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

Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
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PMID:Pathophysiology and treatment of posttransplant hypertension. 193 42

Noradrenaline (NA) and dopamine (DA) have opposite effects on the kidney; NA causes vasoconstriction and increased sodium reabsorption while DA promotes vasodilation and natriuresis. In 15 patients investigated for renin-mediated hypertension measurements of plasma renin activity (PRA), NA and DA concentrations were made in arterial and renal venous blood from both kidneys before and after acute stimulation of renin release by i.v. dihydralazine. Nine patients had unilateral renin secretion and were classified as renin-positive, while the remaining six patients were renin-negative. Renin-positive patients had higher arterial and renal venous PRA, NA and DA levels than the negative ones. In the renin-positive group V-A differences for NA and DA were present on both sides despite unilateral secretion of renin. NA but not DA levels were higher in the renin-secreting kidney, which can partly be explained by the reduced plasma flow to the involved kidney. After dihydralazine the arterial NA and DA rose similarly in renin-positive and renin-negative patients, while PRA rose only in the renin-positive cases. In the renin-positive patients where stimulation of renin secretion caused a marked increase of the PRA gradient on the affected side only, renal gradients for NA and DA increased bilaterally. The increase in DA was more pronounced than that of NA yielding a rise in DA/NA ratio on the affected side. Arterial PRA was positively correlated to the plasma concentrations of NA and DA. V-A differences for PRA and NA or DA were positively correlated on the involved renin-secreting side. In summary, patients with renin-dependent hypertension have elevated plasma NA and DA concentrations. Stimulation of renin release by dihydralazine increases the DA/NA ratio in arterial and renal venous blood indicating release of 'precursor dopamine' from noradrenergic fibres and/or activation of dopaminergic nerves. There seems to be a relationship between renal nerve activity and renin release in renin-dependent hypertension.
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PMID:Plasma noradrenaline and dopamine in renin-mediated hypertension. 240 2

The acute blockade of the renin-angiotensin system has been made it possible to investigate its role in the maintenance of blood pressure and aldosterone secretion in normotensive and hypertensive subjects. The administration of saralasin or captopril and, in the near future, of renin inhibitors induces a fall in blood pressure that is variable from one subject to the other according to the sodium balance and the level of activation of the system. These blockers also decrease the angiotensin II-dependent aldosterone production and increase renin secretion according to the circulating level of angiotensin II and the functional state of adrenal and juxtaglomerular receptors. In practice the definition of an abnormal response to renin-angiotensin blockade is difficult to define precisely, but the hypotensive effect has been tentatively used for the diagnosis of renin-dependent hypertension, especially renovascular hypertension and primary hyperaldosteronism. In renal artery stenosis the most convincing results mainly concern the lateralization of an abnormal unilateral renin secretion, which is potentiated by an acute blockade of the renin-angiotensin system. The acute administration of converting enzyme inhibitor is also useful to detect the absence of decrease in plasma aldosterone, which is characteristic of a solitary tumor or of other anatomical and functional disorders of the adrenal glands.
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PMID:Acute inhibition of the renin-angiotensin system: interest and limits to detect surgically curable hypertension. 241 19

A 41-yr-old woman with bilateral renal artery stenosis (RAS) and renovascular hypertension is presented. In this patient, the routine [99mTc]diethylenetriaminepentaacetic acid renal scintigraphy without Captopril was normal and the subsequent study with Captopril showed a marked decrease in glomerular filtration rate of the right kidney alone. Percutaneous transluminal angioplasty of the functionally affected right kidney immediately evoked new renin-dependent hypertension caused by the untreated left RAS. This patient illustrates two major points: (a) as a diagnostic tool, the sensitivity of Captopril renal scintigraphy may be compromised by an inability to detect bilateral RAS, but (b) after angioplasty, it can be useful for evaluating the treated kidney and in revealing contralateral disease that may benefit from angioplasty.
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PMID:Captopril renal scintigraphy in a patient with bilateral renal artery stenosis. 268 93

In 30 patients with renovascular hypertension, 50 with hypertension in a course of arteries, 71 hypertensive subjects with coexisting parenchymal nephropathy and in 63 with primary hypertension the captopril test was performed after 8 hours night rest and within high sodium diet. Positive test result was stated in 76.67% of patients with renovascular hypertension, in 70.59% of patients with arteritis, in 53.52% of patients with hypertension and coexisting parenchymal nephropathy and in 63.49% of patients with primary hypertension. Significant correlation between increase of plasma renin activity and blood pressure decrease after captopril administration was only stated in patients with renovascular hypertension and in those with arteritis. Results of performed studies impaired the captopril test value in diagnostics of renin-dependent hypertension.
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PMID:[Diagnostic value of the captopril test in patients with arterial hypertension]. 269 83

The renin-angiotensin system has been shown to play a significant role in maintaining blood pressure and sodium balance in health and disease states. The development of various pharmacologic probes that inhibit the RAS at different and specific points in the renin-angiotensin cascade has facilitated the elucidation of the role of angiotensin II in renovascular hypertension. In a clinical regard, inhibitors of the RAS have been instrumental in screening patients for renovascular hypertension, and in predicting curability with a high degree of reliability. Moreover, use of these drugs in an out-patient setting has been determined to be safe, practical, and reliable, making the work-up for renin-dependent hypertension cost effective and accurate.
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PMID:Pharmacologic probes to identify patients with renovascular hypertension. 288 24

Technical aspects of percutaneous transluminal angioplasty in renovascular hypertension include knowledge about the pathophysiology of dilation, certain radiological and physiological markers, criteria for patient selection, and, finally, the catheter technique. Important factors for a successful procedure are overdilation and adequate pressure and time of balloon inflation. Radiological markers are inflation and deflation profiles of the balloon as well as determination of the pressure gradient across the stenosis. Main criteria for patient selection are renin-dependent hypertension and less frequent improvement of kidney function. Following dilation the most common adjunct medical therapy is low-dose application of aspirin for a period of 6 months.
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PMID:Technical aspects of percutaneous transluminal angioplasty in renovascular disease. 294 14

The case of a young woman presenting with a renin-secreting soft tissue sarcoma is described. The primary extrarenal tumour as well as metastatic disease were associated with severe hypertension and both required surgical treatment. The location of these rare malignant tumours and their association with renin-dependent hypertension is discussed. In cases of this type, reappearance of hypertension suggests tumour recurrence.
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PMID:Epithelioid sarcoma of soft tissues: a case of extrarenal renin-secreting tumour. 307 40

In order to improve on the technique of noninvasive detection of renal artery stenosis, we studied the effects of angiotensin converting enzyme inhibition with captopril on individual kidney hemodynamics and function as assessed by technetium-99m diethylenetriaminepentaacetic acid [( 99mTc]DTPA) renal flow studies and iodine-131 orthoiodohippurate [( 131I]hippuran) renography in experimental Goldblatt's hypertension. In two-kidney, one-clip (renin-dependent) hypertension, captopril (1.5 mg/kg bolus with 1.5 mg/min infusion) reduced mean arterial pressure (MAP) and ipsilateral glomerular filtration rate (GFR) without changes in the contralateral kidney. Captopril infusion resulted in alterations in both the [99mTc]DTPA and [131I]hippuran studies, which were most evident in the 15-min [99mTc]DTPA renal flow studies. In one-kidney, one-clip (volume-dependent) hypertension, captopril reduced MAP but did not alter GFR, renal plasma flow, or the radionuclide studies. These studies suggest that the [99mTc]DTPA renal flow study coupled with captopril challenge may unmask intrarenal angiotensin II-dependent functional and hemodynamic changes of the stenotic kidney, and offers promise in the detection of renin-dependent hypertension.
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PMID:Captopril renography in two kidney and one kidney Goldblatt hypertension in dogs. 329 73

This study tested the hypothesis that interactions of endogenous angiotensin II (AII) with the noradrenergic neuroeffector junction are important in renin-dependent hypertension. In the in situ blood-perfused rat mesentery, in normal rats exogenous AII potentiated mesenteric vascular responses to periarterial (sympathetic) nerve stimulation (PNS) more than vascular responses to exogenous norepinephrine (NE). In 2-kidney-1-clip (2K-1C) rats with renovascular hypertension mesenteric vascular responses to PNS and NE were greater than in sham-operated rats, and renovascular hypertension mimicked the effects of exogenous AII with respect to enhancing responses to PNS more than responses to NE. In 2K-1C rats, but not in sham-operated rats, 1-Sar-8-Ile-AII markedly suppressed vascular responses to PNS, without influencing responses to NE. Finally, 1-Sar-8-Ile-AII attenuated sympathetic nerve stimulation-induced neuronal spillover of NE in 2K-1C rats, but not in sham-operated rats. These data indicate that renovascular hypertension enhances noradrenergic neurotransmission, and that this enhancement is mediated in part by AII-induced facilitation of NE release.
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PMID:Angiotensin II-noradrenergic interactions in renovascular hypertensive rats. 330


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