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

The purpose of this study was to examine the systolic blood pressure and plasma renin activity (PRA) responses to chronic stress in normotensive rats and in rats with one hypertensive parent. Twenty-four male Wistar-Kyoto (WKY) and 24 male F1 offspring of spontaneously hypertensive and WKY rats (BHR) were randomly assigned to 3 groups of 8 each. Experimental (E) animals were subjected to 2 hr daily of shock-shock conflict. Each response produced a 0.2 sec, 0.2-0.4 mA cutaneous electric shock. Failure to respond in 10 sec resulted in a train of 5 shocks (0.2 sec each sec). Yoked animals (Y) received the same shocks as E but had no control over their presentation. Finally, a control group (C) for maturation received no shocks. The E and Y animals were subjected to 14 weeks of conflict and were then monitored an additional 14 weeks in the absence of shock. All animals had their tail cuff blood pressures taken weekly except for 3 times when bloods were obtained for PRA assays. Analysis of blood pressure data revealed that:(1) BHR animals showed more of a blood pressure response to shock than WKY animals; (2) Y animals showed more of a response to conflict than E, especially for the BHR group; and (3) BHR shocked animals remained permanently elevated compared to BHR control animals even in the 14 week post-conflict period during which no shocks were given. Although PRAs for BHR animals were significantly higher than for WKY at the beginning of study, the stress-induced hypertension was associated with either normal or suppressed PRA values, suggesting that the hypertension in these animals is not a high renin hypertension.
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PMID:Blood pressure and plasma renin activity responses to chronic stress in the borderline hypertensive rat. 637 56

A nomogram based on the relationship between plasma renin activity and urinary sodium excretion in normal subjects has been used to classify 956 patients with essential hypertension into low, medium and high renin subgroups. Patients with low renin hypertension (27 percent of all patients) were older (P less than 0.001) than patients with medium or normal renin hypertension. They also contained more women (P less than 0.01) and had higher systolic blood pressures than patients with medium renin hypertension. Creatinine clearance, albumin concentration and hematocrit were lower in low renin patients than in patients with medium renin activity. Serum potassium levels were lower, but urinary potassium excretion was higher in low renin patients. Most of the differences in clinical and biochemical parameters could be explained by the differences in age and male:female ratio between the subgroups. Despite lower renin values, aldosterone excretions were similar between the subgroups. Differences in renin activity and differences in aldosterone-renin ratio could not be explained by differences in age, duration of hypertension and sex ratios. Patients with low renin hypertension showed evidence of increased adrenal sensitivity to angiotensin II-induced aldosterone secretion. Patients with high renin hypertension (11 percent of all patients) were younger than patients with medium or normal renin hypertension. Other differences in biochemical characteristics between these renin subgroups included a slightly higher albumin concentration and hematocrit in patients with high renin levels. These differences and the difference in renin activity between patients with high and patients with medium renin essential hypertension could not be explained by differences in age and/or sex ratio between the two subgroups. Despite the higher renin activity, aldosterone excretion was similar between the high and medium renin subgroups. Therefore, patients in the high renin subgroup are characterized by signs of volume contraction and by a relative unresponsiveness of the adrenal gland to angiotensin II-induced aldosterone secretion. The possible role of these differences in the sensitivity of the adrenal gland in sustaining hypertension has yet to be defined.
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PMID:Renin subgroups in essential hypertension. 675 52

Renovascular hypertension and high renin hypertension were found to be associated with an excess prevalence of carotid artery atherosclerotic lesions and to a higher risk of stroke, respectively, as compared to low-to-normal renin hypertension. Primary aldosteronism, being characterized by hypertension and a chronically suppressed plasma renin activity, should be accompanied by a low prevalence of carotid artery lesions. To verify this hypothesis we investigated prospectively, by a high resolution duplex ultrasound technique, the prevalence of extracranial carotid artery lesions in a case-controlled study of 34 (22 women and 12 men, aged 22 to 76 years) patients with no history or symptoms of cerebrovascular disease. Primary aldosteronism was diagnosed in 17 patients; 12 had a surgically confirmed unilateral aldosterone-secreting adenoma; and 5 had idiopathic hyperaldosteronism. Each primary aldosteronism patient was individually matched with a control with primary hypertension for sex, race, age, body mass index, casual blood pressure levels, duration of hypertension, smoking, diabetes mellitus, total serum cholesterol, and triglycerides. After the matching, the two groups were similar in terms of demographic features and overall cardiovascular risk profile (all P = NS). However, plasma renin activity and aldosterone levels were significantly lower and higher, respectively, in primary aldosteronism than in primary hypertensive patients. In primary aldosteronism the overall prevalence of carotid artery lesions at duplex was 59%, not significantly different from that (53%) found in primary hypertensives. Thus, at variance with renovascular hypertension, primary aldosteronism is not associated with an excess prevalence of carotid artery lesions.
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PMID:Prevalence of extracranial carotid artery lesions at duplex in primary aldosteronism. 842 67

The renin angiotensin system is one of the most important humoral factors underlying the mechanism of hypertension. The genes constituting the renin angiotensin system have been expected to be candidates for essential hypertension. DNA polymorphisms of angiotensinogen and angiotensin II type 1 receptor genes are reported to be significantly related with the incidence of human hypertension, but further investigation is needed to clarify the relationship between the genes of the renin angiotensin system and hypertension. The renin angiotensin system exists not only in circulating blood, but also in extrarenal organs and tissues. Tissue renin angiotensin systems in the brain, blood vessels, and adrenal glands are considered to play important roles in the pressor mechanisms in low renin as well as high renin hypertension. Gene expressions of the constituents of the tissue renin angiotensin system are affected in part by circulating angiotensin II, but they are regulated mostly by their own specific control mechanisms in each organ and tissue. In future, laboratory tests in clinical medicine may be necessary to determine the DNA polymorphisms and tissue gene expression of renin angiotensin system, in deciding the diagnosis, prognosis and therapy of hypertension.
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PMID:[Role of renin angiotensin system in the vasopressor mechanisms of hypertension--gene analyses and tissue renin angiotensin system]. 855 76

In order to lower arterial blood pressure, antihypertensive drugs decrease cardiac output, total peripheral resistance or both. Diuretics, beta-blockers, and central adrenergic inhibitors decrease cardiac output. ACE inhibitors, angiotensin II antagonists, calcium antagonists, alpha-blockers, central adrenergic inhibitors, and after a delay also diuretics and beta-blockers decrease peripheral resistance. Diuretics are first line therapy for treating low renin hypertension. Beta blockers are used for treating high renin hypertension and patients suffering additional coronary artery disease. ACE inihibitors can be given for treating high renin hypertension particularly in conjunction with diabetes, heart failure or left ventricular hypertrophy. Combining ACE inhibitors with diuretics potentiates the antihypertensive effect. Angiotensin II antagonists exert fewer side effects and better renal protection than ACE inhibitors. The main indication for calcium antagonists is low renin hypertension, their advantages being strong blood pressure reduction as well as in preventing stroke. Central alpha2 receptor agonists and other vasodilators are chosen only in selected cases and mostly in combination with other antihypertensive drugs.
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PMID:[Pharmacological basis of antihypertensive drug therapy]. 1519 36

In the 1970s, pharmacological therapy interrupting the renin-angiotensin system was considered beneficial for patients with high-renin hypertension. This gave rise to the development of ACE inhibitors. Surprisingly, the ACE inhibitors proved to be effective not only in patients with high renin hypertension, but also in many patients with normal levels of plasma renin activity. At present ACE inhibitors have a significant position in a wide range of chronic illnesses such as atherosclerosis, hypertension, myocardial infarction, diabetic complications, stroke etc. They are combined safely with drugs like angiotensin receptor blockers, calcium channel blockers and thiazides with varying degree of benefits. Though they are safe drugs, patients need monitoring for renal insufficiency, hypotension, hyperkalemia etc. The safety of these drugs in paediatrics patients is not established. It is better to avoid these drugs during pregnancy.
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PMID:Therapeutic dimensions of ACE inhibitors--a review of literature and clinical trials. 1865 May 98

Tissue kallikrein has been suggested to be involved in blood pressure regulation and in protection against hypertension. However, this hypothesis remains debated. Recently, murine genetic models of kallikrein deficiency have been engineered and partial genetic deficiency in kallikrein activity has been characterized in humans. Studies in kallikrein-deficient mice indicate that kallikrein indeed influences blood pressure in the setting of mineralocorticoid excess and salt retention but not in normotensive animals and in high renin hypertension. These observations suggest that kallikrein can have antihypertensive function in physiological situations where sodium retention can trigger blood pressure elevation.
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PMID:Tissue kallikrein, blood pressure regulation, and hypertension: insight from genetic kallikrein deficiency. 2332 81

There are various causes of Reno Vascular Hypertension in children reported in the literature. Amongst these, Page kidney gets a rare mention. This phenomenon is a result of the accumulation of blood or urine in the perinephric or subcapsular space, resulting in compression of renal parenchyma, microvascular ischemia, alteration in the renin-angiotensin apparatus, and high renin hypertension. It has been well documented and studied in adults. Only a few cases are reported in the paediatric population. We report a rare presentation of Page kidney in a 5 year 8 months old girl. She initially presented with Dietl's crisis secondary to left Pelviureteric Junction obstruction (PUJO) causing massive hydronephrosis. She developed Page kidney phenomenon after spontaneous rupture of the pelvicalyceal system formed a tight compressive urinoma. She was managed successfully with internal JJ stenting and ultrasound-guided aspiration of the urinoma followed by elective delayed Pyeloplasty. To our knowledge, this is the first documented case of Page kidney in a child with severe PUJO.
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PMID:Page Kidney in a Child with Severe Pelviureteric Junction Obstruction. 3288 53


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