Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the interaction between the renin angiotensin aldosterone system and the renal prostaglandin (PG), urinary excretion of PGE, urinary excretion of main urinary metabolite (MUM) of PGF2a, urinary excretion of aldosterone, and plasma renin activity were measured before and after infusion of 1-Sar-8-Ile-Angiotensin II, a specific competitive inhibitor of angiotensin II, in 18 patients with essential hypertension under normal and low sodium diets. The values of urinary sodium excretion in these patients before the infusion of the peptide were 160.8 +/- 13.3 and 27.0 +/- 2.7 mEq per day on normal and low sodium diet, respectively. On normal sodium diet, urinary excretion of PGE was found to correlate with the level of plasma renin activity before the infusion (r = 0.6977, p less than 0.01), and it was decreased slightly from 0.37 +/- 0.05 ng/min to 0.26 +/- 0.04 ng/min after the infusion of the antagonist. On low sodium diet, urinary excretion of PGE was not significantly changed by the infusion of the peptide and showed no correlation with the level of plasma renin activity before the infusion, while urinary excretion of PGE showed a significant correlation with the excretion of urinary aldosterone (r = 0.6719, p less than 0.02). Excretion of PGF2aMUM decreased after the infusion of this peptide on both sodium diets, but the changes were not statistically significant. The present data suggest that angiotensin II influences the synthesis or release of renal PG in patients with essential hypertension on normal sodium diet, but not when they are on low sodium diet.
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PMID:Effects of 1-Sar-8-Ile-angiotensin II on urinary prostaglandin excretion in patients with essential hypertension. 60 75

Eighteen patients with advanced or malignant hypertension due to essential hypertension, systemic lupus erythematosus or chronic glomerulonephritis were infused intravenously with 1-Sar-8-Ile-Angiotensin II, a competitive antagonist of aniotensin II. The spectrum of responses was broad from a mild elevation to a marked fall in blood pressure. The changes in mean blood pressure caused by this peptide showed a significant correlation with the level of peripheral plasma renin activity immediately before the infusion (r=0.5652, p less than 0.02). This peptide infusion reduced blood pressre in 12 patients (responders), but not in 6 (non-respnders). There were no differences with age, sex and severity of hypertension except for the level of peripheral plasma renin activity between the two groups. Our retrospective study showed that in 12 responders propranolol reduced blood pressure to near the normal level, while in 6 non-responders furosemide induced similar depressor response. It is concluded that the vasodepressor effect of this peptide correlates with the levels of peripheral plasma renin activity and that the responses to this drug can be used as a guide for the selection of effective antihypertensive drugs.
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PMID:Clinical evaluation of angiotensin II antagonist in advanced hypertension. 88 41

The range of arterial pressures in non-pregnant women between the ages of 15 and 44 years in Ile-Ife, Western Nigeria, has been determined from a randomly selected group of 626 women. The survey showed a low range of arterial pressures in the women. Blood pressures within the group showed a tendency to rise with age except in those who were aged 40 to 44 years, where the small numbers may have yielded the unexpected lower arterial pressure levels. Parity did not seem to have exerted any clear influence on the blood pressures of the subjects. The exception is in the age group 30 to 34 years where increasing parity was associated with a lower systolic blood pressure. The results of the survey suggested that essential hypertension and chronic renal disease were not likely to be significant factors in the high incidence of pre-eclampsia and eclampsia in the community.
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PMID:Arterial pressures in non-pregnant women of child-bearing age in Ile-Ife, Nigeria. 95 82

The pharmacological effects of 1-Sar-8-Ile-angiotensin II on blood pressure and plasma renin activity (PRA) were studied in 5 normal subjects and in 19 patients with hypertension of various etiologics including malignant hypertension, renovascular hypertension, essential hypertension, and primary aldosteronism. Intravenous administration of this peptide induced a significant pressor response in normal or low PRA subjects at infusion rates of 100-600 ng/kg/min. Similar pressor response was also observed in renovascular hypertensives with normal PRA who were cured later by surgical treatment. The blood pressure in high PRA group was lowered remarkably by infusion of this angiotensin II inhibitor. A significant increase in PRA was obtained in subjects with malignant hypertension following the infusion of this peptide. However, there was no detectable rise in PRA in other subjects with normal or high PRA. The present data show that circulating angiotensin II plays an important role in maintaining high blood pressure in high PRA patients, especially in malignant hypertension, while it is not directly involved in the maintenance of high blood pressure in human chronic renovascular hypertension.
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PMID:Effects of 1-sarcosine-8-isoleucine-angiotensin II on blood pressure and plasma renin activity in various types of hypertension. 117 25

L-2H-Leu, L-2H-Val, L-2H-Ile, L-2H-Phe, 14N-Lys were chosen for comparing their metabolic kinetic variables among those with prominent genetic predisposition of essential hypertension (FH*, 10 subjects), of stroke (FS*, 12 subjects) and those without (F-, 12 subjects) groups by gas chromatography-mass spectrometry. Results showed that only the metabolic kinetics of phenylalanine was dearranged: (1) The plasma pools of FH* and FS* groups were enlarged; (2) The turnover rate constant between plasma pool and cell pool of FH* was constricted; (3) The cell pool of FH* was larger, while the turnover rate constant was smaller than that of FS* group. The aberration of phenylalanine metabolism in essential hypertension and stroke might relate with hyperfunction of sympathetic nervous activity genetically. These diseases possibly belong to the category related to the inherited amino-acid metabolic aberration.
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PMID:[Inherited metabolic aberration of phenylalanine in the family members of patients with essential hypertension and stroke]. 165 82

1. We carried out investigations on specific atrial natriuretic peptide (ANP) and angiotensin II (ANG) binding sites in capillaries isolated from the cerebral cortex of spontaneously hypertensive rats (SHR), an animal model of human essential hypertension, and also from Wistar Kyoto rats (WKY). 2. In an equilibrium binding study done in the presence of increasing concentrations of the radiolabeled ligands, the binding of 125I-rat alpha-ANP (1-28) [ANF-(99-126)] (125I-rANP) and 125I-ANG (5-L-isoleucine) (125I-ANG) to the cerebral capillaries was single and of a high affinity. 3. The maximum binding capacity (Bmax) and dissociation constant (Kd) in the 125I-rANP binding of 20-week-old, hypertensive SHR was significantly lower than in age-matched, normotensive WKY. Conversely, a significant increase in the Bmax of 125I-ANG binding of adult SHR was observed, with a significant decrease in the Kd. 4. There was no differences in the Bmax of 125I-rANP and 125I-ANG binding between 4-week-old, prehypertensive SHR and age-matched WKY. However, there was a significant decrease in the Kd of 125I-rANP binding of SHR. 5. As a dramatic change in the binding kinetics of 125I-rANP and 125I-ANG was noted in the cerebral capillaries of adult sustained-hypertensive SHR, the possibility that ANP and ANG play a role in the etiology of dysfunction of the blood-brain barrier complicated with hypertension, by interacting with specific receptors, would have to be considered.
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PMID:Atrial natriuretic peptide and angiotensin II binding sites in cerebral capillaries of spontaneously hypertensive rats. 252 58

We examined the time course and extent to which central and peripheral mechanisms contribute to the short-term effects of a 500-mg oral dose of alpha-methyldopa on supine mean arterial pressure, cardiac output, and total peripheral resistance, as well as its effects on total urinary excretion of norepinephrine and its metabolites, in five subjects with essential hypertension. Total peripheral resistance was reduced significantly 1 hour after alpha-methyldopa administration and remained so for the ensuing 7 hours of the study (p less than 0.05). A small but significant reduction in mean arterial pressure occurred 7 hours after the dose (p less than 0.05), while cardiac output did not change significantly. Total 24-hour urinary norepinephrine and metabolite excretion was reduced by 8.1 mumol (35% compared with placebo). The relative distribution of urinary norepinephrine metabolites was unaffected by alpha-methyldopa, and the catecholamine metabolites of alpha-methyldopa, alpha-methylnorepinephrine and alpha-methylnormetanephrine did not account for this reduction. Competitive inhibition of methyldopa transport across the blood-brain barrier and into the central nervous system by large oral doses of isoleucine antagonized most of the effect of alpha-methyldopa. The effects on total peripheral resistance were completely abolished, and small, insignificant changes during the 7-hour study were similar to those observed after placebo. Changes in mean arterial pressure were not significant; however, 24-hour total urinary norepinephrine and metabolite excretion increased by 6.1 mumol to 22.7 mumol (24.7 mumol excreted after placebo). Adding benserazide to the alpha/methyldopa-isoleucine dose regimen in an attempt to inhibit any residual, presumably peripheral, effects of alpha-methyldopa caused little, if any, further antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for a predominantly central hypotensive effect of alpha-methyldopa in humans. 394 83

In this study, the effects of angiotensin II (A II, Asn-Arg-Val-Tyr-Val-His-Pro-Phe) and angiotensin III (A III, Arg-Val-Tyr-Ile-His-Pro-Phe) on blood pressure (B.P.), pulse rate, several hormones [plasma renin activity (PRA), plasma aldosterone (PA), ACTH, plasma cortisol (PC), urinary catecholamines and urinary aldosterone] and urinary electrolytes were investigated in 9 male patients with essential hypertension [mean age 36.2 +/- 4.1 (S.E.) years]. A II and A III infusions (8 ng/kg/min, 60 min) were started from 0900 h and blood samples were drawn before, at 15, 30, 45, 60 min after the beginning of the infusions, and at 15 min after their cessation. Urinary samples were collected within 2 hrs before and after the infusions, respectively. A II significantly increased B.P.(p less than 0.01) during the infusions, whereas A III did not increase B.P.. PRA significantly decreased after the infusions of A II and A III (p less than 0.05), but the potency of A II was significantly greater than that of A III (p less than 0.01). PA was increased after both infusions, but in response to A III, a peak was observed at 30 min after the infusion and subsequently, the levels decreased gradually. Significant differences between both responses were found at 45 and 60 min (p less than 0.05) after the infusions. ACTH was unchanged during the infusions, but PC was equipotentially suppressed during the infusions, with the suppression of A II being similar to that of A III. In the responses of urinary catecholamines, noradrenaline and dopamine were equipotentially decreased after the infusions (p less than 0.05). The results of the present study clearly indicate that several differences exist between the biological activities of A II and those of A III. Further systematic experimental studies are needed to resolve the details.
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PMID:[Changes in responses of blood pressure and several hormones to infusions of angiotensin II and angiotensin III in patients with essential hypertension]. 609 61

Under various conditions of sodium balance, 1-sarcosine-8-isoleucine angiotensin II was infused into 15 normotensive controls and 82 patients with benign essential hypertension. Changes in mean blood pressure induced by the analogue were correlated with the logarithm of plasma renin activity (r = -0.763, p less than 0.001 for the controls; r = -0.776, p less than 0.001 for the patients). Although the coefficients of determination were much the same, 0.95 confidence limits of the regression line did not overlap at renin levels over 7 ng/ml/h. At those levels, a decrease in the mean blood pressure induced by the analogue was greater in the hypertensive patients. A pressure-renin index was defined as a product of the logarithm of plasma renin activity and the mean blood pressure measured before the analogue infusion. The correlation between the analogue effect and the pressure-renin index was highly significant (r = -0.763, p less than 0.001 for the controls; r = -0.777, p less than 0.001 for the hypertensive patients). The regression line (0.95 confidence limit) for the hypertensives coincided with that for the normotensives. Thus, the blood pressure level should be taken into account when attempting to evaluate plasma renin activity.
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PMID:Evaluation of plasma renin activity by blood pressure level (pressure-renin index) in patients with essential hypertension. 705 Apr 56

As part of the multicenter project entitled "Pathobiological Determinants of Atherosclerosis in Youth (PDAY)," we are testing polymorphisms in candidate genes of atherosclerosis and hypertension for associations with arterial lesions in autopsied young persons. In this study, we used temperature gradient gel electrophoresis (TGGE) to type the Met235-->Thr polymorphism in exon 2 of the angiotensinogen gene (AGT) that is associated with essential hypertension in some human populations. In addition to Met235-->Thr, we detected and sequenced four other TGGE variants in exon 2 of AGT. These included two new amino acid substitutions (Thr209-->Ile and Leu211-->Arg) that were found only among black PDAY cases. The frequency of the Ile209 mutation was 0.002 and the frequency of the Arg211 was 0.006 in 260 black PDAY cases. The other two TGGE variants were Tyr248-->Cys and a T-->C substitution at nucleotide position 171 that had been identified in previous studies. We also developed restriction isotyping for rapid typing of each AGT variant using PCR amplification and digestion with diagnostic restriction enzymes.
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PMID:Detection and characterization of new mutations in the human angiotensinogen gene (AGT). 760 42


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