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

To investigate the influence of hereditary on plasma renin activity (PRA), plasma aldosterone concentrations (PAC), blood pressure, and the renal excretion of sodium and potassium following volume expansion and contraction in normal man, we studied 37 pairs of monozygotic (MZ) and 18 pairs of dizygotic (DZ) twins. Volume expansion was achieved by the intravenous infusion of 2L normal saline; volume contraction was accomplished by a low-sodium diet and 120 mg oral furosemide. The presence of genetic variance was tested by calculating the within pair and among component estimates of genetic variance. Outpatient 24-hour-urine collections suggested that MZ and DZ twins ingested diets similar in sodium and potassium content, and failed to reveal genetic influences on the dietary preferences for these electrolytes. The PRA values suggested heritable influences during both the volume expanded and contracted state with the added stimulus of upright posture. Heritable influences were observed on PAC and were most apparent in the basal state on the day of volume expansion. An influence of heredity on blood pressure was most apparent during volume contraction. Urinary sodium excretion (UNaV), urinary potassium excretion (UKV), fractional excretion of sodium (FENa), and fractional excretion of potassium (FEK) revealed evidence of significant genetic variance under the condition of volume expansion. in that state, systolic blood pressure was directly correlated with PRA, PAC, and inversely with FENa. The data suggest that the renal regulation of sodium and potassium excretion is in part influenced by heritable factors that may in turn contribute to the development of hypertension in some individuals.
Hypertension
PMID:Genetic influences on renin, aldosterone, and the renal excretion of sodium and potassium following volume expansion and contraction in normal man. 39 49

The renin-angiotensin-aldosterone system, electrolyte and water balance, body fluid, and neurogenic tone and reactivity of the vasculature were studied in hypertension induced in uninephrectomized rats by repeated injection of renin-rich kidney extract and 1% saline drinking. The control rats were injected with physiological saline. Various measurements were made in conscious rats on the 10th day of the treatment. As compared with the control, plasma renin concentration and serum sodium increased significantly, while plasma aldosterone and renal excretory function did not differ. Blood volume (BV) expressed as per body weight increased significantly, but absolute BV, absolute or body weight-related plasma volume and hematocrit were not significantly different. The hypotensive effect of 1-Sar-8-Ile-angiotensin II was negligible 12 hours after the preceding injection of kidney extract. It was small but significant 1 hour after the injection. Increase in water turn-over and fractional sodium excretion occurred during the development of hypertension. Spironolactone did not significantly modify the developmental course. We observed increased depressor response to hexamethonium and increased reactivities to noradrenaline and angiotensin II (A II); these response curves relatively resembled those of spontaneously hypertensive rats. Hypertensive vascular changes were seen in the kidney and heart by histology. Thus, it was suggested that a direct vascular action of A II played a partial role in this hypertensive process while aldosterone played little role. The significance of BV increase and possible contribution of A II's other actions were discussed.
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PMID:Pathophysiological studies on hypertension induced in rats by kidney extract and salt. 39 83

Renin is a hormone secreted by the juxtaglomerular cells of the kidney; it interacts with a plasma protein substrate to produce a decapeptide prohormone angiotensin I. Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. The biosynthesis and control of renin secretion are not well understood, and the question as to whether renin is synthesized and stored in a larger precursor form is as yet unresolved. Whether or not higher molecular weight or inactive forms of renin in plasma have a role in controlling renin activity or whether they simply represent a degradative pathway for renin is as yet uncertain. The availability of several inhibitors of the renin-angiotensin system has served to define the role of renin both in normal cardiovascular homeostasis and in renovascular hypertension. It appears that renin plays an important role in maintaining blood pressure in the salt- or volume-depleted state and that it is responsible for the initial phases of renovascular hypertension in any model of this disease process. Renin's part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), renin continues to play a significant role during the chronic phase.
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PMID:The role of renin in the control of the circulation and in hypertensive disease. 39 5

The recognition of secondary causes of hypertension, such as renovascular disease and aldosteronism, can be enhanced by stimulation and suppression of the 2 limbs of the renin angiotensin system. Normal values have been established in unstimulated and stimulated conditions. Saline infusion suppresses plasma aldosterone normally. Patients with proved adenomas do no suppress renin and are outside the well established ranges of normal suppression. Likewise, furosemide will stimulate renin release. Patients with proved aldosteronism are outside the normal ranges of plasma renin activity. These maneuvers also are useful in discriminating renovascular hypertension, particularly when achieving differential renal venous collections under stimulated conditions (after furosemide and tilting). By stressing this system (with furosemide stimulation or saline suppression) one can discriminate better secondary hypertension by the failure to respond normally.
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PMID:Evaluation of patients for secondary hypertension. 39 53

Five hundred and seventy-four ambulatory subjects with blood pressures ranging from 94/58 to 250/145 mm Hg were studied on their usual dietary and sodium intake. Renin, renin substrate, angiotensin II, aldosterone and urinary sodium and potassium were compared with blood pressure to access the contribution of these variables to the blood pressure variance. Our analyses revealed that renin substrate was highly and positively correlated with diastolic blood pressure (r = +0.39; p < 0.00001) but all other components of the renin-aldosterone system exhibited a significant negative correlation with blood pressure. A highly significant relationship between potassium, the renin-aldosterone system and blood pressure was found but no such relationship could be demonstrated for sodium. Subjects with higher blood pressures had lower urinary potassium concentrations and lower potassium/creatine ratios. These findings raised the possibility of a significant pathogenetic relationship between potassium and high blood pressure. Multiple linear regression reveals that influences of the renin-angiotensin-aldosterone system can only account for less than 20% of the variance exhibited by the blood pressure in these subjects.
Hypertension
PMID:Relation between blood pressure and renin, renin substrate, angiotensin II, aldosterone and urinary sodium and potassium in 574 ambulatory subjects. 39 40

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

Diurnal 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) pattern was studied with RIA technique in 33 hypertensive patients in supine position and on normal sodium diet. The compound was evaluated every 2 h from 0800-2000 h. Simultaneously, plasma aldosterone and cortisol were measured. Abnormal 18-OH-DOC behavior was observed in only 2 out of 4 patients with Cushing's disease, while sporadic and slight elevations, synchronous with F, were seen in 5 out of 24 stable essential hypertensive patients [1 with normal plasma renin activity (PRA), 1 with low PRA, and 3 with high PRA]. 18-OH-DOC was normal in 2 cases of hypertension due to renal artery stenosis, in 1 patient with nephrosclerosis, and in 1 patient with horseshoe kidney. From these results, 18-OH-DOC does not seem to play an important pathogenetic role in stable essential hypertension, considering also the low mineralocorticoid activity of the compound.
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PMID:Diurnal 18-hydroxy-11-deoxycorticosterone pattern in human stable hypertension. 40 Jul 33

Experimental toxemia of pregnancy was induced in 8 pregnant monkeys (Macacamulatta) by reducing the abdomiinal aorta to one-third of its original diameter during the last month of gestation. It was characterized by hypertension and proteinuria. In the kidney, light and electron microscopy and immunofluorescence revealed findings similar to those in human toxemia. Focal necrosis in the liver and diffuse hemorrhagic infarctions in the placenta were also observed. Plasma renin activity and aldosterone levels, as determined in blood from the uterine vein, were elevated. None of these changes were found in 4 control animals.
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PMID:Experimental toxemia of pregnancy in the monkey, with a preliminary report on renin and aldosterone. 40 16

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.
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PMID:Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion. 42 Mar 14

The renin-angiotensin-aldosterone system in patients with acromegaly was evaluated by infusing [sarcosine1, isoleucine8]angiotensin II, a competitive angiotensin II antagonist, into five acromegalic patients with hypertension and three normotensive acromegalics. The drug was infused at a rate of 600 ng/kg . min for 30 min, 1 h after iv injection of 40 mg furosemide. In addition, before the infusion, plasma samples were obtained for determination of PRA and plasma aldosterone concentration. A significant pressor response to [sarcosine1, isoleucine8]angiotensin II was observed in all eight patients. Preinfusion PRA and plasma aldosterone concentration were significantly lower than in normal controls. It is concluded that in acromegaly, the renin-angiotensin-aldosterone system is suppressed and that this system is probably not involved in maintenance of the high blood pressure observed in some acromegalic patients.
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PMID:Blood pressure response to an angiotensin II antagonist in patients with acromegaly. 42 97


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