Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Moderate salt restriction lowers blood pressure in many patients with essential hypertension. The effectiveness of the salt restriction in lowering blood pressure appears to be directly related to the severity of the blood pressure and suppression of the renin-angiotensin system. Patients with more severe hypertension, older patients or black patients will respond best. Salt restriction is additive to the effect of blood pressure lowering drugs particularly those that block the renin-angiotensin system such as beta-blockers and converting enzyme inhibitors. All patients with high blood pressure and, particularly those already on drug treatment, should be instructed on how to cut back their salt intake moderately. Most patients find it easy to reduce salt intake to around half of their present consumption.
 ...
PMID:Salt restriction in the treatment of hypertension. 386 23

Three controlled intervention studies were carried out in North Karelia to study the possible role of dietary fat in the control of human blood pressure. All studies included middle-aged free-living couples (families) and a baseline (BS, 2 weeks), an intervention (IN, 6-12 weeks) and a switch-back (SB, 4-6 weeks) period. During IN the families were instructed to eat low fat (less than 25 en% instead of 39 en%), high P/S ratio diet (0.4-1.1 instead of 0.2). Salt and energy intake and other lifestyles were kept constant. In the first study the P/S ratio of the IN diet was 1.1. Both systolic and diastolic blood pressures decreased significantly during IN and increased back again during SB. The same results were obtained in the second study at P/S level 0.9 when a randomized group with 60% salt reduction and a control had little change in their blood pressure levels. In the third study the blood pressure reduction was again repeated during a 12 week IN period. The reduction was similar in two randomized groups with P/S 0.4 and 0.9, when both group had less than 25 en% of total fat. The results strongly support the hypothesis that dietary fat is related to human blood pressure, and that modification of dietary fat should be considered in the non-pharmacological prevention and management of hypertension.
 ...
PMID:Role of dietary fat in blood pressure control. 386 27

The effects of chronic dietary salt-loading and nifedipine therapy on hypertension-prone (SBH), -resistant (SBN) and parental (SB) Sabra rats were investigated. Salt diet for 12 weeks resulted in a sustained hypertension and heart hypertrophy only in SBH. Nifedipine therapy (300 p.p.m. = 300 mg/kg of food) introduced after week 7 on a salt diet, achieved small changes in salt-loaded SBN and SB rats, but resulted in a marked decrease in blood pressure in SBH rats within 1 week and in a regression of cardiac hypertrophy. Plasma renin activity rose slightly in nifedipine treated SB and SBN rats, but decreased significantly in treated SBH rats. Histopathological investigations revealed hypertensive vasculopathy in three out of nine untreated SBH rats, whereas there were no morphological changes in the treated rats.
 ...
PMID:Salt-induced hypertension in the 'Sabra' rat strain: influence of nifedipine treatment. 388 35

The influence of renal dysfunction (induced by ischaemic injury) on the development of salt hypertension was studied in rats which were exposed to 60 min of renal ischaemia when either immature or adult. Saline-drinking age-matched animals served as controls. The blood pressure, plasma urea concentration, extracellular fluid volume (ECFV) and renal mass were measured 21 and 50 days after renal ischaemia. Increments of plasma urea concentration and ECFV were considered to be indicators of renal dysfunction. Increased renal mass was used as an estimate of the degree of renal injury. In adult rats, both plasma urea concentration and ECFV were increased 3 weeks after renal ischaemia. This correlated with a pronounced increase of renal mass. A similar relation of renal mass to ECFV was still present 50 days after renal ischaemia. In rats treated when immature the increment of plasma urea concentration was much smaller and ECFV did not differ significantly from the control volumes. A mild salt hypertension developed only in those rats which were treated when immature. On the other hand, the blood pressure tended to decrease in animals treated when adult. It is concluded that mild renal dysfunction facilitates the development of salt hypertension in immature rats. This is in contrast with the reversed effects of extensive renal dysfunction in adult animals. It is suggested that the age of animals is more important for the induction of salt hypertension than the degree of renal dysfunction.
 ...
PMID:Age-dependent blood pressure response to increased salt intake in rats influenced by a transient renal ischaemia. 395 8

The haemodynamic, antianginal and antihypertensive effects of nicardipine, a vascular selective calcium antagonist, were studied in experimental animals. In the canine isolated coronary artery, nicardipine relaxed potassium-induced contraction and suppressed 3,4-diaminopyridine-induced rhythmic contractions more effectively than nifedipine, verapamil or diltiazem. In anaesthetised rats, nicardipine prevented the elevation of ST segment induced by intracoronary injection of methacholine. In anaesthetised dogs, nicardipine produced a greater vasodilatation in vertebral, carotid, and coronary vessels than in mesenteric, femoral, and renal vessels and did not affect myocardial oxygen consumption. In conscious monkeys, nicardipine given intravenously lowered blood pressure and gave rise to reflex tachycardia but did not prolong the A-V conduction time. Nicardipine given orally lowered blood pressure in spontaneously hypertensive rats (SHR), renal hypertensive rats (RHR), and deoxycorticosterone acetate/salt hypertensive rats (DOCA/Salt), as well as in normotensive rats. Long-term treatment with nicardipine given orally for 12 weeks effectively lowered high blood pressure in the three types of hypertensive rats, reduced cardiac hypertrophy in SHR and DOCA/Salt rats, and prevented mortality from stroke in DOCA/Salt rats. Combined treatment with nicardipine and a beta-adrenoceptor blocking agent (indenolol) showed an antihypertensive effect similar to that obtained with nicardipine alone. Conscious renal hypertensive dogs given repeated oral administration of nicardipine for 14 days did not develop tolerance to the hypotensive activity of nicardipine. Under the same conditions, tolerance to hydralazine developed within 4 days.
 ...
PMID:Cardiovascular pharmacology of nicardipine in animals. 402 53

Adrenal-enucleated, mononephrectomized rats given a high salt diet rapidly develop malignant hypertension, characterized by the presence of necrotizing vascular lesions in a number of organs and tissues. If a normal salt intake is provided, or if hydrochlorothiazide is given together with a high salt diet, there is, instead, the delayed onset of benign hypertension which either stabilizes or increases in intensity extremely slowly; Such animals display few, if any, pathologic vascular changes other than occasional focal glomerular hyalinization, show insignificant cardiac enlargement, and do not exhibit alterations in the serum sodium or potassium. Occasional animals behave atypically and develop malignant hypertension despite normal salt consumption, demonstrating that in susceptible rats excess salt is not essential to this disorder. Hydrochlorothiazide given to rats that imbibed distilled water postoperatively prevented hypertension entirely for 97 days, when one of eight rats developed mild hypertension and some others reached what is regarded as a prehypertensive range. It is concluded that adrenal regeneration provides a physiological milieu favorable to the development of benign hypertension, which is not, as a rule, manifest until regeneration is complete. Salt excess converts the response into one in which malignant hypertension begins during regeneration and worsens rapidly thereafter until death. The course and findings are compared with those of the benign and malignant phases of clinical essential hypertension, and the implications of the similarities are discussed.
 ...
PMID:Benign and malignant hypertension after adrenal enucleation in the rat. Relationship to salt intake, response to hydrochlorothiazide, and similarity to essential hypertension. 602 46

Cerebral aneurysms were induced in rats treated with unilateral ligation of the common carotid artery and hypertension produced by renal infarction with or without beta-aminopropionitrile, one of the lathyrogens. In this experiment, cerebral aneurysms developed more frequently than in the previous experiments in which hypertension induced by deoxycorticosterone and salt had been used. It was demonstrated that deoxycorticosterone was not essential to the development of the lesion. Regardless of its type, hypertension combined with carotid ligation played a primary role in the production of cerebral aneurysms in rats. Sodium chloride enhanced the systolic hypertension and thus increased the incidence of lesions. The role of hypertension in the development of cerebral aneurysms in humans is discussed.
 ...
PMID:Experimentally induced cerebral aneurysms in rats: Part VI. Hypertension. 611 49

In urethane-anesthetized rats, vasodepressor neuron pools were located bilaterally in and adjacent to the A1 area of the ventrolateral medulla by injecting the neuroexcitatory amino acid, L-glutamate. Ventrolateral vasodepressor areas included the caudalateral part of the nucleus reticularis gigantocellularis, the rostrolateral part of the nucleus reticularis ventralis, and the dorsal nucleus reticularis lateralis. In the ventrolateral vasodepressor areas L-glutamate elicited a transient fall in blood pressure (BP) and heart rate (HR). The opiate agonist (D-ala2-met5)-enkephalinamide (DAME) was used to stimulate opiate receptors in vasodepressor sites, identified with L-glutamate. In these sites, bilateral injections (0.1 microliter/site) of DAME caused a dose-related (2.5-500.0 ng) increase in blood pressure and heart rate, as well as exaggeration of the response to occlusion of the carotid. The effects of DAME on blood pressure were completely abolished by alpha-adrenergic blockade (phentolamine, 2 mg/kg, i.v.) and all effects of DAME were reversed by the administration of naloxone HCl (1 mg/kg, i.v.). Naloxone reversal was accompanied by an unexpected "rebound" hypertension. Saline had no significant effects when injected, or administered intravenously, in the absence or presence of DAME. It was concluded that stimulation of opiate receptors in the ventrolateral vasodepressor areas activated sympathetic outflow. An enkephalinergic system in this area of the brain stem may serve to modulate blood pressure, heart rate and cardiovascular reflexes.
 ...
PMID:Hypertensive response following stimulation of opiate receptors in the caudal ventrolateral medulla. 614 14

Seventeen young normotensive men with a family history of hypertension in two generations (H) and 15 age-matched control subjects (C) were studied with respect to blood pressure (BP), intraerythrocyte sodium content (IeNa), sodium influx, and rate of sodium efflux. The investigations were done during normal salt intake and after 4 weeks of ordinary intake plus 12 g NaCl daily. BP did not increase significantly in either of the two groups during increased salt intake. During normal salt intake H had a significantly (p less than 0.01) higher IeNa (9.5 +/- 1.5 mmol/L) compared with C (8.2 +/- 1.4 mmol/L). During high salt intake IeNa in H decreased significantly to 8.1 +/- 1.2 mmol/L, the difference from C (7.6 +/- 1.2 mmol/L) not being significant. While the Na influx was similar in the two groups, the rate constant for Na efflux was significantly lower during normal salt intake in H (0.23 +/- 0.08 vs 0.29 +/- 0.1 h-1, p less than 0.05). Salt intake increased the efflux rate constant significantly in H (0.28 +/- 0.08 h-1, p less than 0.05), while it did not change significantly in C (0.32 +/- 0.08 h-1) compared with the value for normal salt intake. Our results suggest that young men with a hereditary predisposition to hypertension have a higher IeNa secondary to a lower rate of Na efflux, while a normal Na influx indicates normal cell permeability to Na. The findings in H during high Na intake--a decreased IeNa and an increased efflux rate of Na--do not favor the existence of a sodium transport inhibitor, in subjects predisposed to hypertension, increasing during high salt intake and volume expansion and acting through inhibition of the Na efflux.
 ...
PMID:Blood pressure, intraerythrocyte content, and transmembrane fluxes of sodium during normal and high salt intake in subjects with and without a family history of hypertension: evidence against a sodium transport inhibitor. 620 56

Research of the past 30 years has produced information showing the close interrelationships of neural mechanisms, the renin-angiotensin-aldosterone system, and salt balance as determinants of arterial pressure, both normal and elevated. Contemporary emphases are on central sites of neural regulation of arterial pressure, and an interesting sidelight of the conventional approaches is the possibility that the endorphin-enkephalin system may have a role in hypertension. Salt balance is critically important for people with salt-dependent hypertension; mechanisms of this dependency have not been defined but possible candidates are activation of the sympathetic nervous system, release of a natriuretic factor that causes vasoconstriction as well as salt loss, and renal-neural interactions.
Hypertension
PMID:Physiologic regulation of arterial pressure. An overview. 628 83


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>