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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Present knowledge of the mechanisms regulating release of renin is reviewed with particular emphasis on neural factors. Evidence is given for a direct effect of renal innervation on beta adrenergic receptors in juxtaglomerular cells, and for the involvement of reflex release of renin in conditions such as tilting and acute salt depletion. Participation of neural and nonneural mechanisms of control is also shown to occur in other conditions, such as aortic constriction and hemorrhage. The view is held that neural sympathetic factors might explain some of the renin disturbances found in essential hypertension. First, in patients with high renin hypertension part of the hypertension is renin-dependent, and these pressor levels of renin seem to be neurally induced since they can commonly be suppressed by beta adrenoreceptor blocking agents. Second, the hypothesis is presented that patients with low renin hypertension, at least those who have no volume disturbance, have a blunted sympathetic control of renin release. Therefore a sufficiently precise test of sympathetic activity, and possibly of body fluid volumes, should be associated with renin profiles for a better understanding of the pathophysiology of arterial hypertension and as a better guide to therapeutic management. Indeed, most of the available antihypertensive drugs act on sympathetic activity, body fluid volume or renin, and this multifaceted profile would provide more rational guidelines for treatment.
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PMID:Control of renin release: a review of experimental evidence and clinical implications. 0 64

Plasma catecholamines, indexes of sympathetic nervous tonicity, were measured simultaneously with renin both supine and after standing plus furosemide in patients with primary hypertension and normotensive volunteers. Seventy percent of hypertensive patients with high renin levels had increased catecholamines compared with a 14% incidence in the combined group with low and normal renin (P less than 0.001). Basal catecholamines were related directly to renin in the hypertensive patients and to blood pressure in the normal (P less than 0.05), but not in the high and low renin subgroups, and inversely to percent increase of catecholamines after standing plus furosemide in hypertensive and normotensive patients (P less than 0.01). Sympathetic nervous hypertonicity may be responsible for the elevation of blood pressure and for the activation of the renin-angiotensin system in patients with high renin hypertension.
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PMID:Increased plasma catecholamines in high renin hypertension. 99 17

In patients with essential hypertension a gradual decrease in basal and stimulated renin secretion was found with increasing age. Stimulated plasma aldosterone decreased similarly; however, the observed changes were less pronounced. Young patients (less than 35 years) with high renin hypertension had lower diastolic blood pressure than patients with low renin hypertension in the same age group. Contrary to these findings, a markedly higher diastolic blood pressure was observed in patients over 35 years of age with high renin hypertension than in the group of patients with low renin hypertension. These results indicate that neither high nor low renin essential hypertension patients represent homogeneous groups. Furthermore, the dissociation between changes in renin activity and plasma aldosterone points to a disturbed relationship between the renin angiotensin system and aldosterone secretion in essential hypertension.
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PMID:[Plasma renin activity and plasma aldosterone in essential hypertension: effect of age and diastolic blood pressure]. 101 95

The anti-hypertensive effect of spironolactone and thiabutazide was tested on 47 unselected patients with primary hypertension. They were divided into two groups according to the change in plasma-renin activity in response to furosemide administration: those with and those without response to stimulation, and sub-groups with low, normal or high plasma-renin activity (low renin hypertension; normal renin hypertension; high renin hypertension). During both 4-week treatment periods there was a distinct fall in systolic blood pressure, most marked in the patients without plasma renin stimulation (after spironolactone of about 26.2 mm Hg, after thiabutazide 29 mm Hg), the diastolic pressure fall being only slight in all groups (about 5-10 mm Hg). The plasma-renin activity and plasma-aldosterone concentration increased in all groups, after both spironolactone and thiabutazide three-to fourfold compared with the basal value, even in patients without change in plasma-renin activity after furosemide injections. Serum sodium content decreased after administration of spironolactone, increasing again after subsequent thiabutazide administration. Serum potassium content increased after spironolactone, decreasing after thiabutazide. There was no significant difference between either individual groups or different treatment periods with spironolactone or thiabutazide as far as weight, urine volume or electrolyte excretion in 24-hour urine was concerned.
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PMID:[Spironolactone and thiabutazide in the treatment of essential hypertension (author's transl)]. 116 22

Subjects with high renin hypertension tend to be sodium-resistant showing paradoxical blood pressure responses to alterations in sodium intake. Of twenty-five subjects with high renin essential hypertension (ten females, 15 males, mean age 30 years), 14 were noted to have a decrease in mean arterial blood pressure (MAP) when sodium intake was increased from 10 to 100 mmol/d. The percentage response of plasma renin activity was greater in these patients than in those with an increase in MAP (-55.4 +/- 5.4 v -33.6 +/- 6.9, P = .018). Overall, the response of MAP was directly correlated to the percentage response of plasma renin activity (r = .549, P = .005), and inversely related to the change in serum calcium concentration (corrected for changes in serum albumin) (r = -.547, P = .005). No intercorrelation between the changes in plasma renin activity and serum calcium concentration was detected. The blood pressure response to increased sodium intake in high renin hypertension would appear to be divergent and related not only to the suppression of plasma renin activity, but also to changes in circulating calcium.
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PMID:Blood pressure and serum calcium responses to altered sodium intake in high renin hypertension. 264 17

Whilst plasma renin values are elevated in a minority of patients with essential hypertension, there is no indication that high renin hypertension is a distinct entity and even where renin levels are elevated, they are usually less than those observed in renovascular hypertension. It is still possible for the renin-angiotensin system to be important, if blood pressure is maintained by renin activity within the arterial or arteriolar walls. Accordingly, renin-like activity or rat aortic wall homogenate and plasma renin concentrations were measured simultaneously. Both plasma and aortic renin (measured with an incubation pH of 6.5) rose in salt-depleted and fell in salt-loaded rats. Both were elevated in Goldblatt 2-kidney hypertension. However, aortic renin fell gradually over 24 h after bilateral nephrectomy, whilst plasma renin had reached its nadir by 1 h. To assess the importance of arterial as opposed to plasma renin the renin-angiotensin system was blocked with the converting enzyme inhibitor Sq20881. A blood pressure fall attributable to renin-angiotensin blockade could be demonstrated for at least 6 h after bilateral nephrectomy. This supports the hypothesis that renin in the arterial and arteriolar wall, rather than plasma renin, is responsible for blood pressure maintenance. Nevertheless, in steady state conditions such as essential hypertension, plasma and arterial renin are closely related.
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PMID:Vascular renin in hypertension. 615 22

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