Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between left ventricle-to-body weight ratio (LV/BW), mean arterial pressure (MAP, the average of 12 h of intra-arterial monitoring in conscious animals) and plasma renin activity (PRA) was assessed at 12 weeks after unilateral clipping or sham operation in twenty-four one-kidney rats and twenty-six two-kidney rats. The degree of hypertension and left ventricular hypertrophy were similar in one-kidney and two-kidney groups. There was a close linear relationship between LV/BW and MAP which was similar in one-kidney and two-kidney rats. PRA was significantly elevated only in two-kidney rats and was not related to the degree of hypertrophy after accounting for the effect of PRA on MAP. These data suggest that activation of the renin-angiotensin system does not contribute directly to myocardial hypertrophy in rats with renal-clip hypertension.
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PMID:The renin-angiotensin system and hypertensive left ventricular hypertrophy in the rat. 624 Mar 58

The objective of this study was to investigate the relationship between the high activity of the renin-angiotensin-aldosterone system (RAAS) and the control of blood pressure and aldosterone in the canine puppy. The effect of the angiotensin II analog saralasin on arterial pressure (MAP), plasma renin activity (PRA), plasma renin concentration (PRC), and aldosterone (PA) was studied in unanesthetized normal, salt-loaded and salt-depleted puppies aged 9 to 30 days. Salt-loading was performed by daily intraperitoneal administration of 10 mEq sodium/kg body weight for 5 days and salt-depletion by furosemide injections. Saralasin infusion, 6 micrograms/kg/min, during 60 min significantly decreased MAP and increased PRC not only in salt-depleted puppies, as has been observed in adult salt-depleted dogs, but also in normal puppies (mean fall, 6.6 mm Hg). Although any developmental changes in the RAAS and MAP and in their relationship could not be ascertained, the fall in MAP during saralasin in normal puppies was significantly correlated to presaralasin renin values (r = 0.76, P less than 0.01, N = 11). PA did not change in both groups of puppies. In salt-loaded puppies saralasin caused no change of MAP, PRC, and PA. We conclude that the high renin levels at young age contribute to the basal arterial pressure in puppies.
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PMID:Effects of angiotensin II blockade in the canine puppy under different salt-intake. 639 82

Factors contributing to the blood pressure (BP) response to changes in dietary sodium intake were studied in 25 patients with essential hypertension (EH). Relevant clinical, biochemical and haemodynamic variables were measured after two weeks on a low sodium diet (LS, 50 mmol) and after two weeks on a high sodium diet (HS, 300 mmol). BP was significantly higher during HS. The difference in mean arterial pressure between HS and LS (delta MAP) was taken as a measure of sodium sensitivity. delta MAP was directly related to age, initial BP, plasma noradrenaline during HS and changes in forearm vascular resistance. It was indirectly related to plasma aldosterone during LS. No correlation was found with renin or with the excretion of urinary kallikrein. It is concluded that sodium sensitivity in EH is related to age and blood pressure and is predominantly mediated by changes in vascular resistance to which aldosterone and adrenergic mechanisms are likely to contribute.
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PMID:Clinical biochemical and haemodynamic correlates of sodium sensitivity in essential hypertension. 640 Jan 14

Changes in hemodynamics, plasma catecholamines, and PRA in response to controlled hypotension induced with ISDN (n = 10, mean dose 15.5 micrograms kg-1 min-1) and NTG (n = 7, mean dose 5.5 micrograms kg-1 min-1) were studied during neuroleptanesthesia in patients undergoing facial and neck surgery. Before the commencement of vasodilator infusion the patients were pretreated with metoprolol 0.1 mg kg-1. In addition, enflurane was used to obtain the desired hypotensive level. During ISDN induced hypotension, MAP was reduced from 83 to 63 mm Hg (p less than 0.001). Continuous infusion of NTG resulted in a decrease of MAP from 81 to 53 mm Hg (p less than 0.01). In both groups, HR decreased by 10% (p less than 0.05). For both vasodilators the reduction of MAP was associated with a marked decrease in SVRI (p less than 0.01), while Cl remained largely unchanged. The hemodynamic responses to the two vasodilators were similar, except that NTG reduced PAMP (p less than 0.01) and increased intrapulmonary shunt volume (p less than 0.01). The anesthetic technique attenuated catecholamine and renin release, suppressed reflex tachycardia, and prevented rebound hypertension.
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PMID:Hemodynamic and hormonal response to induced hypotension with isosorbide dinitrate and nitroglycerin during anesthesia. 642 Oct 7

Regulation of aldosterone secretion by sodium chloride is impaired in a group of essential hypertensives: high-salt diet fails to suppress aldosterone in these patients despite low renin values. The mechanism of this impaired regulation of aldosterone has not been clarified so far. We tested the sensitivity of aldosterone secretion and blood pressure to A II in 20 normotensive controls (aged 20-60, MAP 92 +/- 3 mm Hg), in ten normotensives with one or two parents with hypertension, and in 21 patients with essential hypertension (aged 17-65, MAP 119 +/- 4 mm Hg). After a period of 6 days on high-salt intake (300-320 mEq Na+/day), A II (0.1, 0.5, 1.0 and 2.0 ng/kg/min) was infused, each concentration for 30 min. According to aldosterone excretion during sodium loading, patients were divided into group A with complete suppression (n = 12, aldosterone excretion 3.6 +/- 0.4 microgram/day) and in group B with insufficient suppression (n = 9, aldosterone excretion 15.5 +/- 2.3 micrograms/day). Despite similarly low plasma renins, rise of serum aldosterone levels during A II infusion was significantly higher in group B patients than in group A patients and normotensive controls. Rise in mean arterial blood pressure, however, brought about by graded A II infusion was similar in both groups of hypertensives and in normotensive controls. The results demonstrate an increased adrenal sensitivity to A II in a subgroup of essential hypertensives only. A similar adrenal hypersensitivity to A II found by others in patients with hyperaldosteronism due to adrenal hyperplasia supports the hypothesis that the same mechanism underlies both disorders.
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PMID:Cardiovascular and adrenal sensitivity to angiotensin II in essential hypertension. 652 58

In order to determine factors contributing to sodium induced changes of blood pressure, 20 patients with essential hypertension were studied when on their regular sodium intake and after two weeks of a low sodium diet (50 mmol daily) and two weeks of a high sodium diet (300 mmol daily). There were two periods of regular sodium intake, one of four weeks at the beginning and one of two weeks at the end of the study. The change in mean arterial pressure between the high and low salt diets (delta MAP) was regarded as a measure of sodium sensitivity, and was directly correlated with age and initial blood pressure. Compared with non-responders, responders (delta MAP 10 mmHg or more) showed a lesser activation of the renin-angiotensin-aldosterone system during the low salt period. The response to the administration of intravenous frusemide was not helpful in predicting sodium sensitivity. A significant but relatively small (4.2 mmHg) reduction in MAP was obtained during low salt period compared with the first period of regular sodium intake. The data suggest that moderate dietary sodium restriction can help to reduce the blood pressure of the relatively older patient with hypertension.
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PMID:Sodium sensitivity in essential hypertension: role of the renin-angiotensin-aldosterone system and predictive value of an intravenous frusemide test. 653 May 38

In a prospective, double-blind, intraindividual, cross-over, placebo-controlled multicenter study, clinical and biochemical effects of once daily postprandial dose regimens of 50, 100, and 200 mg spironolactone were investigated in 45 outpatients with primary hypertension, WHO (World Health Organization) Stage I-II. Each of the three active therapy periods, which were randomly allocated to patients, were of 2 months' duration, with intervening placebo periods, Clinical and biochemical parameters, including furosemide-stimulated plasma renin activity (PRA), were recorded at regular intervals. All three spironolactone doses resulted in statistically significant blood pressure (BP) reductions independent of initial pretreatment levels and yielded satisfactory BP control in more than half of the patients. The 200 mg daily dose of spironolactone was found to be more effective than 50 but not 100 mg. When, correlating blood pressure response (delta MAP) to PRA, the profiling for positive spironolactone responders was characterized by high age and low PRA, irrespective of sex. Spironolactone therapy resulted in decreased serum sodium and magnesium values; potassium, creatinine, urate, and triglyceride levels were increased. However, all treatment values were within normal ranges. Side effects were infrequent and mainly of endocrine nature.
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PMID:Clinical and biochemical effects of spironolactone administered once daily in primary hypertension. Multicenter Sweden study. 699 72

1. To determine if increases in plasma sodium concentration P[Na] have any sustained effects of the renin-aldosterone system, P[Na] was increased in a group of six dogs over a period of 6 days by increasing sodium intake from 10 to 200 mmol per day while a fixed 700 ml per day water intake was maintained along with a continuous i.v. infusion of antidiuretic hormone (ADH) at a rate of 2.4 units per day. 2. P[Na] rose from 137.3 +/- 2.0 to 153.6 +/- 6.5 mmol/l during the high intake period. Plasma potassium concentration, 22Na space, and mean arterial pressure all remained near control levels in response to Na loading. 3. Plasma renin activity (PRA) averaged 1.0 +/- 0.1 ngAI/ml per hour on the final low Na day and fell transiently to 0.6 +/- 0.2 ngAI/ml per hour on the first day of sodium loading. For the duration of the study it remained at the control level. Plasma aldosterone concentration fell from the low Na level of 15.4 +/- 2.4 ng/100 ml to 10.5 +/- 1.5 ng/100 ml on the final day of high Na intake. 4. We conclude that increases in P[Na] in the absence of concomitant changes in P[K], 22Na space and MAP do not have a sustained effect on control of renin release but may exert a negative effect on aldosterone secretion.
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PMID:Effect of sustained hypernatraemia on the renin-aldosterone system in the dog. 701 64

Acute renal hypertension was produced in Sprague-Dawley female rats by the AL between the origins of the renal arteries. These were compared with an LN group. A sham group in which the ligature was placed but not tied was also prepared. MAP was recorded, and the animals were sacrificed at 1, 2, or 4 days after surgery. The hearts were examined histologically, and the lesions, consisting of focal or confluent necrosis of myocardial fibers with mononuclear cellular infiltrate, were scored. In the AL group the intensity of the lesions increased with time. The score on day 1 was 0.92 +/- 0.09; on day 2, 1.37 +/- 0.08; and on day 4, 1.75 +/- 0.01. Values at comparable intervals in the LN group were 0.14 +/- 0.04, 0.27 +/- 0.12, and 0.09 +/- 0.07, respectively (p less than 0.001). No coronary lesions were found. Arterial pressures were significantly elevated in the AL group but not in the LN or sham groups. Ventricular water and potassium were unchanged with the exception of a significant decrease of [K+] in the AL group 2 days after ligation. It is concluded that rats with acute renal hypertension develop cardiac necrosis, with a secondary fall in myocardial [K+]. The possibility that this is due to endogenous renin-angiotensin will require further study.
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PMID:Cardiomyopathy produced in rats with acute renal hypertension. 735 29

NO synthase is present in magnocellular neurons of supraoptic and paraventricular nuclei as well as in the posterior pituitary gland and may participate in control of vasopressin secretion. To test this possibility, experiments were performed in conscious, chronically prepared rabbits to determine the effect of NO synthesis inhibition with NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) on basal vasopressin secretion and vasopressin responses to increased plasma osmolality (hypertonic saline infusion; P osm) and decreased blood pressure (nitroprusside infusion). L-NAME infusion (0.5 mg.kg-1 x min-1 i.v.) increased mean arterial pressure [MAP; 82.6 +/- 3.4 to 93.0 +/- 3.0 mmHg (P < 0.02)], decreased heart rate [HR; 242 +/- 12 to 209 +/- 9 beats/min (P < 0.02)], decreased plasma renin activity [PRA; 3.1 +/- 0.6 to 2.0 +/- 0.6 ng.ml-.2 h-1 (P < 0.001)], and increased plasma vasopressin concentration [P AVP; 2.2 +/- 0.3 to 4.5 +/- 1.0 pg/ml (P < 0.05)]. P(osm) did not change. Hypertonic saline infusion did not change MAP or HR but decreased PRA [4.3 +/- 0.8 to 0.9 +/- 0.2 ng.ml-1 x 2 h-1 (P < 0.01)], increased P(osm) [284 +/- 1 to 305 +/- 2 mosmol/kg H2O (P < 0.001)], and increased PAVP [2.8 +/- 0.3 to 12.7 +/- 2.7 pg/ml (P < 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of inhibition of nitric oxide synthesis on vasopressin secretion in conscious rabbits. 751 50


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