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

Hypertension is a major medical problem with significant short- and long-term sequelae. Previous investigators have reported childhood hypertension to be secondary and when sexondary, renal. However, recent studies have shown primary (essential) hypertension to be more prevalent than secondary. Children with blood pressures at the 95th percentile for age deserve comprehensive evaluation and follow-up. Those with systemic evidence of side-effects will require therapy. Modern therapy should be based on pathophysiologic principles which include an understanding of volume-dependent and renin-dependent hypertension. The stepwise approach to therapy will produce the maximal therapeutic benefit.
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PMID:A pathophysiologic basis for the diagnosis and treatment of the renal hypertensions. 34 67

Hypertension in patients on chronic hemodialysis is thought to be largely of two types--volume dependent or renin dependent. If renin-dependent hypertension is mediated by angiotensin II, then angiotensin II antagonism should lower blood pressure. To test this hypothesis, the angiotensin II antagonist saralasin was given to 15 hypertensive patients on chronic hemodialysis. Patients were separated into two groups by their blood pressure response. In responders blood pressure was 191/112 mm Hg and fell to 147/85 during saralasin administration (P less than 0.01). In contrast, nonresponders had blood pressures of 190/111 mm Hg before and 188/110 during saralasin administration. Five responders subsequently ahd nephrectomies with normalization of their blood pressures. Plasma renin activity averaged 70 ng/ml . 3 h of angiotensin I in responders and increased to 110 after saralasin (P less than 0.05), while nonresponders had values of 21 before and after saralasin. These results offer strong support for the hypothesis that renin-dependent hypertension is an important mechanism in certain patients on chronic hemodialysis and that such patients will respond to angiotensin II antagonism.
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PMID:Effect of saralasin in hypertensive patients on chronic hemodialysis. 61 54

We evaluated propranolol effects on blood pressure, plasma renin activity, and erythrocyte production in nine chronically hemodialyzed and four nondialyzed patients with hypertension and high plasma renin concentrations. Propranolol, at a maximum daily dose of 240 mg, controlled blood pressure in 12 of the 13 patients. During propranolol treatment of dialyzed patients, mean blood pressure fell from 133 +/- 1 to 113 +/- 4 mm Hg (P less than 0.005) and plasma renin activity from 3093 +/- 423 to 689 +/- 218 ng/dl 3h (P less than 0.001). Similar results were obtained in nondialyzed patients. In both groups hematocrit and red cell mass were unchanged, although ferrokinetic measurements suggested a decrease in erythropoiesis. Thus propranolol alone reduces blood pressure and renin activity in chronically dialyzed patients with hypertension and high renin concentrations. No hematologic complications or other side effects were observed. These findings suggest that propranolol may be an effective alternative to bilateral nephrectomy in the control of renin-dependent hypertension in selected patients.
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PMID:Propranolol effects in long-term hemodialysis patients with renin-dependent hypertension. 63 24

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

The reliability of the angiotensin II (AT II)-antagonist Saralasin in the diagnosis of AT II-dependent forms of hypertension was investigated in 61 cases of hypertension of different etiology. In 14 patients, lowering of blood pressure by Saralasin suggested an AT II-dependent hypertension which could be ascertained in 8 patients (5 had undergone successful surgery) by increased levels of plasma-renin-activity (PRA), AT II, PRA-ratio in renal vein blood and by angiography. Besides, depressor reactions by Saralasin yielded additional information in three patients with renovascular hypertension but normal levels of PRA and AT II, in two patients with high renin essential hypertension and one patient with pheochromocytoma. This test seems to be valuable in the diagnosis of renin-dependent hypertension.
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PMID:[Critical analysis of the saralasintest in the diagnosis of hypertension (author's transl)]. 89 3

Renal artery thrombosis or embolism associated with the use of an umbilical arterial catheter can cause renin-dependent hypertension in the neonate. The tip of the catheter should therefore be kept well below the origin of the renal arteries and the infant's blood pressure monitored. Moreover, since the pressor hypertension may be transient and kidney function may return, a period of medical management should be attempted before proceeding to nephrectomy.
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PMID:Conservative management of neonatal renal artery embolism. 98 37

In children with reflux nephropathy renin-dependent hypertension may develop. Two girls with reflux nephropathy, hypertension, elevated plasma renin activity, but normal (Case I) and near normal (Case 2) serum creatinines are described. These cases suggest that reflux nephropathy can activate the renin-angiotensin system and that the renin inhibitors, methyldopa and propranolol, an useful in managing this type of hypertension.
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PMID:Renin-dependent hypertension in children with reflux nephropathy. 127 3

We describe methods for using ameroid constrictors to develop renin-dependent hypertension in dogs. A vascular-access-port was implanted in each dog and mean arterial blood pressure was monitored. Via a small flank incision, an ameroid constrictor was placed on the left renal artery and mean arterial blood pressure, plasma renin activity, and the response to angiotensin-converting enzyme inhibition measured during the subsequent 4 weeks. Placement of the constrictor on the left renal artery resulted in a significant increase in plasma renin activity which was accompanied by a significant hypertension (blood pressure greater than 140 mmHg). The greatest increase in plasma renin activity and blood pressure occurred at week two which coincided with the greatest response to angiotensin-converting enzyme inhibition, when mean arterial blood pressure decreased more than 30 mmHg after administration of either captopril or enalapril (1 mg/kg, i.v.). The results of this study indicate that ameroid constrictors provide a reliable method for establishing renin-dependent hypertension in dogs.
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PMID:Use of ameroid constrictors in the development of renin-dependent hypertension in dogs. 131 13

Administration of adenosine results in profound hypotension without the expected activation of reflex sympathetic and renin mechanisms in most animal models. This action can be explained by the vasodilatory and neuroinhibitory effects of adenosine. It is generally considered an inhibitory neuromodulator because it inhibits the release of virtually all neurotransmitters studied and produces hyperpolarization of neurons. In contrast, adenosine produces vasoconstriction of some vascular beds, including the renal and pulmonary circulations. Renal vasoconstriction is caused by activation of A1 receptors and involves an interaction with angiotensin II. In other vascular beds adenosine releases eicosanoids, including thromboxane, also resulting in vasoconstriction. Adenosine-induced vasoconstriction is transient and species dependent. Neither the receptor type, the molecular mechanisms of these actions, nor their significance to pathophysiological processes have been defined. Adenosine also has an apparent excitatory effect in the nucleus tractus solitarii. Microinjections of adenosine into this brain stem nucleus lead to decreased sympathetic tone and hypotension similar to those produced by the excitatory amino acid glutamate. The mechanism that explains this action has recently been explored and involves the release of glutamate by adenosine. Adenosine also stimulates afferent fibers mediating sympathetic activity, including renal and myocardial afferent nerves, and carotid and aortic chemoreceptors. Afferent nerve activation seems to be more pronounced in humans and may explain most of the cardiovascular and respiratory actions of adenosine in this species. Finally, animal studies suggest that endogenous adenosine plays a role in the regulation of the baroreceptor reflex and restrains the full expression of renin-dependent hypertension.
Hypertension 1992 Oct
PMID:Contrasting excitatory and inhibitory effects of adenosine in blood pressure regulation. 139 81

Unlike the non-renin-dependent hypertension associated with infrarenal aorta banding, an abnormal accumulation of fibrillar collagen occurs within the adventitia of intramural coronary arteries and neighboring interstitial space of the left and right ventricles in arterial hypertension associated with primary or secondary hyperaldosteronism. Based on these findings it was suggested that this interstitial and perivascular fibrosis was mediated by mineralocorticoid excess (i.e., elevated plasma aldosterone relative to dietary sodium) and not ventricular loading. To further address the importance of mineralocorticoid excess, we examined the fibrous tissue response after 8 weeks in the following uninephrectomized rat groups receiving a high-sodium diet: D-aldosterone (ALDO) infusion (0.75 micrograms/hr sc, n = 16); deoxycorticosterone acetate (DOCA) administration (100 mg/kg/wk sc, n = 8); and administration of a mineralocorticoid-like substance, glycyrrhizic acid (GA; 1 gm kg/wk sc, n = 8). Compared with ALDO infusion and sodium deprivation (n = 9), untreated controls (n = 14), and uninephrectomized rats with high dietary sodium and no mineralocorticoid administration (n = 15), we found (1) hypertension and left ventricular hypertrophy with all forms of mineralocorticoid excess; (2) a rise in collagen volume fraction with ALDO, and an increase in perivascular collagen with DOCA; and (3) no observance of myocardial fibrosis with GA or experimental controls, including ALDO infusion and sodium deprivation. Thus, in the presence of enhanced sodium intake, chronic administration of ALDO or DOCA are associated with collagen accumulation in the myocardium, whereas with the mineralocorticoid-like compound GA, myocardial fibrosis was not seen.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mineralocorticoid excess, dietary sodium, and myocardial fibrosis. 145 2


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