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

We describe the natural recovery from the aggravated hypertension, hypokalemia and suppression of the renin-aldosterone axis after the glycyrrhizin discontinuation in two mild hypertensive women aged 71 and 68 years, who had been administered 273 to 546 mg glycyrrhizin daily for 1.5 and 6 months, respectively, for the treatment of liver disease. About one month after the glycyrrhizin discontinuation, acceleration of hypertension, hypokalemia and suppression of the renin-aldosterone system still continued in both patients. At this stage, sodium restriction resulted in the normalization of blood pressure with weight loss and the subsequent sodium repletion produced a rapid increase in blood pressure to hypertensive levels observed before sodium restriction, with weight gain. Plasma renin activity and plasma aldosterone were low and did not respond to sodium restriction. Inappropriately excessive amounts of potassium were also excreted in the presence of hypokalemia. About one and a half months later, the improvements of aggravated hypertension, hypokalemia and suppressed renin-aldosterone system gradually occurred in both patients. Sodium restriction performed about three months later in case 2 no longer produced the changes in blood pressure and body weight. Plasma renin activity and plasma aldosterone responded subnormally to sodium restriction. These results demonstrate that both patients had a prolongation of the syndrome resembling primary aldosteronism except the low plasma aldosterone level about one month after the glycyrrhizin discontinuation. The possible mechanisms by which this prolongation was caused are discussed.
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PMID:Prolonged pseudoaldosteronism induced by glycyrrhizin. 39 3

Circadian changes in plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in normal and hypertensive rats were determined by measurements at 8 a.m., 4 p.m. and 12 midnight (MN). For the normals, PRA and PAC were highest at 4 p.m. Animals made hypertensive by constriction one renal artery with the other kidney intact were studied after 4, 5, 7 and 10 weeks; the clear-cut circadian rhythm for PRA in normals had disappeared but for PAC the circadian rhythm was present in the 4-, 5- and 10-week groups. Both PRA and PAC were elevated in all four hypertensive groups compared with the normal controls and there was a highly significant correlation between PRA and PAC. The 4 p.m. peak value for PAC was much higher in relation to the 8 a.m. and 12 MN values values in the hypertensive animals than in the normals. Sodium balance studies failed to demonstrate any appreciable differences among the groups. When the hypertensive animals were divided into two groups on the basis of the level of hypertension, the rats with moderate hypertension showed an average elevation in PRA which was significant in only the 4- and 7-week groups whereas PRA was elevated in all four groups with severe hypertension. Thus, the present data help to define the activity of the renin-angiotensin-aldosterone system in two-kidney, one clip hypertension in the rat.
Hypertension
PMID:Circadian changes in plasma renin activity and plasma aldosterone concentration in two-kidney hypertension rats. 39 40

The effects of continuous intrarenal prostaglandin E2 (PGE2) infusion (7 days) on sodium and water balance, plasma renin activity (PRA), and sodium and water balance, plasma renin activity (PRA), and mean arterial pressure (MAP) were examined in conscious, unilaterally nephrectomized dogs maintained on a fixed sodium intake of 55 meq/day. PGE2 infusion (2 microgram/min) resulted in a sustained threefold increase in both urine output and water intake without a measurable change in glomerular filtration rate. PRA increased from 0.4 +/- 0.1 during the control period to 2.2 +/- 0.9 ng AI.ml-1.h-1 on day 1 and averaged 3.6 +/- 0.5 for the remaining 6 days of PGE2 infusion. Concurrently, MAP increased from 102 +/- 3 to a maximum of 117 +/- 4 mmHg on day 5; changes in PRA and MAP were significantly correlated (r = 0.96, P less than 0.001). Sodium excretion increased from 54.5 +/- 3 to 88.0 +/- 19 meq/day on day 1, and then declined to an average of 64.8 +/- 1 meq/day for the remaining 6 days of infusion. All variables returned to the control level during the recovery period. Intravenous infusion of PGE2 (2 microgram/min) yielded directionally similar but statistically insignificant effects. It is concluded that chronic intrarenal PGE2 infusion results in marked diuresis, polydipsia, a moderate loss of sodium, enhanced PRA, and mild hypertension.
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PMID:Prostaglandin E2-induced hypertension in conscious dogs. 49 30

Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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PMID:Plasma catecholamines determination using high pressure liquid chromatography and their roles in blood pressure regulation and experimental hypertension in rats. 50 4

A 33-year-old man is described with hyperkalaemia, hypertension and acidosis. The blood pressure was 160 to 200 mmHg systolic and 90 to 110 mmHg diastolic and the plasma potassium was between 6.0 and 7.0 mmole per litre. There was no renal disease and creatinine clearance was 103 ml per minute. Plasma renin activity was low and plasma aldosterone was at the lower limit of normal. Sodium deprivation or oral frusemide had little effect on blood pressure, plasma potassium, renin, aldosterone or arginine vasopressin. However, bendrofluazide caused a rapid fall of blood pressure and plasma potassium, and rise of plasma renin, aldosterone and plasma arginine vasopressin. Hypertension and hyperkalaemia is rare in the absence of renal failure. Four similar patients reported previously are reviewed. We suggest that our patient, and perhaps some of those reported earlier had primary abnormality of renal tubular function with impaired secretion of potassium and excessive tubular reabsorption of sodium. The plasma renin activity could be due to volume expansion and the low plasma aldosterone was probably caused by the antagonistic effects of low renin depressing synthesis and hyperkalaemia increasing it. A minor similar tubular abnormality might be the explanation in some of the patients with essential hypertension who have low plasma renin activity.
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PMID:Hypertension and hyperkalaemia responding to bendrofluazide. 50 50

The effect of indomethacin on plasma renin activity (PRA) and renal function was examined in conscious dogs with chronic renovascular hypertension before or after volume expansion. PRA did not change following the infusion of indomethacin: PRA was 5.18 +/- 1.46 ng/ml/h during control periods and was 5.01 +/- 0.95 ng/ml/h (p greater than 0.1) after 80 min of infusion of indomethacin. Mean arterial blood pressure (MABP) was 121.6 +/- 7.4 mm Hg during control periods and was 122.0 +/- 4.6 mm Hg (p greater than 0.1) after 80 min of infusion of indomethacin. Infusion of indomethacin into these dogs undergoing diuresis did not change inulin or p-aminohippuric acid clearance. Sodium excretion (UNaV) showed slight but not signifcant decreases with the infusion of indomethacin. UNaV was 109.3 +/- 25.7 muEq/min during control periods and was 69.6 +/- 21.0 muEq/min (0.05 less than p less than 0.1) after 80 min of infusion of indomethacin. The results suggest that renin release, sodium excretion, and blood pressure in the dog with chronic renovascular hypertension in uninfluenced by indomethacin.
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PMID:Effect of indomethacin on renal function and plasma renin activity in dogs with chronic renovascular hypertension. 51 27

Sodium restriction has become an integral part of the medical management of hypertension. In general the degree of sodium restriction recommended by physicians depends upon the severity of the disease. The commonly prescribed sodium restricted diets are classified as mild and moderate. Mild sodium restriction refers to a diet in which 3.0-4.0 gm of sodium are allowed per day. Moderate sodium restriction is indicated when hypertension is more severe; 1-2 gm of sodium are allowed daily. Sodium added in the processing of foods contributes significantly to the sodium content of the diet. "Convenience" and "fast" foods are high in sodium and are not allowed the hypertensive patients. Significant advances have occurred in the past decade in the medical management of hypertension. The sodium-restricted diet remains the cornerstone of effective blood pressure control. Therefore, nutrition must become an integral part of the hypertensive treatment program.
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PMID:The relationship of diet to blood pressure control. 52 19

A new method was developed for separate kidney function studies by catheterizing the ureters and exteriorizing the catheters through the urethra into the vagina. Renal artery plication was performed to reduce blood flow to one kidney by 66 +/- 5%. Arterial pressure increased from 107 +/- 2 to 131 +/- 3 mmHg and remained elevated for 28 days. Plasma renin activity was increased for the first 7-10 days only. Sodium and water excretion were markedly reduced in the kidney with the stenosed renal artery and after the first 2 days Na and water excretion were incresed in the contralateral kidney. These changes in Na and water excretion were frequently associated with similar directional changes in glomerular filtration rate (GFR) and renal plasma flow. An exception was noted in that renal sodium and water excretion remained low throughout the 28 days in the kidney with the constricted renal artery, whereas GRF returned to near the control level by the end of 2 wk. Altered filtration fraction did not appear to be a determining factor in control of the rate of Na excretion. It is suggested that GFR, the renin-angiotensin-aldosterone system, and other as yet undefined factors are involved in salt and water homeostasis during unilateral renal artery stenosis with hypertension.
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PMID:Separate renal function studies in conscious dogs with renovascular hypertension. 69 70

Sodium and calcium contents of cardiovascular tissue in spontaneously hypertensive rats (SHR) and DOCA hypertensive rats were investigated. The effect of salt loading on these contents of SHR and control Wistar rats was also investigated. Calcium content increased with the development of hypertension, but not sodium content particularly in salt loading rats and at the sustained stage of DOCA hypertensive rats. These results suggest that calcium rather than sodium is more intimately related to the increase in blood pressure.
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PMID:Studies on sodium and calcium contents of cardiovascular tissue in experimental hypertension. 83 30

A sodium-rich diet was given 20 rabbits with 2-kidney hypertension (clipping of one renal artery with an intact contralateral kidney), 19 rabbits with 1-kidney hypertension (clipping of one renal artery with contralateral nephrectomy), and 13 normal rabbits. Sodium content of the diet was twice as much as the regular diet. The sodium load was started 10 weeks after clipping of the renal artery and lasted for 2 weeks. During the sodium load blood pressure did not show any significant changes but hematocrit was reduced in all 3 groups. Plasma renin activity (PRA) was clearly suppressed in 10 of 19 animals with 1-kidney hypertension and in 6 of 13 normal animals, but only in 4 of 20 animals with 2-kidney hypertension (p less than 0.04). The results indicate that PRA was more easily suppressed in animals with 1-kidney hypertension than in those with 2-kidney hypertension by a sodium-rich diet and the suppressive response is not associated with alterations in blood pressure.
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PMID:Responses of plasma renin to sodium load in two types of experimental renal hypertension. 84 42


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