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

Fifteen patients whose renovascular hypertension was cured or improved by renal artery reconstructive surgery or nephrectomy (or both) underwent studies of their renin-angiotensin systems preoperatively. These studies included measurements of peripheral venous renin activity in the erect position without diuretic preparation, blood pressure response to blockade of endogenous angiotensin II with a saralasin infusion in the acutely sodium-depleted state, and levels of renal venous renin activity, also after sodium depletion. In 13 of these 15 patients who had benefitted from surgical intervention for relief of renovascular hypertension, at least one index of renin dependency was positive. Two patients had negative results in all of the tests. On the basis of these findings, we concluded that cure or improvement of renovascular hypertension is possible even though these three parameters of renin-angiotensin overactivity are negative.
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PMID:Renovascular hypertension. Relationship of surgical curability to renin-angiotensin activity. 65 81

A change in vascular reactivity was characterized in the pig during the development of deoxycorticosterone acetate (DOCA) hypertension. Pigs, 8-12 weeks of age, were subjected to unilateral nephrectomy and instrumented with an electromagnetic flowprobe on the ascending aorta and with Tygon catheters in the aorta and thoracic vena cava. Approximately 2 weeks after surgery, Silastic strips impregnated with DOCA (100 mg/kg) were implanted subcutaneously. Within the first 3 days after implantation, mean arterial pressure (MAP) began to rise and reached levels approximately 40% greater than control during the 4th week. Graded intravenous infusions of norepinephrine or angiotensin II were given to unanesthetized pigs before, and at intervals during, the development of hypertension. Changes in total peripheral resistance were calculated from recordings of MAP and cardiac output. Comparison of pre-DOCA response curves with those obtained at intervals following DOCA implantation demonstrated a significant increase in vascular smooth muscle sensitivity (decrease in threshold infusion rates) to both drugs post-DOCA. There also was a shift to the left in the dose-response curves. These changes in systemic vascular reactivity occurred at the time the arterial pressure began to rise. The temporal relationship suggests that the increase in vascular reactivity may initiate the increase in mean arterial pressure.
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PMID:Whole body vascular reactivity during the development of deoxycorticosterone acetate hypertension in the pig. 65 35

To study whether the renin-angiotensin system is related to hyperuricemia in hypertension, the serum concentration of uric acid was determined in 96 patients with various types of hypertension and various degrees of plasma renin activity (PRA). In malignant hypertension, both PRA and the serum uric acid level were higher than in essential hypertension; but in primary aldosteronism or desoxycorticosterone-excess hypertension, they were lower than in the essential type. In renovascular hypertension, PRA was higher than in essential hypertension, but the serum uric acid levels were similar. There were no differences in PRA and serum uric acid concentration between Cushing's syndrome and essential hypertension. The serum uric acid level in high-renin essential hypertension was higher than in either the normal-renin or the low-renin type. There was a significant correlation between serum uric acid concentration and PRA in the basal state, and between the change in PRA and the change in serum uric acid induced by administration of furosemide. Apparently the close correlation between the renin-angiotensin system and the concentration of serum uric acid is related to changes in extracellular fluid volume, although an intrarenal effect of angiotensin II cannot be excluded.
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PMID:Serum uric acid and the renin-angiotensin system in hypertension. 65 66

1. Rats with indwelling aortic and right atrial cannulae were maintained on a sodium-free diet before and after renal arterial constriction combined with contralateral nephrectomy. Control animals underwent the same protocol except that non-constricting clips were used. 2. Plasma volumes in the salt-deprived animals were lower than previously determined values in animals with free access to sodium. After clipping plasma volume increased in the hypertensive animals. Extracellular fluid volume was increased equally in both normotensive and hypertensive animals on the second postoperative day only. 3. Before clipping and contralateral nephrectomy plasma angiotensin II values were higher than normal. After the operation angiotensin II concentrations fell to normal over a period of 14 days without significant differences between experimental and control groups. 4. It is concluded that high blood pressure after clipping may be in part maintained by increases in plasma volume. However, the results strongly suggest that other renal mechanisms are likely to be of major pathogenic importance.
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PMID:Determinants of high blood pressure in salt-deprived renal hypertensive rats: role of changes in plasma volume, extracellular fluid volume and plasma angiotensin II. 66 71

In 35 patients with moderate or severe essential hypertension (EH) four groups could be identified by plasma angiotensin II (AII) (formula: see text) and by exchangeable sodium (ENa) (formula: see text) determination. In 6 patients with high AII (135.9 pg/ml +/- 26.29) and normal ENa (98.83% +/- 1.40) propranolol significantly lowered both blood pressure (BP) and AII, suggesting that these forms of EH are renin dependent. In 15 patients with normal AII (36.43 pg/ml +/- 2.27) and high ENa (124.23 +/- 2.78) and in 6 patients with low AII (8.36 pg/ml +/- 3.39) and high ENa (125.16% +/- 5.71) the maximal hypotensive effect was achieved after ENa reduction with thiabutazid. These forms of EH appear to be volume-sodium dependent. In 8 patients with increase of both AII (76.53 pg/ml +/- 5.72) and ENa (112% +/- 1.72), propranolol associated with thiabutazid lowered the BP, AII and ENa suggesting that these cases are mixed forms. ENa determination appears to be a reliable index for renin profiling; such a renin-sodium profile allows to identify some pathophysiologic forms of arterial hypertension.
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PMID:Renin-sodium profile and its therapeutical implications in arterial hypertension. 67 43

Pressor responses to norepinephrine (NE) infusions were examined in normal rabbits, in rabbits with renal artery stenosis of over 30 days' duration (chronic renal hypertensive rabbits), and in rabbits with renal artery stenosis of 3 days' duration (3-day clipped rabbits). The 3-day clipped rabbits did not have hypertension, but they showed the same increased pressor responses to NE as did the chronic renal hypertensive rabbits, which was about 2.5 times that of the normal rabbits. Plasma renin activity (PRA) was the same in the 3-day clipped rabbits as in the normal group, but in the chronic renal hypertensive rabbits the PRA was significantly below normal. Infusions of angiotensin II (A II) in either subpressor or pressor amounts potentiated the pressor responses to NE in normal rabbits, whereas, in 3-day clipped rabbits and chronic renal hypertensive rabbits, A II in subpressor or pressor doses did not alter the pressor responses to NE. Infusion of the A II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, did not alter the pressor responses of normal rabbits to NE, but this A II analogue completely abolished the pressor hyperresponsiveness to NE in the 3-day clipped rabbits and greatly reduced the NE hyperresponsiveness in the chronic renal hypertensive rabbits; this A II antagonist did not alter the control arterial pressure in any of the three groups of rabbits. These studies show that the increased pressor response to NE in rabbits with renal artery stenosis occurs before the onset of hypertension and thus is not merely a result of the hypertension. Also, these results provide evidence that A II plays an important role in the increased pressor responses to NE in hypertensive and prehypertensive rabbits.
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PMID:Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. The role of angiotensin II. 67 26

A central stimulatory effect of angiotensin II (AII) on the secretion of arginine-vasopressin (AVP) has been described. The competitive blocker of AII, saralasin (SAR) has been used for diagnostic purposes in angiotensin-dependent hypertension. In addition SAR has a partially agnoistic effect. The aim of the present study was to demonstrate whether AVP-levels can be influenced during SAR-induced renin stimulation. In 9 patients with essential hypertension blood pressure dropped significantly under SAR (10 microgram/kg/min over a 30 min period). Before and after SAR plasma renin activity (PRA) and AVP were measured by RIA, SAR evoked significantly increments of PRA in all patients and of AVP in 6 patients. The increased serum concentrations of AVP following SAR may be explained either by the depressor effect of SAR, its diminished concentration at the central receptor, or a partial AII-agonistic effect.
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PMID:[Effect of saralasin on plasma renin activity and arginine-vasopressin in patients with angiotensin-dependent hypertension (author's transl)]. 68 28

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.
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PMID:SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension. 68 62

We isolated and perfused both the "clipped" and "contralateral" kidneys from Goldblatt renal hypertensive and sham-operated control rats, 1--104 days postoperatively. Responses to renal nerve stimulation were depressed in clipped kidneys from hypertensive rats (1 day postoperative), and these kidneys were supersensitive to exogenous norepinephrine (1--31 day) when compared with the contralateral organ of the same animal. Similar alterations were found between clipped and contralateral kidneys from sham-operated control rats. There was no difference in responses to renal nerve stimulation of norepinephrine between clipped kidneys from hypertensive and control rats, but clipped kidneys from hypertensive rats were supersensitive to angiotensin II (17 and 31 days). Comparison of contralateral kidneys from hypertensive and control rats revealed no change in norepinephrine sensitivity or in responses to renal nerve stimulation, but there was a reduction in the slope of the dose-response curve to norepinephrine and of the maximal effect of the catecholamine (104 days) and a pronounced supersensitivity to angiotensin II (17--104 days) in the hypertensive rats. These results indicate that (1) renal nerve function and norepinephrine sensitivity of the isolated renal vasculature are unchanged in renal hypertension, but clipping partially denervates the kidney causing depressed nerve function and unilateral norepinephrine supersensitivity, unrelated to hypertension; (2) the prolonged high pressure load on the contralateral kidney may impair the function of the vascular smooth muscle; and (3) bilateral supersensitivity to angiotensin II is associated with hypertension but is not solely a consequence of the high pressure.
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PMID:Increased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal hypertensive rats. 68 57

The mechanisms involved in residual or recurrent hypertension following operation to correct renal artery stenosis were studied in 10 patients by performing angiotensin II blockade with Saralasin (Sarcosine, alanine, angiotensin II) before and after operation. Peripheral renin and renal vein renin determinations, angiography, and renography were done as well. The limitations of renin determinations are cited and the application of angiotensin II blockade as a specific method of detecting renin-dependent hypertension before and after operation are presented. Saralasin infusion under the controlled conditions of our study proved to be a sensitive method for detection of renin-dependent hypertension. The results of Saralasin infusion correlated closely with peripheral and renal vein renin determinations. Thus angiotensin II blockade before and after operation may supercede more invasive and less specific diagnostic methods.
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PMID:Evaluation of surgical response in renovascular hypertension using angiotensin II blockade. 71 82


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