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

Hypertension that is truly resistant to modern antihypertensive therapy is uncommon. In the majority of cases, apparent resistance is more likely associated with poor patient adherence, interacting drugs, drug interactions, and inappropriate drug dosages. Sodium and fluid volume play a major role in resistant hypertension. There is considerable evidence to support the role of dietary sodium restriction in successful nonpharmacological treatment of hypertension. Salt sensitivity in humans appears to represent at least one factor determining individual susceptibility to variable salt intakes. Sodium and water retention may lead to refractoriness to many antihypertensive agents, and there is evidence to suggest that extracellular fluid volume expansion also plays a role in many hypertensive patients. While retention of sodium and water is well established early in patients with renal parenchymal disease, hypertension associated with progression of renal parenchymal disease is complicated by other factors that include interactions between hemodynamic and humoral factors, functional changes in adrenergic responses, and structural vascular disease. The role of other cations such as potassium, calcium, and magnesium in resistant hypertension has yet to be established.
Hypertension 1988 Mar
PMID:The patient with resistant hypertension. Cations, volume, and renal factors. 328 Apr 98

We investigated the status of circulating kinins in rats with severe hypertension caused by drinking 1% NaCl (saline) and treatment with deoxycorticosterone (DOC, 25 mg/kg/wk s.c.) for 5 weeks. Saline-drinking rats treated with DOC had a higher systolic blood pressure (210 +/- 4 mm Hg) than did rats without DOC treatment drinking water (138 +/- 3 mm Hg) or saline (141 +/- 3 mm Hg). The concentration of kinins in the inferior vena cava plasma of DOC-salt hypertensive rats did not differ from the venous plasma kinin concentration in normotensive rats drinking water or saline. In contrast, the arterial plasma kinin concentration in DOC-salt hypertensive rats (7.0 +/- 0.8 pg/ml) was lower (p less than 0.002) than that in water-drinking controls (14.0 +/- 2.2 pg/ml); it also was lower (p less than 0.005) in saline-drinking rats (8.1 +/- 0.9 pg/ml) than in water-drinking controls. Infusion of bradykinin (20 micrograms/kg/min i.v.) increased arterial plasma kinins in all the groups. Nonetheless, the arterial plasma kinin concentration achieved during bradykinin infusion in DOC-salt hypertensive (1590 +/- 130 pg/ml) and in saline-drinking rats (1540 +/- 100 pg/ml) was lower than that in water-drinking rats (2140 +/- 210 pg/ml). On the other hand, during infusion of the kininase II inhibitor captopril (80 micrograms/hr i.p.) for 3 days, neither DOC-salt hypertensive rats nor saline-drinking normotensive rats exhibited significant reduction of arterial plasma kinins relative to the level in water-drinking controls. These data indicate that high salt intake, irrespective of the level of blood pressure, causes the arterial plasma concentration of kinins to fall.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1988 May
PMID:Plasma kinin concentration in deoxycorticosterone-salt hypertension. 328 20

In earlier investigations it has been found that high arterial blood pressure of salt-sensitive DAHL rats (DAHL-S) that received a diet containing 8% NaCl could be normalized by chronic treatment with specific calcium antagonists, as for instance, nitrendipine or anipamil. Parallel measurements on heart and arterial vasculature with atomic absorption spectrometry revealed that there was a rise in absolute calcium content upon development of hypertension, whereas under the influence of nitrendipine, not only the blood pressure and heart weight but also myocardial (and arterial) tissue calcium content remained in the physiologic range. In the present study, an additional determination of the free intracellular calcium ion concentration with Ca-sensitive microelectrodes was carried out. For technical reasons, the measurements were restricted to isolated resting rat papillary muscles (stretched to optimal length in a perfusion bath of 1.5 ml at 30 degrees C in normal Tyrode solution). The impalement of the electrodes was considered adequate when the heights of Ca potential and membrane potential were constant for more than twenty minutes. In order to produce severe systemic hypertension, a group of six-week-old DAHL-S rats was fed with an 8% NaCl diet over five weeks. Another group of DAHL-S rats received additionally 150 mg/kg nitrendipine twice a day orally. Salt-resistant DAHL-R rats, also fed with an 8% NaCl diet, served as controls. The findings of this preliminary study are as follows (n = 5 in each group): (table; see text).
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PMID:Restriction by nitrendipine of excessive concentration of free intracellular calcium ions in ventricular myocardium of hypertensive rats. 335 26

Pressor responses to arginine-vasopressin (AVP) and norepinephrine (NE) were studied in deoxycorticosterone (DOC)-salt hypertensive and prehypertensive rats. DOC-salt rats received weekly subcutaneous injection of DOC acetate (30 mg/kg) and given 1% saline for drinking. Salt and control rats received injections of sesame oil and given 1% saline or tap water, respectively. On the 5th day (prehypertensive stage) and at 6th week (hypertensive stage) after treatment had started, pressor responses were studied by measuring changes in mean arterial pressure recorded from the iliac artery in response to i.v. injections of AVP or NE under urethane anesthesia. Pressor response to AVP was enhanced both in DOC-salt hypertensive and prehypertensive rats compared with that in salt and control rats. Pressor response to NE tended to be enhanced in DOC-salt hypertensive rats, however, the enhancement was not observed in the rats in prehypertensive stage. Enhanced pressor response to AVP in DOC-salt prehypertensive rats was not due to the structural change of vascular beds, because peripheral resistance in isolated hindlimb preparations was similar in the three groups. Thus, pressor response to AVP was enhanced even in the prehypertensive stage in DOC-salt rats and the enhancement might be involved in the pathogenesis of hypertension in DOC-salt rats.
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PMID:Pressor response to vasopressin and norepinephrine in DOC-salt hypertensive and prehypertensive rats. 338 Dec 22

The mechanism by which excessive sodium chloride intake raises blood pressure has not been fully clarified. The present study was therefore undertaken in patients with essential hypertension to investigate the possible role of an intracellular calcium-dependent mechanism in salt sensitivity. The difference in mean blood pressure between a week of low sodium chloride diet (3 g/day) and a week of high sodium chloride diet (20 g/day) was studied in relation to the intracellular free calcium concentration in lymphocytes and an acute hypotensive response to a 10-mg sublingual dose of nifedipine in 12 inpatients. Sodium chloride loading induced significant increases in mean blood pressure (from 111 +/- 12 to 122 +/- 11 mm Hg; p less than 0.01), intracellular free calcium in lymphocytes (from 133 +/- 13 to 145 +/- 9 nmol/L; p less than 0.01), and the hypotensive response to nifedipine (from 19 +/- 6 to 31 +/- 10 mm Hg; p less than 0.01). In addition, serum total calcium concentration was decreased while urinary calcium excretion was increased. The elevation of mean blood pressure was closely and positively correlated with the increase in intracellular free calcium concentration (r = 0.71, p less than 0.05) and the increase in the hypotensive effect of nifedipine (r = 0.91, p less than 0.01) after sodium chloride loading. However, changes in these values had no relation to the change in serum concentration or urinary excretion of calcium. These data suggest that change in the cellular calcium-dependent vasoconstriction mechanism may be associated with salt sensitivity of patients with essential hypertension.
Hypertension 1988 Jun
PMID:Role of cellular calcium in salt sensitivity of patients with essential hypertension. 339 81

Effects of sodium load on the development of hypertension, plasma renin activity (PRA) and kininogen were studied in rats with renal artery constriction and untouched contralateral kidney. After the operation or sham-operation, 0.9% NaCl or water were given as drinking fluid. A marked hypertension (systolic pressure greater than 150 mmHg) developed in all operated rats on saline, but only in 2/3 of operated rats on water. In none of the sham-operated controls did systolic pressure exceed 150 mmHg during 7 postoperative weeks. Within the operated group on water, hypertensive rats had significantly higher PRA values than normotensive animals (P less than 0.05). Salt load slightly suppressed the PRA in sham-operated rats but not in animals with constriction renal artery, compared to sham-operated controls on water. The operated rats on salt excess had higher plasma kininogen levels than the operated normotensive rats on water (P less than 0.05), but there were no other significant differences in kininogen values between different study groups, regardless of whether blood pressure was increased or not. The results indicate that in this form of hypertension, the high blood pressure can be maintained without any increase in PRA if animals are subjected to a sodium load which sensitizes vascular beds to angiotensin. The increase in plasma kininogen, suggesting suppression of kallikrein-kinin system, is unlikely associated with the increase of blood pressure.
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PMID:The effect of sodium load on the development of hypertension, plasma renin and kininogen in rats with renal artery constriction. 352 27

We describe for the first time a non-human primate model of mineralocorticoid-salt hypertension. Baboons instrumented for chronic, direct measurement of arterial pressure, underwent sodium chloride loading (8.6 or 17.1 mEq/kg/day) by different routes for several weeks and deoxycorticosterone acetate (DOCA) 5 mg/2 days i.m., in addition to sodium chloride, for periods lasting up to several months. Salt loading alone at 8.6 mEq/kg/day had no chronic effect on mean arterial pressure (MAP). Salt loading at both doses in combination with DOCA produced increases in MAP within a few days which became progressively larger over weeks to months. DOCA-salt hypertension was associated with hyporeninemia and mild hypokalemia, without consistent changes in heart rate or plasma catecholamines. A biofeedback procedure applied to three animals failed to reduce tonic blood pressure. In two of these animals, administration of clonidine or atenolol also had no antihypertensive effect, whereas a diuretic combination (hydrochlorothiazide and triamterene) rapidly abolished the hypertension. The absence of amelioration of the hypertension by a central sympatholytic agent or a beta-adrenoceptor blocker, coupled with the absence of increased plasma catecholamines, suggests that increased sympathetic activity may not contribute to the hypertension in contrast with findings in lower animals but consistent with clinical reports.
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PMID:Production and reversal of DOCA-salt hypertension in baboons. 358 84

The response of known hypertensives to advice on sodium restriction was examined as part of a 5-year study on hypertension screening in family practice. The study comprised 34 family practices, pair-matched for location, activity level, and length of time in present practice. One practice in each matched pair was randomly allocated to an experimental or a control group. All hypertensive patients in each experimental practice were exposed to a management program which included dietary counseling to restrict sodium intake. A sample of hypertensive patients (N = 1,001) in both control and experimental groups was interviewed 3.5 years into the study. Although more subjects in experimental practices reported not adding salt (22.9%) compared with those in control practices (17.3%), the results of multivariate analysis showed that type of practice (experimental or control) was not significantly associated with salt use. Salt avoidance was strongly related to lower levels of education and to sex (men were less likely to use salt). Subjects who did not use salt also tended to avoid high-sodium foods. The response to nutritional advice was less favorable than expected. Difficulties in compliance with dietary recommendations are discussed.
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PMID:Lack of impact of salt restriction advice on hypertensive patients. 358 62

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.
Hypertension 1987 Nov
PMID:Role of prostaglandins and kinins in the renal pressor reflex. 366 64

Weanling Dahl salt-sensitive (DS) and salt-resistant (DR) rats were used to compare effects of feeding high or low NaCl diets on taste preference for, and intake of, a wide range of saline concentrations. The DS and DR were fed either 8.0 or 0.4% dietary NaCl for 4 weeks. Then, with all animals fed the 0.4% NaCl diet, their taste preferences for 0.0001 to 0.56 M saline were assessed using three 24-hour two-bottle preference tests of each solution versus distilled deionized water. Saline preference and intake were influenced by concentration and its interaction with genotype, with DS exhibiting higher preferences than DR for hypotonic saline. The DS preexposed to 8.0% dietary NaCl showed elevated consumption levels of water and total fluid (saline + water) that persisted throughout the 5-week test period, despite transfer to the 0.4% NaCl diet before the initiation of preference testing. Findings indicate that genotype, dietary NaCl levels in weaning diet, and saline concentration of preference test solutions interact to influence saline preference and saline and water intake in Dahl rats.
Hypertension 1986 Nov
PMID:Salt level in weaning diet affects saline preference and fluid intake in Dahl rats. 377 Aug 65


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