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

Minoxidil, a new peripheral vasodilator, given orally to hypertensive men in single doses of 5-25 mg, produced no haemodynamic changes within one hour after administration. After repeated oral doses within 24 hours to a total of 15-45 mg and after 10 mg t.i.d. orally for one week, moderate decreases in BP were seen concomitant with tendencies to increased heart rate and cardiac output. Clinically, oral minoxidil 10-50 mg daily in combination with diuretics and adrenergic beta-receptor blocking agents achieved an improved BP control in five patients with sustained arterial hypertension and unsatisfactory response to previous treatment. However, in four of the five patients minoxidil had to be withdrawn because of side-effects. It is concluded that minoxidil, producing a hypotensive effect of slow onset, may find a place as a therapeutic addition to symptomatic patients with severe and therapy-resistant hypertensive cardiovascular disease, provided adequate measures are taken to counteract side-effects, especially water retention and development of oedemas.
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PMID:Minoxidil--haemodynamic and clinical experiences with a new peripheral vasodilator. 23 65

The authors reports the results of 171 cases of portal systemic by pass operations out of a total of 200 cases operated on between 1968 and 1974. These 171 patients all presented with a syndrome of portal hypertension with oesophageal varices and all had previously bled. Their age lay in 70 p. cent of cases between 40 and 60 years and the cause of hypertension was in 96 p. cent of cases an intra-hepatic block. 41 p. cent were included in the risk group A according to Child's classification, 51 p. cent in Group B and 8 p. cent in Group C. The routine operation was side-to-side portacaval anastomosis (75 p. cent). The operative mortality was 5.2 p. cent in all with 1 p. cent in cases with risk A, and 15 p. cent in cases with risk C. The fall in portal pressure was on average 15 cm of water, i.e. 41 p. cent of the initial pressure. The overall survival after 5 years was 65 p. cent, 70 p. cent for risk A and 26 p. cent for risk C. In 69 p. cent of cases the cause of death was liver failure. Encephalopathy, studied in 76 patients over an average period of 3 years, occurred in 39 p. cent of cases, and in 13 p. cent of the latter it was serious. In the 12 p. cent of survivors, we noted recurrent hemorrhage, but in only 2.5 p cent of cases did the bleeding definitely come from oesophageal varices. In the light of these results, the authors judge positively the surgical treatment of portal hypertension.
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PMID:[Immediate and late results of 171 therapeutic portal systemic by pass operations (author's transl)]. 30 46

Studies on the Kyoto (SHR) and the New Zealand (GHR) strains of genetically predisposed hypertensive rats have shown that in the SHR neurogenic influences, primarily of higher central origin, play an important role in the initiation of hypertension. Studies on human essential hypertension indicate that this may also be true for man, although it is far from being the sole explanation. Brookhaven hypertension-prone rats illustrate the interaction between genetic and exogenous factors since they require an overload of salt for the development of high blood pressure. The Milan hypertensive rats (MHS), on the other hand, illustrate a genetic deviation of renal function with imbalance between glomerular filtration and tubular resorption of sodium and water, which may simulate at least some variants of the relatively mild forms of low renin hypertension in man. Structural adaptive vascular changes have been demonstrated in SHR and GHR and in nongenetic renal hypertension in rats, and there are several indications of their presence in MHS. Thus, regardless of the nature of the initiating factors, these secondary but rapidly established changes occur and greatly contribute to the maintenance and acceleration of the hypertensive state. The vascular changes can even be regarded as a common denominator for chronic hypertension and serve as an element which, in fact, reinforces the initiating mechanisms. The progress of the vascular changes can be interfered with by reducing the pressure load. Lowering the blood pressure by pharmacologic treatment is most effective when the treatment is initiated as such an early age when the cardiovascular structural adaptation is still minimal. Treatment in later phases is less successful since the adaptive increases in cardiac and vessel wall thickness can then no longer be fully normalized by pressure reduction because of increased amounts of collagen and other connective tissue elements in the vessel wall, which regress poorly. An increased wall thickness of the resistance vessels implies a vascular hyperreactivity to constricting influences which, in turn, rapidly brings the blood pressure back to supranormal levels as soon as therapy is stopped.
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PMID:Mechanisms of spontaneous hypertension in rats. 32

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

The effect of high doses of furosemide, 200 to 800 mg daily, has been studied in 12 Nigerias with edema associated with severe chronic renal failure and hypertension. They all responded well and lost their edema fluid during a period which varied from 10 to 57 days. The fecal water content and the frequency of bowel opening while on furosemide were significantly higher than without furosemide in six of these patients. It is concluded that the gastrointestinal tract is a major contributory site of fluid loss in patients with grossly impaired renal function.
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PMID:High-dose furosemide in Nigerians with severe chronic renal failure: effect on fecal water content. 34 52

Present understanding of the physiology of arterial pressure regulation indicates that the renal-body fluid volume system determines the level at which the mean pressure resides over long periods of time. The relationships between blood volume, and size and compliance of the entire vascular system, and intrinsic regulation of tissue blood flow determine the sequence of observed changes in cardiac output and total peripheral resistance. Current evidence is compatible with the concept that functional changes in the renal vasculature or tubular system, either intrinsic or extrinsic in origin, reflect the final common pathway in the genesis of all forms of experimental and human hypertension. At the present time the nature of these renal changes appears to alter the fundamental relationships between renal perfusion pressure and sodium and water excretion. One of the major challenges in the field of hypertension today is to test the hypothesis that changes in renal function, either extrinsic or intrinsic in form, are involved in all forms of hypertension.
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PMID:Perspective on the physiology of hypertension. 35 14

The kallikrein-kinin system in the kidney is localized in the distal nephron, where it appears to be linked to processes that control water and electrolyte excretion. Some evidence exists that the effect of the renal kallikrein-kinin system is partially mediated by the release of prostaglandins. It has not yet been determined whether endogenous kinins affect the function of the nephron directly or indirectly by changes in renal blood flow distribution. Further, a number of studies in animals and humans indicates that kallikrein excretion is decreased in most types of hypertension, with the exception of hypertension caused by an excess of mineralocorticoids (where kallikrein is increased). In rats susceptible to the hypertensive effect of salt, kallikrein is conspicuously decreased. In renal diseases, urinary kallikrein excretion is also decreased. Finally, it still needs to be determined whether or not low kallikrein excretion is a pathogenetic factor in hypertension and renal diseases.
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PMID:The renal kallikrein-kinin system in human and in experimental hypertension. 36 76

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

In the system of long-term maintenance of the arterial pressure level by means of the renal excretion mechanism described by Guyton et al., the renal medulla with its counterflow-concentrating multiplier and powerful source of natural natriuretics, the prostaglandins, plays the role of a "control device", a regulator setting the level of arterial pressure required for fulfilling the complete volume of renal excretion of salts and water. Increase in systemic arterial pressure causes the development of a complex of structural-functional changes in the kidney, the common purpose of which consists in preventing the loss of salts and water by the organism by shifting parameters of the excretory renal function in such a manner that the normal (balanced with the supply of salts and water to the organism) volume of excretion may occur with higher values (kidney "resetting"). The central role in accomplishing this "resetting" is played by the medullary excretory mechanism which is closely connected, due to the absence of autoregulated blood flow in the medulla, with systemic arterial pressure. When the kidney reaches the "resetting" this mechanism provides for a sufficiently full volume of excretion only when the arterial pressure increases, maintaining its fixed (higher) level by means of the feedback mechanism. In hypertension caused by overdosage of corticosteroid hormones or excess of salt in the diet the increase of pressure develops as a compensation for the occurring deficiency of the medullary excretory mechanism.
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PMID:[Kidney in chronic arterial hypertension: "resetting" and the role of the renal medulla in its development]. 39 Feb 6

Indirect systolic blood pressure (SBP) was monitored in male, weanling, spontaneously hypertensive rats (SHR) maintained on water for 16 weeks (group A) or on captopril therapy (100 mg/kg/day in drinking water) for 4 (group B), 8 (group C), 12 (group D), 16 (group E) weeks. Weanling SHR of group A developed typical, time-related hypertension over a 16-week observation period. In marked contrast, SHR receiving captopril did not develop hypertension. Discontinuation of captopril after 4, 8, 12 or 16 weeks resulted in the usual development of hypertension. There was a transient increase in water consumption of drug treated rats which returned to normal by 8 weeks of dosing. Conversely, when captopril therapy was discontinued after 4, 8 or 12 weeks, there was a transient decrease in water intake, the magnitude of which was inversely related to the duration of drug therapy. These results demonstrate that daily captopril therapy was able to completely prevent the development of spontaneous hypertension. Explanations for the mechanism(s) underlying the influence of captopril on blood pressure and water intake remain speculative.
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PMID:Prevention of the development of spontaneous hypertension in rats by captopril (SQ 14,225). 39 24


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