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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A random sample of the rural community (two villages) were examined by means of questionnaire. Seventy-four percent of the community could not denote any risk factors of arterial hypertension. A very low percentage were informed of the role played by sodium chloride in the genesis of hypertension. Moreover, the community was very poorly informed of the adverse effects of overweight, tobacco smoking, and alcohol abuse. Excess use of sodium chloride was likely to be one of the causes promoting high prevalence of arterial hypertension. Some of the people were of opinion that arterial blood pressure might be influenced by definite nutritional and non-nutritional factors. The data obtained point to a low enough level of hygienic knowledge of the rural community regarding arterial hypertension risk factors. It is concluded that high prevalence of arterial hypertension risk factors and the low level of information of those factors provide evidence in favour of carrying out large-scale measures aimed at primary prophylaxis of arterial hypertension in the rural community. It is stressed that one should begin with the raising of the hygienic knowledge standards of the community.
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PMID:[Knowledge of the rural population on factors promoting the emergence of arterial hypertension]. 271 7

An increased central salt sensitivity is thought to be basically involved in hypertension. Therefore, in anaesthetized normotensive (Wistar, WKY) and hypertensive (SHR) rats, small amounts (10 microliters in 20 min) of both isotonic and hypertonic NaCl solutions (0.154 M, 0.3 M, 0.6 M and 1.0 M) were i.c.v. applied and blood pressure (BP) and heart rate (HR) responses registered. Central administration of hypertonic NaCl solution caused an elevation in BP and HR in both strains. The response magnitude was positively correlated to the NaCl concentration used. This increase could be interrupted by i.v. injection of a ganglionic blocker (tetraethylammoniumbromide). Despite of differences in time course, the magnitude of the BP and HR increases were much more elevated in SHR and WKY than in Wistar rats, suggesting strain differences. Considering the results obtained with 1.0 M NaCl solution, the following values were reached: in Wistar: delta syst. BP +15.7 mm Hg, delta HR +23.3 bpm; in WKY: delta syst. BP +40.2 mm Hg, delta HR +51.6 bpm; in SHR: delta syst. BP +46.0 mm Hg, delta HR +48.0 bpm. On the contrary, isotonic NaCl solution, when centrally applied, caused an elevation in HR (+25 bpm) and BP (delta syst. BP +6.2 mm Hg) only in SHR. These results support the idea that an exaggerated central sensitivity to sodium chloride may participate in hypertension.
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PMID:Blood pressure and heart rate responses to intracerebroventricular infusion of sodium chloride solution in normotensive and hypertensive rats. 275 68

High dietary intake of linoleic acid lowers arterial pressure, and, in vitro, linoleic acid inhibits the enzymatic activity of renin. The purpose of the present study was 1) to evaluate the effect of intravenous infusion of linoleic acid on blood pressure in normotensive and hypertensive Sprague-Dawley rats and 2) to determine whether the hypotensive response to linoleic acid infusion is caused by inhibition of circulating renin. Blood pressure was decreased (P less than 0.01) by linoleic acid infusion in normotensive sodium chloride-deprived animals and in animals with two-kidney, one-clip hypertension. In contrast, linoleic acid infusion did not affect blood pressure in normotensive rats on a "normal" or high sodium chloride intake, in rats with deoxycorticosterone acetate (DOCA)-salt hypertension, and in anephric rats. In sodium chloride-deprived rats, the reduction of blood pressure by linoleic acid infusion was associated with increased plasma renin activity (P less than 0.05); serum angiotensin-converting enzyme activity was unchanged. The in vitro enzymatic activity of exogenous renin in plasma of anephric rats was not affected by linoleic acid infusion. In two-kidney, one-clip hypertensive animals, pretreatment with indomethacin did not alter the hypotensive response to linoleic acid. Thus, although linoleic acid infusion lowered blood pressure in high renin but not in low renin states, the reduction of blood pressure was not related to inhibition of circulating renin or to alterations of endogenous prostaglandin biosynthesis.
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PMID:Effect of linoleic acid infusion on blood pressure in normotensive and hypertensive rats. 276 41

This study investigated the effect of chronic intracerebroventricular (IVT) infusion of a hypertonic NaCl (400 mmol/l) artificial cerebrospinal fluid (aCSF) on blood pressure and whole body pressor responsiveness, in control rats (CH) and in rats implanted with deoxycorticosterone acetate (DOCA; DH). An isotonic aCSF was infused into another group of control (Cl) and DOCA (Dl) rats. Indirect systolic blood pressure (SBP) was measured using a tail-cuff technique once a week prior to and during the infusion period. Following 2 weeks of infusion, SBP increased significantly only in the DH and CH groups. In urethane-anaesthetized rats, the pressor response to intravenous infusions of norepinephrine and angiotensin II (Ang II) increased significantly in DH rats. When compared with Cl and Dl rats, those from the CH group also exhibited an enhanced response to norepinephrine and Ang II. However, this increase was not as great as in the DH animal. These results show that whole body pressor responses to norepinephrine and Ang II, increase in rats receiving chronic IVT infusion of hypertonic NaCl. These responses coincide with moderate but significant increases in SBP. These data indicate that sodium chloride acts at a central site to increase norepinephrine and Ang II pressor responsiveness in mineralocorticoid hypertension.
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PMID:Central action of sodium chloride on whole body pressor responsiveness in the DOCA-treated rat. 276 24

Changes in plasma levels of Na+, K+-ATPase inhibitors with salt loading were studied in eight patients with essential hypertension. By improving the assay method of Na+, K+-ATPase inhibitors to distinguish ouabain and vanadate, two types of inhibitors were detected in the plasma of patients with essential hypertension: One was ouabainlike and the other was nonouabainlike. The ouabainlike inhibitor was detected at low KCl concentrations (0.1 mM) in the assay buffer, and the nonouabainlike inhibitor was detected at a high KCl concentration (10 mM). By increasing dietary sodium chloride from 2 g/day for 5 days to 20 g/day for 6 days, systolic blood pressure increased significantly from 122 +/- 3.9 to 138 +/- 3.8 mmHg (p less than 0.005), whereas plasma renin activity decreased significantly from 3.9 +/- 0.8 to 0.8 +/- 0.3 ng/ml/hr (p less than 0.002). Under these conditions, the ouabainlike inhibitor increased significantly from 6.2 +/- 3.9% to 30.5 +/- 5.9% inhibition (p less than 0.005), after increasing dietary sodium. Furthermore, plasma level of the ouabainlike inhibitor correlated significantly with both systolic blood pressure (p less than 0.05) and daily urinary sodium excretion (p less than 0.01). In contrast, the plasma nonouabainlike inhibitor did not change with high sodium intake and did not correlate with blood pressure and daily urinary sodium excretion. These findings suggest that a ouabainlike inhibitor is involved in the maintenance of high blood pressure induced by high sodium intake in patients with essential hypertension. The role of the nonouabainlike inhibitor in blood pressure regulation is still unknown.
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PMID:Increase in plasma ouabainlike inhibitor of Na+, K+-ATPase with high sodium intake in patients with essential hypertension. 283 25

The effects of chronic salt loading on central adrenergic mechanisms were evaluated in spontaneously hypertensive rats maintained on tap water or 1.2% sodium chloride drinking water for 4 weeks. Basal blood pressure was increased by 10% in the high salt group. Central catecholamines were measured spectrofluorimetrically after cation exchange chromatography. Endogenous levels of noradrenaline (NA) were not influenced by salt loading but the NA turnover (disappearance of NA following synthesis inhibition by alpha-methyltyrosine) was increased in the hemisperes. Central alpha 2-adrenoceptor sensitivity was assessed as the clonidine-induced reduction in blood pressure and as the clonidine-induced deceleration of NA turnover and locus coeruleus (LC) NA cell firing rate (single unit recording). The results were slightly disparate but the unchanged sensitivity of clonidine to reduce LC NA cell firing suggests that there were no alterations in central alpha 2-adrenoceptor sensitivity following a salt load. There were also no changes in alpha 1-adrenoceptor function, which was assessed semiquantitatively as the clonidine-induced increase in flexor reflex activity in spinalized rats. In salt loaded rats there was an enhanced blood pressure and heart rate reduction following ganglionic blockade which may be interpreted as an increased basal sympathetic tone. In the periphery the pressor responses to phenylephrine were increased whereas the chronotropic response to isoprenaline was unchanged. In conclusion, in the spontaneously hypertensive rat on a high salt intake the aggravated development of hypertension was not associated with major changes in central alpha 1 and alpha 2-adrenoceptor mediated functions or in neuronal activity of brain stem NA neurons. There were indications of an increased basal sympathetic tone and increased blood pressure response to pressor substances.
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PMID:Chronic salt loading and central adrenergic mechanisms in the spontaneously hypertensive rat. 286 8

Atrial natriuretic factor (ANF) antagonizes vasoconstriction induced by numerous smooth muscle agonists and also lowers blood pressure in intact animals. ANF has particularly marked relaxant effects on angiotensin II-contracted vessels in vitro. Sensitivity to the blood pressure-lowering effect of ANF in vivo appears to be enhanced in renin-dependent models of renovascular hypertension compared with other experimental hypertensive models. The depressor action of low, possibly physiological doses of ANF in two-kidney, one-clip Goldblatt rats is due to a decrease in total peripheral resistance. On the other hand, high doses of ANF can lower cardiac output, particularly in volume-expanded models such as deoxycorticosterone-salt hypertension. ANF markedly inhibits renin secretion in intact animals, probably via increased glomerular filtration rate and load of sodium chloride to the macula densa. This effect is masked when renal perfusion is impaired (e.g., via unilateral renal artery constriction), in which case ANF may stimulate renin secretion slightly. ANF also reduces plasma aldosterone in vivo and inhibits basal and agonist-induced aldosterone release from isolated adrenal cortical cells. This effect appears to be especially marked for angiotensin-induced aldosterone production in vivo and in vitro. These findings indicate that ANF has potentially important interactions with the renin-angiotensin-aldosterone system and suggest a role for ANF in the homeostatic control of blood pressure as well as of extracellular fluid volume.
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PMID:Effects of atrial natriuretic factor on blood pressure and the renin-angiotensin-aldosterone system. 294 Jan 20

Atrial natriuretic factor is postulated to act through atrial stretch receptors as a volume regulatory hormone that stimulates diuresis and natriuresis in response to increased atrial pressure. To characterize the stimuli associated with the release of atrial natriuretic factor in humans, we studied 14 normal subjects, both in the supine position and after 10 minutes in an upright posture, while they were on a regular diet (Day 0) and during 3 days of supplemental sodium chloride intake (8 g/day). Radioimmunoassay of plasma atrial natriuretic factor was performed with rabbit antibody to the human hormone amino acids (102-126). Urinary sodium excretion increased from 111 +/- 13 mEq/day (mean +/- SEM) on Day 0 to 275 +/- 15 mEq/day by the third day (Day 3) of high sodium intake. The level of atrial natriuretic factor in the supine position rose from 17 +/- 4 pg/ml (Day 0) to 76 +/- 13 pg/ml on Day 3 (p less than 0.001) and after 10 minutes in an upright posture on Day 3, the level fell to 32 +/- 10 (p less than 0.005). Plasma concentrations of atrial natriuretic factor correlated positively with spot and 24-hour urinary sodium excretion and weight gain, and correlated negatively with plasma aldosterone and renin activity. We conclude that the response of atrial natriuretic factor to sodium loading and posture change in humans is appropriate for a volume regulatory hormone.
Hypertension 1986 Jun
PMID:Sodium loading and posture modulate human atrial natriuretic factor plasma levels. 294 66

The adrenergic innervation of major arteries and veins was examined in DOCA-NaCl hypertensive rats using a histochemical fluorescent technique to detect the intraneuronal catecholamine content. The possible role of sodium and chloride ions was studied in DOCA-treated rats which were fed a low-salt diet which was supplemented with sodium bicarbonate instead of sodium chloride. Focal defects of adrenergic innervation were observed in blood vessels of DOCA-NaCl hypertensive rats. Nevertheless, the degree of these changes differed according to the vascular bed examined. A maximum decrease of the catecholamine content in varicosities of adrenergic terminals was found in the femoral vessels while there were nearly no changes in tail arteries and veins. Adrenergic innervation was usually more impaired in veins than in corresponding arteries of hypertensive animals. Pronounced changes in blood vessels of rats with DOCA-NaCl hypertension contrasted with the maximum alterations observed in those hypertensive DOCA-treated animals which were fed a NaHCO3-supplemented diet. Thus a chloride overload seems to be more important for alteration of adrenergic innervation than the degree of blood pressure elevation or the sodium overload per se.
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PMID:The adrenergic innervation of arteries and veins in rats with DOCA-NaCl hypertension: the role of sodium and chloride overload. 294

Clinico-biochemical investigation of 76 persons with borderline arterial hypertension (BAH) aged 15 to 64 and 60 controls with assessment of some parameters of lipid, carbohydrate and water-salt metabolism was carried out. Gustatory sensitivity to sodium chloride was studied. Differences in the levels of these indices were revealed in patients with BAH with relation to the presence or absence of basal changes on ECG and fundus of the eye; there were also some differences in risk factors in BAH and essential hypertension.
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PMID:[Clinico-biochemical characteristics of persons with borderline arterial hypertension]. 296 28


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