanism of hypertension and in the inverse circadian BP pressure pattern in TGR.
 ...
PMID:Effects of the angiotensin II receptor antagonist losartan on 24-hour blood pressure profiles of primary and secondary hypertensive rats. 747 45

Liddle's syndrome, a rare cause of hypokalemic hypertension, is characterized by a renal tubular sodium channel defect resulting in excessive sodium absorption and concomitant potassium wasting. In this disorder, although the clinical manifestations resemble primary aldosteronism, serum and urine aldosterone are suppressed. The syndrome is transmitted in an autosomal dominant pattern. It has been reported previously in white and oriental populations but not in the black individuals. We identified four patients (two of whom are black) in our nephrology clinic, with severe hypokalemic hypertension not correctly diagnosed for several years. All patients underwent an extensive work-up for secondary hypertension because of persistent severe hypertension (average blood pressure, 210/130 mm Hg) despite high-dose multi-drug therapy. Primary aldosteronism was excluded because of low serum aldosterone. Cushing's syndrome, pheochromocytoma, renal artery stenosis, and enzymatic deficiencies of cortisol synthesis (11 beta-hydroxylase, 17 alpha-hydroxylase, 5 beta-reductase, and 11 beta-hydroxysteroid dehydrogenase) were ruled out with extensive endocrine and radiologic studies. Once the diagnosis of Liddle's syndrome was suspected, all patients were treated with either triamterene or ameloride, with resolution of hypokalemia and correction of hypertension occurring within 5 to 7 days. Our findings suggest that Liddle's syndrome can occur in the black population. Although the actual incidence of this syndrome remains unknown, it may be significantly more common than we are led to believe since it is inherited in a Mendelian pattern. Whether there is a subset of low-renin, salt-sensitive black hypertensive patients who have the same or similar sodium channel defect remains to be elucidated.
 ...
PMID:Liddle's syndrome, an underrecognized entity: a report of four cases, including the first report in black individuals. 777 90

Renal parenchymal disease is the most common cause of secondary hypertension, accounting for 2.5% to 5.0% of all cases. Hypertension associated with renal parenchymal disease occurs as a complication of a wide variety of glomerular and interstitial renal diseases and may accelerate the decline in renal function if inadequately controlled. Renal parenchymal hypertension most probably represents the combined interactions of multiple independent mechanisms: potential factors include impaired sodium handling leading to volume expansion, perturbations of the renin-angiotensin system, alterations in endogenous vasodepressor compounds, and possibly increased activity of vasoactive substances. The past several years have witnessed newer insights into both the pathophysiology and the therapeutics of this disorder. The characterization of endothelin and the nitric oxide (NO)-arginine pathway and their roles in biology and medicine has provided additional new insights with regard to the pathogenesis of hypertension in renal parenchymal disease. For example, methylated L-arginine derivatives that possess NO synthase inhibitor capabilities including NG-N-dimethylarginine and N-monomethyl-L-arginine are found in human plasma and in urine. Patients with chronic uremia have impaired elimination of these compounds, and circulating concentrations of these compounds may increase sufficiently to result in inhibition of NO production. Thus, accumulation of endogenous NO synthase inhibitors might contribute to the hypertension of advanced renal failure. Similarly, it has been proposed that increased endothelium-derived endothelin that results from hypertensive injury to vascular endothelium could lead to further vasoconstriction and worsening of hypertension. Additional insight into this fascinating problem must await further biochemical characterization of some of the mediators and a more precise delineation of their pathophysiological role.
 ...
PMID:Renal parenchymal disease and hypertension. 777 24

Renovascular hypertension is one of the more common causes of secondary hypertension. The true prevalence of this condition is not known, because only a selected few with hypertension are considered for thorough diagnostic work-up. The higher incidence figures come from centers with a special interest in this disease. The ability of a clinician to detect renovascular hypertension has improved substantially, thanks to the advances in radiology. The predominant mechanism of blood pressure elevation from renal ischemia is activation of the renin-angiotensin system. Clinically, the pathological lesions that cause renal artery stenosis are atherosclerosis and fibromuscular dysplasia; the former is typically seen in older men, and the latter is typically found in young women. Suspicion of the presence of renovascular disease should prompt the physician to obtain appropriate screening and confirmatory tests. Once diagnosed, the management of patients with renovascular hypertension requires a carefully planned multidisciplinary approach to offer the patient a best possible therapeutic option, with surgical revascularization or balloon angioplasty, or chronic medical therapy. However, these options are not mutually exclusive. The best long-term results are obtained with surgical therapy. Although balloon angioplasty is being increasingly used perhaps as the preferred initial therapeutic procedure for many patients with renal artery stenosis, long-term results comparable with surgery are not yet available. The ideal rational therapy for patients with renal artery stenosis is reperfusion of the ischemic kidney either by surgical correction or by balloon dilation. The aim is not only to improve the blood pressure control, but also to prevent and at times to reverse renal failure. Although effective antihypertensive drugs have become available, the role of medical management of renovascular hypertension is shrinking and should be limited to patients who have contraindications to or unwilling to undergo corrective procedures to relieve renal ischemia.
 ...
PMID:Renovascular hypertension. 777 25

A 30-y-old female presented with a history of hypertension and a modest degree of hyperkalemia. There was a mild degree of contraction of her ECF volume on clinical examination, with elevated levels of renin and aldosterone in plasma. No causes for secondary hypertension were found. Laboratory investigations revealed a slightly reduced glomerular filtration rate (GFR) and a subnormal kaliuretic response to exogenous mineralocorticoids. When a further degree of ECF volume contraction was induced, she was unable to conserve Na+ and Cl- appropriately. Moreover, expansion of the ECF volume led to a significant suppression of the levels of both renin and aldosterone in plasma. We speculate that these findings could be explained by a diminished net rate of reabsorption of Na+ in the cortical collecting duct. Such a reduction could lead to a diminished generation of an electrical gradient to favour the net secretion of K+ and lead to hyperkalemia with renal salt wasting. The resultant contraction of the extracellular fluid volume with the release of renin and aldosterone (and probably other vasoactive hormones) might have predisposed her to hypertension. This hypothesis was supported by the finding that NaCl supplements led to a significant drop in her blood pressure. This case could represent a new syndrome of hyperkalemia and "salt sensitive" hypertension.
 ...
PMID:Hyperkalemia with mild ECF volume contraction: studies to provide a possible physiologic interpretation. 786 45

Clinician questions in nephrovascular hypertension are: 1) Is hypertension secondary to nephrovascular disease? 2) Is vascular obstruction susceptible of surgical management? 3) Which is the best technical approach? In this review of recent international literature we have focused diagnostic value of echo-color Doppler in the screening of patients with secondary hypertension. The sensibility and specificity of this diagnostic test reach 89% and 99.5%. Respectively when the stenosis is over 70%. Anyway when the stenosis is under 70% the accuracy of this examination is lower. Angiography remains the gold standard test in patient eligible for surgery, although its invasiveness. Diagnostic tests of the renin-angiotensin axis (e.g. Captopril test) are useful too, but morphologic evidence is not provided. Surgical approach is the best choice in elective patients.
 ...
PMID:[The clinician's need in renovascular hypertension]. 788 60

Hypertension secondary to an activated renin-angiotensin system without renal artery stenosis can be detected by angiotensin-converting enzyme (ACE) inhibitor renography. Two cases of renin-mediated hypertension without major or branch vessel stenosis supplying the kidney with parenchymatous disease were discovered by ACE inhibitor renography.
 ...
PMID:Renin-dependent renal parenchymatous hypertension detected by angiotensin-converting enzyme inhibitor renography. 826 28

The usefulness of the captopril test as a simultaneous screening method for primary aldosteronism (PA) and renovascular hypertension (RVH) was evaluated in 111 patients with essential hypertension, and in 79 patients with secondary hypertension, which included 16 patients with PA and 18 with RVH. Plasma renin activity (PRA, ng/mL/h) and plasma aldosterone concentration (PAC, ng/dL) were determined before and 90 min after administration of 50 mg of captopril in the supine position on a normal NaCl diet. A cutoff point or a discriminant function in the screening was determined by discriminant analysis. A quadratic discriminant function of PRA and PAC after the captopril test identified patients with PA with a false negative rate of 6.3% (1/16), and a false positive rate of 0.6% (1/174) which was significantly lower than that of 3.4% at the basal state (P < .05). In the screening for RVH, the criterion of a postcaptopril PRA of greater than 10.6 ng/mL/h had a false negative rate of 5.6% (1/18) and a false positive rate of 15.1% (26/172). This false positive rate was also significantly lower than that using a criterion for precaptopril PRA of 2.21 ng/mL/h (P < .05). Accordingly, the captopril test was a useful method in the simultaneous screening for PA and RVH, and it may be particularly applicable in specialized hypertension clinics.
 ...
PMID:The usefulness of the captopril test as a simultaneous screening for primary aldosteronism and renovascular hypertension. 830 62

Automatic, around-the-clock blood pressure measurements have increased our understanding of hypertension in humans. Patients with essential hypertension display patterns similar to those observed in normotensive subjects, whereas those with secondary hypertension frequently show abnormal circadian rhythms characterized by a failure to reduce blood pressure at night. We have modeled this situation in rats. Normotensive Wistar-Kyoto and Sprague-Dawley rats, spontaneously hypertensive rats, and rats made hypertensive by transgenic implantation of the mouse salivary gland renin gene (TGR[mRen-2]27) underwent chronic implantation of a device that telemetrically monitored their blood pressures, heart rates, and motor activities. In either normotensive or hypertensive rats, motor activity peaked during the dark phase, indicating that animals from all strains were nocturnal. In both normotensive and spontaneously hypertensive rats, the 24-hour blood pressure and heart rate profiles showed peak values during the rats' active phase at night, ie, between midnight and 3 AM. In the transgenic rats, on the other hand, blood pressure values were at maximum during the day around noon, when the rats were in their resting phase. The heart rate of the transgenic rats nevertheless still peaked around midnight. These data suggest that normotensive rats and those with primary and secondary hypertension display circadian rhythms of blood pressure and heart rate analogous to those observed in normotensive and primary or secondary hypertensive humans, respectively. The TGR(mRen-2)27 strain may be a useful model with which to investigate the mechanisms responsible for alterations in circadian rhythms of blood pressure and heart rate in forms of secondary hypertension.
 ...
PMID:Circadian blood pressure variation in transgenic hypertensive rats. 831 99


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>