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)

The present study was undertaken to examine the possible relationship between dietary sodium intake and arginine vasopressin (AVP). In 12 normotensive men (aged 23-26 years) urinary AVP excretion decreased from 6.7 +/- 1.0 to 3.9 +/- 0.3 ng/h (P less than 0.01) when sodium excretion by dietary intervention for one week was reduced from 188 +/- 18 to 16 +/- 2 mmol/24 h. At a high sodium intake (300 mmol/day), AVP excretion increased to 10.0 +/- 1.2 ng/h during the first day (P less than 0.01) and remained high throughout one week of sodium load. These results are compatible with a major physiological role of sodium in AVP secretion in man. A sodium-AVP relationship may play a role in the pathogenesis of essential hypertension since recent reports suggest elevated plasma AVP in essential hypertensive states.
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PMID:Dietary sodium intake and vasopressin excretion in man. 659 75

In this study we found that, in 31 normal subjects, close to 90% of circulating arginine vasopressin (AVP), measured by radioimmunoassay, was associated with platelets. By using routine methods of centrifugation, which do not completely separate platelets, the normal range of plasma vasopressin was higher by twofold than the normal range in platelet-free plasma prepared by differential centrifugation, which was 1.4 +/- 1.0 sd pg/ml. Platelet vasopressin was 12.9 +/- 5.7 pg/ml. Patients with congestive heart failure had, on average, an elevated platelet-free plasma AVP, as did two patients with thrombocytopenia and one with thrombocytosis. Patients with essential hypertension had slightly high levels of platelet-free plasma AVP and demonstrated an abnormal inverse relationship between platelet-free plasma AVP and serum osmolality. Immunoreactive platelet vasopressin was slightly low in patients with essential hypertension and was subnormal in patients with congestive heart failure. These studies demonstrate that platelets normally present in centrifuged plasma cause an overestimation of the plasma vasopressin levels. Until the physiological meaning of plasma and platelet-bound AVP is understood, studies of circulating vasopressin should probably assess both plasma and platelet AVP levels.
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PMID:Plasma and platelet vasopressin in essential hypertension and congestive heart failure. 682 23

1. This study was designed to compare the response of plasma arginine vasopressin (AVP) to head-up tilt in hypertensive patients and in normals. 2. As expected, plasma AVP showed a consistent increase (P less than 0.005) in normal subjects after tilt while plasma volume decreased significantly (P less than 0.02). On the contrary, in hypertensive patients, after tilt both plasma AVP (P less than 0.025) and plasma volume (P less than 0.05) decreased. 3. These findings, thus, indicate that essential hypertension is characterized by an inverted response of arginine vasopressin to postural change.
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PMID:Inverted response of arginine vasopressin to postural change in patients with essential hypertension. 704 28

The relationship of arterial pressure (AP) to plasma arginine vasopressin (AVP) and sodium (Na) intake was determined in untreated essential hypertensive (H) and normotensive (N) subjects. The AP of H subjects averaged 147/101 mm Hg and that of N subjects, 124/79 mm Hg. Plasma AVP was elevated significantly in H subjects, averaging 8.5 pg/ml compared to 4.7 pg/ml in N subjects. Multivariant regression analysis yielded a significant correlation (r2 = 0.34) between diastolic pressure, urine Na concentration, and changes in plasma AVP. Plasma Na of H subjects averaged 2.0 mEq/liter less and urine Na concentration 22 mEq/liter less than in N subjects. Sodium intake appeared to have no influence on the plasma AVP of N subjects, but H subjects excreting Na in excess of 250 mEq/day averaged a plasma AVP twice as high as that in H subjects excreting less than 150 mEq/day. In H subjects, the influence of Na intake appeared to be related to age. In subjects less than 50 years of age, Na intake did not appear to influence chronic levels of plasma AVP, while in subjects older than 50 years who were excreting Na in excess of 250 mEq/day, plasma AVP levels were twice (13.5 pg/ml) those observed in hypertensives of the same age excreting less than 150 mEq/ day (6.5 pg/ml). The data indicate that plasma AVP tends to be elevated in moderate essential hypertension. Reduced concentrating ability of the kidneys of these subjects is suggested by decreased urine Na concentrations despite elevated plasma AVP. The observed increases of plasma AVP could be exerting a direct influence on extra- and intravascular volumes by renal and systemic vasoconstriction.
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PMID:Vasopressin elevation in essential hypertension and increased responsiveness to sodium intake. 726 83

In this study, the concentration of plasma arginine vasopressin (AVP) and substance P (SP) in normotensive subjects as well as patients with essential hypertension was measured. The results showed that: (1) The concentration of plasma AVP in patients with essential hypertension (21.83 +/- 1.30ng/L) was significantly higher than that in normotensive subjects (11.02 +/- 1.05 ng/L) (P < 0.001). The level of plasma SP in hypertensive subjects (276.60 +/- 21.35 pmol/L) was obviously lower than that in normotensive subjects (958.20 +/- 31.13 pmol/L) (P < 0.001). (2) The level of plasma AVP decreased (from 24.88 +/- 1.63 to 8.69 +/- 1.39 ng/L, P < 0.001) and that of plasma SP increased (from 331.40 +/- 48.18 to 958.80 +/- 39.30 pmol/L, P < 0.001) after antihypertensive drug treatment. (3) A negative correlation was found between the level of plasma AVP and SP in patients with essential hypertension (r = -0.564, P < 0.001), but no correlation was found between them in normotensive subjects (r = -0.096, P > 0.05). It is suggested that the abnormal level of plasma AVP and SP plays a role in the pathogenesis of hypertension.
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PMID:[The role of arginine-vasopressin and substance P in the pathogenesis of hypertension and their interrelation]. 750 32

Parathyroid hormone (PTH) is hypotensive in mammals and is a potent coronary vasodilator. Parathyroid hormone-related peptide (PTHrp) has been reported to have similar vascular activity. In the present study, the effects of human PTH (hPTH) and human PTHrp (hPTHrp) were compared in various in vivo and in vitro assays. In vivo studies included blood pressure measurement and coronary blood flow determination with labeled microspheres in anesthetized and cannulated normotensive rats. Isolated rat tail artery and portal vein helical strips were used in studying tension development in vitro. In the blood pressure assay, PTHrp was several times more potent than PTH. PTHrp was also significantly more potent than PTH in relaxing tail artery precontracted with arginine vasopressin (AVP). PTHrp and PTH both inhibited the spontaneously contracting portal vein, but again PTHrp was significantly more potent. PTHrp (1 microgram/kg) produced a greater increase in coronary blood flow as compared with the same dose of PTH. These data suggest that PTHrp is more potent than PTH in its cardiovascular actions. It is possible that PTHrp is the endogenous vasodilating ligand, and the structural similarity between PTH and PTHrp may explain the pharmacological action of PTH. It is therefore unlikely that PTH or PTHrp may be involved in the genesis or maintenance of hypertension. Because the parathyroid gland seems to be involved in some forms of essential hypertension, factor(s) other than PTH or PTHrp may be responsible.
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PMID:Cardiovascular effects of human parathyroid hormone and parathyroid hormone-related peptide. 751 45

Intravenous (i.v.) infusion of the selective vasopressin (V2) agonist 1-desamino-8-D-arginine vasopressin (DDAVP, Desmopressin) in humans causes a fall in blood pressure, an increase in heart rate, and a rise in plasma renin and noradrenaline. The present study was designed to demonstrate the vasodilatory properties of DDAVP in the renal circulation and to describe the effect of DDAVP on renin secretion. Seven male subjects (31-63 years) with hypertension, who showed no signs of renal parenchymal disease, received an i.v. infusion of DDAVP (400 ng/kg in 10 minutes). They were studied at the time they were undergoing renal vein renin sampling and renal angiography as part of the diagnostic work-up of their hypertension. 131I-Hippurate clearance was used to measure effective renal plasma flow (ERPF). True renal plasma flow was calculated as ERPF divided by the renal extraction ratio of 131I-hippurate. 125I-Thalamate clearance was used to measure glomerular filtration rate (GFR). Measurements were made before and 15-20 minutes after administration of DDAVP. Angiography was performed in the same session after the last blood samples had been collected. In all patients the renal arteries were normal and the extraction ratios of 131I-hippurate and 125I-thalamate (Ehip, Ethal) were not different for the left and right kidney, and in all seven patients a diagnosis of essential hypertension was made. After DDAVP systolic blood pressure decreased by 14.4 mmHg (2.0-26.8) (mean, 95% confidence interval, p < 0.05). Diastolic blood pressure decreased by 12.1 mmHg (2.9-21.7, p < 0.01). Heart rate increased by 17.5 bpm (11.7-23.2, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of DDAVP on renal hemodynamics and renin secretion in subjects with essential hypertension. 795 85

Plasma concentrations of beta-endorphin (beta-EP), leucine enkephalin (LEK), arginine vasopressin (AVP), neurotensin (NT), renin activity (PRA) and angiotensin II (AT-II) were determined before and after the treatment with clonidine in 117 patients with essential hypertension. Before the treatment, the patient group had lower levels of beta-EP and LEK (P < 0.001), higher levels of AVP, PRA and AT-II (P < 0.05-0.01), as compared with those in control group. After 14 days of the treatment, plasma levels of beta-EP, LEK increased significantly (P < 0.001), and correlated negatively with the decrease of the mean artery pressure (r = -0.369 and r = -0.441, respectively, P < 0.01). PRA and AT-II decreased significantly (P < 0.05, P < 0.01). Decrease of AVP level was also observed, but did not reach the statistical significance. NT did not change both before and after the treatment. These data suggest that beta-EP and LEK may be involved in pathogenesis of hypertension and in hypotensive action of clonidine.
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PMID:[Changes in plasma neuropeptides before and after clonidine in patients with essential hypertension]. 824 25

The aim of this study was to determine platelet intracellular free calcium with respect to age, sex, race, and agonist stimulation in patients with essential hypertension compared with normotensive subjects. Intracellular free calcium was measured, using Fura-2-AM, in 42 normotensive and 52 patients with untreated essential hypertension. Of these, 22 pairs were age, sex, and race matched. The intracellular free calcium response to agonist stimulation was measured in the presence of 1 mumol/L arginine vasopressin (AVP). Intracellular calcium was significantly raised in patients with hypertension in both the matched and unmatched groups with values (means +/- SEM) in the matched group of 68.4 +/- 2.6 nmol/L for the hypertensives and 60.2 +/- 2.1 nmol/L for the normotensives (n = 22; P < or = .02) and in the unmatched group of 63.3 +/- 1.8 nmol/L (n = 52) and 57.6 +/- 1.4 nmol/L (n = 42, P < or = .02), respectively. There was no sex difference but intracellular calcium was significantly lower in black hypertensives compared with white hypertensives (P < .005). A significant correlation with blood pressure was only observed in the combined normotensive and hypertensive group (r = 0.23; P = .030). There was no significant correlation with age in any group (even when excluding the black individuals), but in the hypertensive group there was a significant correlation with serum cholesterol (r = 0.34, P = .02; n = 46).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Determinants of platelet intracellular free calcium in essential hypertension and effect of stimulation by arginine vasopressin. 846 8

We conducted a double-blind, crossover study comparing the antihypertensive effects of isradipine versus captopril in patients with essential hypertension. Seventeen patients (8 men, 9 women; 6 whites, 11 blacks) completed both phases of the study, which consisted of two 5-week treatment periods separated by 2 weeks of placebo treatment. Each drug was randomly allocated to half the patients as the first drug and half as the second drug they received. Ambulatory blood pressure (BP) monitoring was carried out on the day before treatment and the last day of each active treatment. Both drugs were effective and well tolerated but isradipine was more effective overall than captopril in lowering BP (9.4% vs 3.9%, respectively; P < 0.02). Black patients had significantly higher BP at baseline than white patients; furthermore, black patients responded better to isradipine than to captopril. White patients had a smaller decrease in blood pressure with both drugs than did black patients, but white patients still attained a lower diastolic BP with captopril than did black patients (88 +/- 2 mm Hg vs 96 +/- 9 mm Hg; P < 0.01). There was no correlation between the pretreatment plasma levels of pressor hormones (plasma renin activity, catecholamines, and arginine vasopressin) and the magnitude of BP response to either drug, but the decrease in BP in response to captopril correlated significantly with the increase in plasma renin activity during treatment (r = -.84; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isradipine versus captopril in patients with essential hypertension. 856 28


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