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

Renal disease and hypertension is a continuing challenge to the nephrologist. At present there are few effective methods of dealing with the common renal diseases such as glomerulonephritis, but fortunately there is now a wide selection of potent antihypertensive agents. Drug resistant hypertension should be a rarity in clinical practice. Malignant hypertension remains a therapeutic emergency. If a patient with hypertension has renal functional impairment it is essential to lower the blood pressure to normal. In the presence of renal failure this should be done with caution so as to avoid a further deterioration in the glomerular filtration rate. However, if the blood pressure is controlled and especially if the renal failure is a result of hypertension alone, renal function may stabilise or even improve, often dramatically.
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PMID:The kidney and antihypertensive therapy. 0 53

In 21 of 23 patients with hypertension unresponsive to other treatment minoxidil, a new antihypertensive drug acting via peripheral vasodilatation, lowered their blood pressure from 191 +/- 19/117 +/- 12 MM Hg to 147 +/- 13/117 +/- 12 mm Hg. The drug causes a reflex tachycardia and must therefore be combined with beta-blockers. Furthermore, an effective diuretic must also be used because minoxidil causes sodium retention. Hypertrichosis is an important side-effect for which the drug may have to be discontinued, especially in young women. Orthostasis did not occur in the reported series. The authors recommend that the drug be made available for the treatment of malignant hypertension.
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PMID:[Minoxidil in the treatment of malignant hypertension (author's transl)]. 2 86

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.
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PMID:Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain). 9 26

Estrogenic compounds are the most important group of drugs that can induce hypertension. Studies have shown an incidence of significant hypertension amounting to less than 1% after 1 year of taking oral contraceptives and about 2% after 5 years. The ratio of the incidence of hypertension among ''takers'' to that of ''nontakers'' has been assessed at 1.8 by 1 study and 2.6 by another. Small but significant increments in systolic and diastolic pressures can be discerned during the first 2 years of treatment. Cessation of treatment has resulted in pressures returing to pretreatment levels within 3 months. In those previously normal the highest readings during oral contraceptive use were only 155/90 mm of Hg. Severe hypertension is more likely to occur in the predisposed, and malignant hypertension has been reported. Previous hypertension, toxemia of pregnancy, obesity, and nephropathy are predisposing conditions. Although progestagens, used alone, do not cause clinical hypertension the incidence of hypertension associated with an estrogen-progestogen combination was directly related to the dose of progestagen used. Weight gain is often observed in oral contraceptive users and is occasionally accompanied by edema and hypertension. There is a marked increase in the circulating level of renin substrate (angiotensinogen) which is caused by the estrogen component of the pill. The increase in renin substrate is associated with increase in plasma levels of renin activity, angiotensin 2, and aldosterone, together with a fall in plasma renin concentration. The suppression of plasma renin concentration can persist for weeks after stopping the pill. The factors responsible for hypertension are probably intrinsic and may be either neural, vascular, or renal. Patients taking oral contraceptives should have blood pressure checks at 6-month intervals, and more frequently in high risk cases. In the management of those with only mild blood pressure elevation, such patients should change to a preparation with the lowest available estrogen dosage, 30 mcg of ethinyl estradiol, or reserve the method for use during crucial periods of family planning. With moderate hypertension the oral contraceptive should be suspended for 3-6 months. If the blood pressure falls, oral contraceptives should not be resumed but another method recommended. Continuing hypertension requires further study and possibly elective sterilization. Severe hypertension requires withdrawal of the pill, urgent investigation, and treatment. Other drugs may cause hypertension. Management of these patients is outlined. Structural formulae of progesterone, norethisterone acetate, medroxyprogesterone acetate, and norgestrel are shown.
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PMID:Drug-induced hypertension: pathogenesis and management. 18 40

1. Saralasin and converting enzyme inhibitors SQ 20881 and captopril induced increases in plasma renin activity to greater than 14 ng h-1 ml-1 in 43 out of 44 patients with untreated renovascular hypertension when studied in the seated position and on normal sodium intake. This degree of response was absent in patients with normal-renin essential hypertension and present in only three out of 26 with high-renin essential hypertension. 2. Reductions of greater than approximately 9% in diastolic pressure in response to these three drugs occurred regularly in renovascular hypertension (95%) but also frequently in high-renin (65%) and normal-renin (26%) essential hypertension. 3. Prior sodium depletion abolished the specificity of the renin and depressor responses to angiotensin blockage for renovascular hypertension. 4. Some patients with bilateral renovascular and all with malignant hypertension also exhibited these responses to angiotensin blockade that are characteristic of unilateral renovascular hypertension.
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PMID:Reactive hyper-reninaemia to angiotensin blockade identifies renovascular hypertension. 23 24

The evolution of malignant hypertension was studied under metabolic balance conditions in 11 uninephrectomized rats given deoxycorticosterone acetate and 1% NaCl as drinking water. Changes in sodium and potassium balance were related to changes in blood pressure, plasma renin activity, hematocrit, and kidney histology. After 3-4 weeks of steadily positive sodium balance accompanied by continuously increasing blood pressure up to 185 plus or minus 19 (SE) mm Hg, periods of sodium loss accompanied by evidence of hemoconcentration were observed marking the onset of the malignant phase as defined by the development of fibrinoid necrosis in the kidney. Plasma renin activity remained markedly suppressed both at the fourth week (0.33 plus or minus 0.02 ng/ml hour-1) when the sodium balance was positive and the kidney biopsy negative and at the end of the experiment (0.35 plus or minus 0.36 ng/ml hour-1) when the sodium balance was negative and the kidney histology revealed malignant vasculitis. Infusion of the angiotensin II inhibitor 1-Sar-8-Ala-angiotensin II consistently failed to affect blood pressure, and the kidney tissue norepinephrine level was reduced (0.054 plus or minus 0.01 mug/g) compared with the control level (0.132 plus or minus 0.02 mug/g). We conclude that malignant vasculitis in this model is preceded by hypertension associated with sodium and water retention and is accompanied by negative sodium balance, decreases in body weight, falling blood pressure, and hemoconcentration without demonstrable participation of the renin-angiotensin system or the renal catecholamines.
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PMID:Malignant hypertension resulting from deoxycorticosterone acetate and salt excess: role of renin and sodium in vascular changes. 23 7

Hypertension has been found to imply a disease entity since the beginning of this century. Effective treatment available in the last two decades has changed the outlook remarkably, especially in malignant hypertension. There are more and more evidence that less severe forms of hypertension will benefit from keeping the blood pressure under control.
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PMID:Long-term aspects on essential hypertension. 26 30

In over 95% of women who have for some time taken estrogen preparations or oral contraceptives containing estrogens there is no significant rise in blood pressure. Probably no more than 1 to 2% of young women treated develop clinically significant hypertension. In very rare instances, the preparations may induce potentially fatal malignant hypertension. Old age, a family history of hypertension and toxemia during earlier pregnancies seem to be predisposing factors for estrogen hypertension. Guide lines are given for the supervision of blood pressure in daily medical practice and circulatory contraindications to the prescription of these preparations are suggested.
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PMID:[Hypertension due to hormonal contraceptives and estrogens (author's transl)]. 30 34

The role of hypertension in chronic glomerulonephritis was studied in rats with experimental hypertension and nephrotoxic serum nephritis. Nephrotoxic serum nephritis accelerated the hypertensive course of Godblatt's type of experimental hypertension both in the acute and chronic phases. Malignant hypertension was found to be caused in some rats by the nephrotoxic serum injection in the chronic phase of experimental hypertension. Nephrotoxic serum nephritis was more protracted in SHR than in control rats. These results suggest that hypertensive changes might aggravate glomerulitis, and that nephritic processes also facilitate the hypertensive changes.
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PMID:Hypertensive changes in experimental nephritis combined with experimental hypertension. 32 44


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