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)

We used the neck chamber technique to study carotid baroreceptor control of blood pressure in 18 renovascular hypertensive subjects. Carotid baroreceptors were stimulated or deactivated for 2 minutes by applying graded reductions or increases in the neck tissue pressure (NTP) outside the carotid sinuses. The sensitivity of the baroreflex was separately calculated for these two conditions by the coefficients of the linear regressions relating the changes in NTP to the resulting changes in mean arterial pressure (MAP, catheter measurement). Baroreceptor deactivation increased MAP, and the sensitivity of the baroreflex was 0.12 /+- 0.07 in an early (5 to 1 seconds) and 0.32 /+- 0.05 in a late (90 to 120 seconds) phase of the stimulus application. Baroreceptor stimulation reduced MAP, and the baroreflex sensitivity was in this instance 0.66 /+- 0.08 and 0.05 /+- 0.08 respectively. Both these sensitivities were significantly greater than those obtained for the baroreceptor deactivation. These response entirely reproduced those of essential hypertensive subjects, but differed from those of normotensive subjects in whom baroreflex sensitivity was greater for carotid baroreceptor deactivation than for stimulation. Our findings indicate that carotid baroreceptor control of blood pressure undergoes a marked resetting in renovascular hypertension. The similarity of the baroreflex between renovascular and essential hypertension suggests as secondary origin of the resetting in man.
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PMID:Carotid sinus baroreceptor control of arterial pressure in renovascular hypertensive subjects. 706 Nov 28

the autonomic sympathetic reflexes to sustained handgrip, upright tilt and the Valsalva maneuver, were tested in 26 patients with labile and 26 with fixed essential hypertension. Sustained handgrip increased systolic (SAP), diastolic (DAP) and mean arterial (MAP) pressure, heart rate (HR), cardiac index (CI), tension time index (TTI) (p less than .01), and had no effect on total peripheral resistance index (TPRI) and left ventricular ejection rate index (LVERI) in both groups of patients. However, the response to upright tilt and the Valsalva maneuver was different in the two groups. Upright tilt in labile hypertensives increased DAP, MAP, HR, and TPRI (p less than .001); decreased CI, stroke index (SI) and LVERI (p less than .01) and had no effect on SAP. In fixed hypertensives, it decreased SAP, MAP, CI, SI and LVERI (p less than .001); increased HR (p less than .01) and had no effect on DAP, and TPRI. The diastolic pressure overshoot of the Valsalva maneuver was attenuated in fixed hypertensives compared to labile (p less then .001). Additionally, when the percent changes from control in DAP, MAP, HR and TPRI to sustained handgrip and upright tilt between the two groups were compared, only differences to upright tilt between the two groups were observed. The results of this investigation suggest that upright tilt and the Valsalva maneuver might serve as better predictors of autonomic reflexes in hypertensive patients than the grip test.
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PMID:Hemodynamic correlates of autonomic reflexes in patients with labile and fixed hypertension. 733 96

Peritubular capillary hydrostatic and oncotic forces and their relationship to the renal excretion of sodium (UNaV) were examined in 19 patients with moderate and uncomplicated essential hypertension (HT) and compared with data from 20 normotensive subjects (NT). Observations were made in hydropenia (C) and during sustained isotonic saline volume expansion (E; 3% increase in body weight). The intrarenal venous pressure (IRVP) was used as an index of peritubular capillary hydrostatic pressure, and the efferent arteriolar colloid osmotic pressure (COPeff) was estimated from the arterial COP and the filtration fraction. C values (mean +/- SEM) in HT (and NT) were: arterial pressure (MAP) 110 +/- 3 mm Hg (85 +/- 1, p less than 0.001); glomerular filtration rate (GFR) 122 +/- 4 ml/min/1.73 m2 (128 +/- 3, p greater than 0.05); renal blood flow (RBF) 1172 +/- 38 ml/min/1.73 m2 (1298 +/- 48, p less than 0.05); IRVP 25.0 +/- 1.0 mm Hg (24.8 +/- 0.8, p greater than 0.05); COPeff 33.0 +/- 0.7 mm Hg (31.9 +/- 0.6, p greater than 0.05); and UNaV 140 +/- 13 mumole/min (161 +/- 12, p greater than 0.05). During E, the increase of UNaV in HT was more than double that of NT (p less than 0.001) while IRVP did not change in either group (p greater than 0.05); and COPeff fell by 26% (p less than 0.001) in both groups. GFR and RBF increased by 18% (p less than 0.001) and 19% (p less than 0.001) respectively, in HT, but did not change in NT. MAP remained unchanged in both groups. The results indicate that the peritubular capillary physical factors are normal in established essential hypertension, and that these forces are not involved in the exaggerated natriuretic response to volume expansion in essential hypertension.
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PMID:Renal sodium excretion and the peritubular capillary physical factors in essential hypertension. 746 93

Fourteen subjects with untreated essential hypertension were subjected to 2-h water immersion (WI) study. They were then randomly assigned to two distinct oral antihypertensive regimens with either calcium-channel blocker nifedipine (group 1, n = 7) or the angiotensin-converting enzyme (ACE) inhibitor lisinopril (group 2, n = 7). Three months later, a WI study identical to the first was repeated in the same hypertensive subjects. In group 1, treatment with nifedipine gastrointestinal therapeutic system (30 mg daily) significantly enhanced the natriuretic response to volume expansion by WI (peak value 405 +/- 82 mumol/min during WI plus nifedipine vs. 291 +/- 52 mumol/min during WI alone, p < 0.05). In group 2, treatment with lisinopril (20 mg daily) was associated with a blunted natriuretic response to volume expansion by WI (peak value 189 +/- 54 mumol/min during WI plus lisinopril vs. 320 +/- 53 mumol/min during WI alone; p < 0.025). A significant direct correlation between urinary sodium excretion (delta UNa V) and mean arterial pressure (delta MAP) was noted during WI plus nifedipine. Each long-term drug treatment was associated with a decrease in BP and hormonal changes of the same magnitude. Our data suggest that calcium antagonists could act as "diuretic agents" capable of counteracting the antinatriuretic effect of reduced renal perfusion pressure.
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PMID:Regulation of sodium excretion in human hypertension: long-term effects of calcium antagonist and angiotensin converting enzyme inhibitor. 768 17

ACE-inhibitors are known to have special renal effects, i.e. they increase ERPF, decrease the filtration fraction and lower proteinuria. These effects can be due to a decrease in angiotensin II (AII) levels as well as an increase in bradykinin. New and more specific AII-receptor antagonists may help to distinguish between effects exerted by angiotensin II and those exerted by bradykinin. We investigated the effects of losartan in 9 patients with essential hypertension (sitting mean diastolic blood pressure 95-120 mmHg). Renal hemodynamics were measured by continuous inulin-and PAH-clearance (GFR and RPF) after stopping antihypertensive therapy for 1 week, followed by a 2-week placebo period and after a 4-week treatment phase with losartan (50 mg/die) followed by a therapy with an ACE-inhibitor (ramipril 5mg/die). Additionally, urine albumin excretion (UAE) was measured. Treatment of patients with essential hypertension with losartan resulted in a significant decrease of MAP after three weeks of treatment (121 +/- 8 mmHg under placebo and 114 +/- 10 mmHg under losartan; * = p < 0.05). MAP after four weeks of losartan treatment was 115 +/- 11 mmHg. Regarding changes in renal hemodynamics we could not demonstrate a significant change for neither losartan nor the ACE-inhibitor. Urine albumin excretion was reduced by both treatment regimens in correlation to the magnitude of blood pressure reduction. Our data indicate that losartan induced a significant reduction in MAP in patients with essential arterial hypertension with only moderate effects on renal hemodynamics.
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PMID:Renal hemodynamics in essential hypertensives treated with losartan. 778 Dec 6

Patients undergoing kidney transplantation often suffer from essential hypertension and coronary artery disease, for which perioperative treatment with nifedipine proved to be effective. If calcium-channel blockers and nondepolarizing muscle relaxants are used simultaneously, their synergistic effect at the neuromuscular cleft must be considered. On the other hand because of its extrarenal elimination no significantly altered effects are expected for patients with terminal renal failure. This prospective study comprised 30 patients undergoing kidney transplantation who were 2 kg over normal weight after a preoperative dialysis and infusion of lactated Ringer solution. Fifteen minutes after introduction of balanced anaesthesia with isoflurane, nitrous oxide and fentanyl, patients were assigned to the treatment group (N) with hypertension (mean arterial pressure (MAP > 110 mmHg) and subsequent management with nifedipine or to the control group (0). Treatment was aimed at keeping MAP between 90 and 110 mmHg. The neuromuscular status was electromyographically assessed by the train-of-four-principle. There were evaluated the duration of action of the initial dose of atracurium (0.5 mg/kg) from injection time to T1 = 2% (WZ 2), the dose of atracurium for a continuous neuromuscular blockade (DD 98 in mg/kg/h), the recovery time and the recovery index. Fourteen patients with hypertension received a bolus of 10 micrograms/kg nifedipine. A significant reduction in blood pressure (p < 0.05) to the desired range was achieved by a subsequent infusion of nifedipine of 5 to 40 micrograms/kg/h. In 16 patients MAP was kept between 90 and 100 mmHg without any additional therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anesthesia for renal transplantation: continuous neuromuscular blockade with atracurium and the management of intraoperative hypertension with nifedipine]. 824 Jun 42

We investigated the effect of a 4-day oral salt load (150 mmol NaCl extra per day) on blood pressure, erythrocyte sodium transport and the activity in the renin-angiotensin system in six males with primary hypertension, who had attained normotension on chronic enalapril treatment for 4 years. The design was a placebo-controlled, randomized, two-way cross over, double-blind study, i.e. each patient served as his own control. Intracellular erythrocyte sodium and potassium content were measured by flame photomometry. The increase in the intracellular sodium concentration during 1 h in 37 degrees C incubation of whole-blood with ouabain (compared with no-ouabain) was measured to determine the rate of active sodium efflux. 24-h blood pressure registration was performed with Space-lab equipment (SL 90202) before and at the end of the salt load. Left ventricular morphology was evaluated with echocardiography and the minimal vascular resistance of the hand vascular bed with water plethysmography at baseline and after 4 years on enalapril. Four years' enalapril treatment caused a significant decrease in blood pressure, left ventricular mass and minimal vascular resistance. During the 4-day salt load average 24-h blood pressure was significantly elevated, 129+/-3/85+/-2 mmHg as compared to 124+/-2/82+/-2 mmHg during placebo treatment (p=0.025). The change (delta) in MAP during high salt intake showed a negative relationship to delta-sodium efflux rate constant (r=-0.65, p=0.047). No significant relationship was found between the blood pressure response to the salt load and structural cardiovascular changes. In conclusion, a short-term oral salt load in hypertensive patients on chronic enalapril treatment caused a blood pressure rise, which was related to cellular sodium transport but not to structural cardiovascular changes.
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PMID:Relationship between salt and blood pressure in hypertensive patients on chronic ACE-inhibition. 955 77

Arterial hypertension-related renal damage is an increasingly common problem recently, because approximately 25% of patients currently treated with dialysis were hypertensive before renal replacement therapy was started. Hypertension is also known as a metabolic disease, while carbohydrate, purine and lipid disturbances are the features of this syndrome. On the other hand, the progression of renal disease depends on the extent of tubulointerstitial injury. For this reason, we undertook a study to evaluate the relationship between excretion of the markers of tubular damage (NAG) and some parameters of carbohydrate, purine and lipid metabolism in untreated essential hypertension. Both healthy volunteers (n = 15) aged 32. 6+/-7.8 and essential hypertensives (n = 25) aged 37.24+/-11.39 underwent the same tests. These tests were performed at 2-day intervals: intravenous glucose tolerance test with 0.5 g/kg b.w. as 40% glucose solution and oral fructose load test with 1.0 g/kg b.w. Area under glucose curve (GA) and serum uric acid post-fructose (PUAA) were calculated. Fasting: insulin, total cholesterol and LDL, triglycerides, free fatty acids (FFA) and urine excretion of NAG, albumin were determined. Glomerular filtration rate was estimated as creatinine clearance. Hypertensives showed statistically higher BMI (p<0.007), NAG (p<0.02), total cholesterol (p<0.01), LDL (p<0.007), FFA (p<0.007), insulin (p<0.01), PGA (p<0.01) and PUAA (p<0.03). NAG excretion correlated positively with WHR (r = 0.40), MAP (r = 0.47) and PUAA (r = 0.47) in hypertensives only. We presume that tubular injury at an early stage of renal damage in patients with essential hypertension could be a part of metabolic syndrome X.
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PMID:Hypertensive nephropathy - an increasing clinical problem. 1020 62

In 34 out-patients with essential hypertension, the antihypertensive effect and the trough-to-peak ratios of once-daily enalapril or lisinopril were compared by ambulatory blood pressure monitoring (ABPM) according to a crossover design. The drug dose was titrated and a thiazide diuretic was added if necessary to attain a target office BP of less than 140/90 mm Hg. Both drugs significantly lowered BP but the effect of lisinopril was greater (P < 0.009): day- and night-time mean BP fell from 152/98 and 135/84 mm Hg, respectively to 133/85 and 118/74 mm Hg with enalapril and to 129/83 and 116/70 mm Hg with lisinopril. BP goal was reached with an average dose of 18 mg enalapril with 8 mg hydrochlorothiazide and with 17 mg lisinopril combined with 6 mg diuretic. Trough:peak ratio values, which were calculated after Fourier analysis of ABPM data in individual patients, were independent of drug dose. The combination with the diuretic resulted in slightly higher trough:peak ratios than with ACE inhibitor monotherapy, but the difference was not significant. The median trough:peak ratio in patients when using enalapril-based therapy was 0.48 and, when taking lisinopril-based treatment, it was 0.65 (n = 28, P < 0.005). A significant correlation was found between trough:peak ratio and changes in daytime mean arterial pressure (MAP; Spearman r= 0.43) and night-time MAP (r= 0.66). When 24-h ABPM was performed starting 24 h after last drug intake, both ACE inhibitors still had a significant antihypertensive effect (P < 0.001), which was similar for both drugs. Eleven patients reported minor side effects. Four patients stopped ACE-inhibitor treatment because of cough. The data show that lisinopril has a longer duration of action than enalapril.
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PMID:Lisinopril versus enalapril: evaluation of trough:peak ratio by ambulatory blood pressure monitoring. 1040 91

Renal scarring with and without vesicoureteral reflux (VUR) has been now recognized as an important cause of paediatric hypertension for many years [1-5]. However, its pathogenesis has still remained uncleared. The widespread concept implicated the activation of renin-angiotensin system finding a powerfull support in higher peripheral plasma renin activity (PRA) in children with reflux nephropathy than in controls [6, 7] and in beneficial antihypertensive effects of ACE inhibitors. The latter, in form of captopril, has also been used in captopril test and in renal scintigraphy and isotope renography following the administration of captopril to provide evidence for renin dependent hypertension [8, 9]. Published studies of captopril test have centred on the identification of renovascular as opposed to essential hypertension [10-18, 20-22]. The aim of our study was to assess the usefulness of captopril test in differentiation between hypertensive children with renal scarring from those with essential hypertension. We studied blood pressure (BP) and PRA responses to a single dose of captopril in two groups of hypertensive children. Group A consisted of 29 patients, 14 boys and 15 girls, who had renal scaring as demonstrated by renal 99mTc dimercaptosuccinid acid scan (99m Tc DMSA) and/or intravenous pyelography. Group B included 19 patients, 19 boys and 10 girls who had arterial hypertension, while clinical examination excluded renal and other definable causes of BP elevation, and they were therefore considered to have essential hypertension. At the time of the study all patients had normal glomerular filtration rate and were not salt depleted. They did not receive any antihypertensive medication for at least two weeks. The test was performed in the morning in fasting sitting patients. At the start of the test a small vein in the hand or forearm was cannulated to permit blood sampling. BP was measured 10, 20, and 30 minutes before captopril administration to get baseline BP (mean of these three measurements) and to allow the children to become accustomed to the test procedure. A single oral dose of captopril 0.64 +/- 0.04 mg/kg body weight was given to patients from group A and almost the same dose of captopril, 0.63 +/- 0.05 mg/kg body weight, to patients from group B. The patients remained sitting and BP was measured every 15 minutes during an hour. Blood for PRA was drown in the sitting position (17 patients from group A and 16 patients from group B) before and one hour after the dose of captopril. Samples of blood for basal PRA were collected from 16 patients from group A and in 14 patients from in B in lying position after waking up in the morning. PRA was measured by radioimmunoassay using a commercially available kit, SB-REN 2, from CIS Bio International. According to the criteria of Muller et al. [10] the captopril test was positive if the post-captopril PRA (ng/ml/h) was greater than or equal to 12 with an increase of greater than or equal to 10 and relative increase of greater than or equal to 15% (400% if initial PRA was < 3). The results of our study are presented in Tables 1 and 2 and in Graphs 1 and 2. The age of patients, doses of captopril, initial BP and PRA before the use of captopril did not much differ between studied groups. Fall of BP and PRA increase were highly significant (p < 0.001) both in group A and group B. However, the hypotensive reaction of diastolic BP and MAP were more pronounced in group A (14.45 +/- 1.67% and 15.81 +/- 1.62%) than in group B (6.95 +/- 2.21% and 8.96 +/- 1.75%; p < 0.01), but there were no significant differences in PRA and systolic BP changes and positive results of captopril test between the studied groups. Hypotensive responses of diastolic BP and MAP greater than 10% of initial values were found to be more frequent in group A (79.32% and 79.31%) than in group B (26.61% and 31.57 degrees %; p < 0.001 and p < 0.01). Diastolic BP and MAP were directly related to the dose of cap
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PMID:[The captopril test--an aid in the detection of scarring nephropathy as a cause of arterial hypertension in children]. 1064 99


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