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

To assess a possible heritability of a disturbed calcium metabolism in relation to blood pressure regulation, 28 young normotensive offspring of either hypertensive or normotensive parents were studied while administered a defined diet with daily sodium chloride of 6 and 20 g/day for 7 days each. Before the high salt diet was begun, the cytosolic calcium concentration ([Ca2+]i) in platelets was elevated in offspring of hypertensive parents, whereas serum electrolytes, plasma renin activity, plasma catecholamines, and 24-hour urinary excretion of sodium and calcium showed no difference between the two groups. On exposure to a high salt diet, the mean blood pressure increased (from 80 +/- 2 to 85 +/- 2 mm Hg, p less than 0.05) in offspring of hypertensive parents. These changes in mean blood pressure were positively correlated with the basal platelet [Ca2+]i (r = 0.61, p less than 0.01), whereas [Ca2+]i did not demonstrate any significant changes. When the subjects were administered the high salt diet, plasma ionized calcium decreased (from 2.37 to 2.21 meq/l, p less than 0.05) and 1,25-dihydroxyvitamin D3 increased (from 32.7 to 40.8 pg/ml, p less than 0.05) with a transient relative hypercalciuria in offspring of hypertensive parents. This increase of 1,25-dihydroxyvitamin D3 was significantly correlated with the changes in mean blood pressure (r = 0.62, p less than 0.01). Disturbed intraplatelet and systemic calcium metabolism may be of predictive value in the development of hypertension.
Hypertension 1992 Jun
PMID:Disturbed calcium metabolism in offspring of hypertensive parents. 159 47

Blood pressure in patients with essential hypertension is raised by sodium chloride but not by nonchloride sodium salts. Although a high sodium chloride diet is known to augment the pressor response to norepinephrine and angiotensin II, the effect of nonchloride sodium salts on pressor responsiveness has not been studied so far. To examine whether sodium chloride and nonchloride sodium salts evoke different pressor responses to these agonists, we performed graded norepinephrine and angiotensin II infusions in salt-sensitive (n = 7) and salt-resistant (n = 8) normotensive subjects. The subjects were given a low salt diet (20 mmol/day) for 3 weeks, to which a supplement of 200 mmol sodium per day, provided as either sodium chloride or sodium citrate, or a placebo was added for 1 week each. We found that, although sodium chloride raised mean arterial blood pressure in the salt-sensitive subjects (p less than 0.005), sodium citrate did not. However, under both sodium salts pressor response to norepinephrine and angiotensin II was significantly greater than under placebo (p less than 0.02). Furthermore, with both sodium salts, pressor response in the salt-sensitive subjects was greater than in the salt-resistant subjects (p less than 0.01). This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin II. Since pressor response increased with both sodium salts but resting blood pressure increased only with sodium chloride, enhanced pressor responsiveness alone cannot account for the sodium chloride-induced rise in resting blood pressure.
Hypertension 1992 Jun
PMID:Effects of sodium salts on pressor reactivity in salt-sensitive men. 159 48

The effect of salt intake on the hypertensive response to long-term infusion of endothelin-1 was investigated. Chronically instrumented male Sprague-Dawley rats (325-375 g) were used in a 15-day protocol that included 3 control days followed by 7 days of endothelin-1 infusion at 5.0 pmol.kg-1.min-1 and 5 days of recovery. Rats were maintained on either a normal sodium chloride intake (2.0 meq Na+ per day; normal sodium) or a high sodium chloride intake (6.0 meq Na+ per day; high sodium) throughout the protocol. Control rats received normal or high sodium intakes but not endothelin-1. In high-sodium rats, endothelin-1 produced a significant increase in mean arterial pressure and total peripheral resistance; a significant bradycardia was observed only on the first day after the start of the endothelin-1 infusion. Cardiac output, stroke volume, water balance, and urinary sodium and potassium excretion remained unchanged. Termination of endothelin-1 infusion resulted in rapid normalization of both arterial pressure and peripheral resistance. In contrast, normal sodium rats exhibited no alteration in mean arterial pressure, heart rate, total peripheral resistance, stroke volume, water balance, or urinary sodium and potassium excretion throughout the endothelin-1 infusion protocol. The hypertension produced by endothelin-1 infusion cannot be explained by alterations in salt or water balance since endothelin-1 infusion in high sodium animals produced significant increases in mean arterial pressure with no observable changes in water or electrolyte balance. These results indicate that endothelin-induced hypertension in conscious rats is a salt-dependent model of hypertension.
Hypertension 1992 Jun
PMID:Salt-dependency of endothelin-induced, chronic hypertension in conscious rats. 159 49

To determine the extent to which baroreceptor function is a determinant of salt-dependent hypertension, we studied the cardiovascular and renal responses to increasing dietary sodium chloride in sinoaortic-denervated (n = 9) and sham-denervated (n = 9) Sprague-Dawley rats. Rats were instrumented with an arterial catheter for measurement of arterial pressure and were individually housed for daily measurements of water intake, sodium intake, urinary output, and urinary sodium excretion. Arterial pressure was monitored daily over a 30-minute period by computer. After 3 days of control measurements (0.4% sodium chloride diet), dietary sodium chloride was increased to 8.0% for 21 days, followed by a 3-day recovery period (0.4% sodium chloride). Ingestion of an 8.0% sodium chloride diet resulted in a 20- to 25-fold increase in sodium intake and a fivefold increase in water intake in both groups. In sinoaortic-denervated rats, arterial pressure increased approximately 10 mm Hg on days 5-10, 20 mm Hg on days 11-18, and 30 mm Hg on days 19-21 of 8.0% sodium chloride. Arterial pressure returned to control levels within the first 24 hours of the recovery period. Elevated sodium intake had no significant effect on arterial pressure in the sham-denervated group. Finally, there were no significant differences between groups in urine output or urinary sodium excretion at any time during the study. We conclude that a primary impairment in the afferent limb of the arterial baroreceptor reflex results in salt-dependent hypertension in the Sprague-Dawley rat.
Hypertension 1992 Jun
PMID:Salt-dependent hypertension in the sinoaortic-denervated rat. 159 63

This study examined the contribution of nitric oxide (NO) to the susceptibility or resistance to the hypertensive effects of high sodium chloride (8.0% NaCl) intake in young Dahl/Rapp salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats. Using NG-monomethyl-L-arginine (L-NMMA) as a probe for NO production in vivo, we found that increasing dietary sodium chloride increased NO activity in salt-resistant rats, but not in salt-sensitive rats. Exogenous L-arginine, the substrate for NO synthesis, decreased blood pressure to normotensive levels in salt-sensitive rats made hypertensive for 2 wk from 8.0% NaCl chow. D-arginine had no effect on blood pressure of these rats and L-arginine did not change blood pressure of salt-resistant rats. Intraperitoneal injections of L-arginine and its precursor, L-citrulline, and oral L-arginine, but not D-arginine, prevented the increase in blood pressure in salt-sensitive rats on the high salt chow over 2 wk of observation. In contrast, L-arginine did not alter the development of hypertension in spontaneously hypertensive rats. Mean urinary cGMP levels were higher in salt-sensitive rats on oral L-arginine than salt-sensitive rats on D-arginine. Infusion of L-NMMA acutely decreased, whereas intravenous L-arginine rapidly increased, urinary cGMP in both groups. L-arginine and L-citrulline increased production of NO and prevented salt-sensitive hypertension in Dahl/Rapp rats.
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PMID:L-arginine abrogates salt-sensitive hypertension in Dahl/Rapp rats. 165 45

We determined the kinetic properties--the maximal velocity, Vmax, and the half-maximal activating concentration of K+, km values--of the vascular sodium pump in rats 6, 28, and 50 days after deoxycorticosterone and sodium chloride (DOC-salt) or vehicle treatment. Tail arteries from six or eight rats from each treatment group were pooled, and Na-pump activity was measured in a Krebs medium containing varying K+ (plus 86Rb+) concentrations (0.25-10 mM). Na-pump activity was plotted as a function of [K + 86Rb]. Data were fit to a two-site model to calculate Vmax and km values. Systolic blood pressures were normal after 6 days but high after 28 and 50 days of DOC-salt treatment. No difference in kinetic parameters existed between the treatment and control groups 6 and 50 days after DOC-salt treatment. After 28 days, Vmax was significantly elevated compared with controls; km was not affected. Thus, stimulation of the vascular Na-pump during established hypertension is due to an increase in the maximal velocity of ouabain-sensitive uptake of K+.
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PMID:Vascular sodium pump activity kinetics in early and advanced stages of deoxycorticosterone-salt hypertension in rats. 166 Sep 56

To investigate the calcium dependence of salt-induced hypertension we concurrently measured blood pressure and serum ionized calcium in conscious normotensive female dogs undergoing five infusions: 1) sodium chloride (0.9%) 2) calcium chloride (10 mg/kg), 3) combined sodium chloride and calcium chloride, 4) nicardipine (1 micrograms/kg/min), and 5) combined sodium chloride and calcium chloride in the presence of nicardipine. While saline and calcium chloride infusions individually did not affect blood pressure, saline combined with calcium chloride significantly and consistently raised mean arterial pressure (MAP) (delta MAP = 7 +/- 2 mm Hg, P less than .001 v baseline). Serum ionized calcium (Caio) levels increased within the normal range with the infusion of calcium alone (1.32 +/- 0.03 to 1.48 +/- 0.01 mmol/L, P less than .005). Extracellular Caio rose less with the combined NaCl-CaCl2 infusion (delta Caio 0.10 +/- 0.01 v 0.16 +/- 0.02 mmol/L, P less than .02). The difference in calcium elevations could not be attributed to volume expansion alone, since saline infusion itself did not affect serum ionized calcium (1.32 +/- 0.3 to 1.31 +/- 0.01 mmol/L, P = NS). Furthermore, nicardipine prevented the pressor effect of the combined saline-calcium infusion. (delta MAP = -2 +/- 3 v 7 +/- 2 mm Hg, P less than .001), and restored the rise in extracellular Caio to that seen with the nonpressor calcium infusion (delta Caio 0.15 +/- 0.01 mmol/L v 0.16 +/- 0.02 mmol/L, P = NS). Altogether, these data demonstrate that the rise in blood pressure and ionized calcium following an acute infusion of sodium and calcium chloride are interdependent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The pressor effect of sodium-volume expansion is calcium mediated. 166 68

In anesthetized (chloralose and urethane), paralyzed and artificially ventilated rats, the neurons in the ventrolateral medullary depressor area (VLDA) were chemically stimulated by microinjections of L-glutamate (2.5-5 nmole in 100 nl of 0.9% sodium chloride solution) and the cerebral blood flow (CBF) was determined using a combination of labeled microspheres (57Co, 113Sn and 46Sc). Unilateral chemical stimulation of the VLDA (n = 11) produced a significant (P less than 0.05) decrease in CBF of the cerebral cortex ipsilateral to the stimulated VLDA; the CBF was 41 +/- 5 (mean +/- S.E.M.) and 29 +/- 4 ml.min-1.(100 g)-1 before and during the chemical stimulation of VLDA. The decrease in CBF was not due to the decrease in arterial blood pressure (ABP) caused by the chemical stimulation of the VLDA because the CBF during the chemical stimulation of the VLDA was significantly smaller (P less than 0.01) than the CBF during controlled hemorrhagic hypotension (n = 10). In another group of rats (n = 6), moderate hypertension was induced by blood transfusion. Unilateral chemical stimulation of the VLDA in these rats decreased ABP but it remained within normotensive range. A significant (P less than 0.05) decrease in CBF (from 46 +/- 12 to 29 +/- 7 ml.min-1.(100 g)-1) and a significant (P less than 0.01) increase in cerebrovascular resistance (from 2.7 +/- 0.4 to 4.3 +/- 0.6 mmHg per [ml.min-1.(100 g)-1]) was observed in the ipsilateral cerebral cortex of these rats. Chemical stimulation of the VLDA did not affect the reactivity of the cerebral vessels to hypercapnea (n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chemical stimulation of the ventrolateral medullary depressor area decreases ipsilateral cerebral blood flow in anesthetized rats. 167 25

As part of the International Cooperative Cardiovascular Diseases and Alimentary Comparison (CAR-DIAC) Study surveys to determine the relationship of dietary factors to blood pressure were carried out in 1985 (pilot study) and 1989 (core study). Thirteen men and 16 women, and 102 men and 115 women aged 50-54 in the rural population of Panyu county in Guangzhou were randomly selected for the pilot and core studies, respectively. Blood pressure was measured by an automatic system and 24-h urine collection by aliquot cups. All urinary specimens were analyzed in the WHO Collaborating Center (Izumo, Japan). Seven hypertensive cases and 17 borderline cases of hypertension were found in 1989 but none in 1985. Mean systolic blood pressure (SBP) and diastolic blood pressures (DBP) were increased, and the intake of dietary sodium (Na), sodium chloride (NaCl), and the ratio of sodium to potassium (Na/K) were increased markedly. The intake of magnesium (Mg) was decreased in 1989. Correlation analyses showed that body mass index was positively related to SBP and DBP (p less than 0.05), Na and NaCl were positively related only to DBP (p less than 0.05), and Mg was inversely related to SBP but with no statistical significance. These results indicate that trends of rise of prevalence rate of hypertension and mean values of SBP and DBP in association with increased dietary Na and decreased Mg intake may be due to rapid changes in dietary habits, changes in lifestyle, and the differing socioeconomic status in the area and may highlight the importance of dietary factors in the prevention of hypertension.
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PMID:Trends of diet and blood pressure in Guangzhou, South China. 170 36

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
Hypertension 1991 Jun
PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5


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