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

Renin is a hormone secreted by the juxtaglomerular cells of the kidney; it interacts with a plasma protein substrate to produce a decapeptide prohormone angiotensin I. Converting hormone located on vascular endothelium converts the decapeptide to an octapeptide, angiotensin II, which effects vasoconstriction, the secretion of aldosterone by the adrenal cortex, and retention of sodium by the kidney. The biosynthesis and control of renin secretion are not well understood, and the question as to whether renin is synthesized and stored in a larger precursor form is as yet unresolved. Whether or not higher molecular weight or inactive forms of renin in plasma have a role in controlling renin activity or whether they simply represent a degradative pathway for renin is as yet uncertain. The availability of several inhibitors of the renin-angiotensin system has served to define the role of renin both in normal cardiovascular homeostasis and in renovascular hypertension. It appears that renin plays an important role in maintaining blood pressure in the salt- or volume-depleted state and that it is responsible for the initial phases of renovascular hypertension in any model of this disease process. Renin's part in chronic renovascular hypertension depends on whether or not sodium is permitted to accumulate. If sodium intake is restricted or if sodium excretion is unimpaired (such as in two-kidney renovascular hypertension models), renin continues to play a significant role during the chronic phase.
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PMID:The role of renin in the control of the circulation and in hypertensive disease. 39 5

Five hundred and seventy-four ambulatory subjects with blood pressures ranging from 94/58 to 250/145 mm Hg were studied on their usual dietary and sodium intake. Renin, renin substrate, angiotensin II, aldosterone and urinary sodium and potassium were compared with blood pressure to access the contribution of these variables to the blood pressure variance. Our analyses revealed that renin substrate was highly and positively correlated with diastolic blood pressure (r = +0.39; p < 0.00001) but all other components of the renin-aldosterone system exhibited a significant negative correlation with blood pressure. A highly significant relationship between potassium, the renin-aldosterone system and blood pressure was found but no such relationship could be demonstrated for sodium. Subjects with higher blood pressures had lower urinary potassium concentrations and lower potassium/creatine ratios. These findings raised the possibility of a significant pathogenetic relationship between potassium and high blood pressure. Multiple linear regression reveals that influences of the renin-angiotensin-aldosterone system can only account for less than 20% of the variance exhibited by the blood pressure in these subjects.
Hypertension
PMID:Relation between blood pressure and renin, renin substrate, angiotensin II, aldosterone and urinary sodium and potassium in 574 ambulatory subjects. 39 40

Renin was extracted and purified from human, dog, hog, rat, beef, rabbit and sheep kidneys. The renin "concentration" of these preparations was determined and expressed in international (Goldblatt) units by measuring the pressor effect produced by intravascular injection into normal dogs of a permanent colony. The renin "activity" was determined by bioassay, in the rat, of the angiotensin produced by incubation in vitro with renin substrate prepared from the serum of nephrectomized dogs. The rate of angiotensin formation was proportional to the concentration of renin, independent of the substrate concentration, and rather similar for renin of all seven species (mean rate = 55 x 10(4) ng angiotensin/unit renin/16 hrs). Due to this uniformity, either of the two international reference preparations of renin (human or hog) from the World Health Organization can serve as an internal standard in the assay of reninof each of the seven species, to express their concentration in terms of the international unit. Renin substrate from hog plasma was suitable for the assay of human, dog and hog renin (mean rate = 55 x 10(4)). However, it reacted much more slowly with the renin of rat, beef, rabbit and sheep (mean rate = 9 x 10(4)) and was, therefore, less suitable for their assay.
Hypertension
PMID:Micromethod for the assay of renin of seven species. 39 36

Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.
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PMID:Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling. 49 1

Around the turn of the century it was observed that low dietary salt consumption is frequently associated with reduction in blood pressure in essential hypertension. It has not been established whether this is a specific effect of NaCl or whether it is an unspecific consequence of the weight loss frequently accompanying low salt intake. Changes of the Renin-Angiotension-Aldosterone system do not seem overly important for the understanding of the original lesion in essential hypertension. Hemodynamic studies demonstrate that increased peripheral (arterial) resistance is characteristic for the disease. It was possible to breed a rat strain with an "anlage" for hypertension which could be unmasked by salt supplements. In humans, essential hypertension is associated with increased salt preference suggesting a genetic factor. This increased desire for salt induces a high salt content of the body including the arterial wall. The hypothesis is being discussed that the stimulating effect of NaCl leads to contraction of the arterial wall inducing increased peripheral resistance - the hallmark of essential hypertension.
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PMID:[Sodium chloride and hypertension (an additional, temporary hypothesis)]. 52 31

Renin activity (RA) in peripheral plasma, as well as in renal cortex and brain (cortex, stem and medulla) homogenates of rats with spontaneous, Goldblatt, NaCl, adrenal-regeneration and neurogenic hypertension was biologically assayed. The results suggest that RA exists not only in the brain of normotensive but of hypertensive rats as well. RA in the medulla is higher than in other brain areas and in the kidney, both in normotensive and in hypertensive rats with the exception of rats with adrenal regeneration and NaCl hypertension. In most of the experimental forms of hypertension (neurogenic, renal, spontaneous) in which RA in the medulla is increased, the role of the brain renin-angiotensin system seems to predominate, while in forms in which renal RA is elevated (adrenal regeneration) the kidney renin system most probably plays a more important role. A definite inverse interrelation between the brain and the kidney renin-angiotensin systems was established. The interrelation between the two renin systems in NaCl hypertension could not be evaluated, since exogenous factors (Na), which interfere with the kidney renin system, play a considerable role in the pathogenesis of NaCl hypertension.
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PMID:Renin activity in the brain, the kidneys and the peripheral plasma or rats with different experimental models of hypertension. 59 8

To learn more about the regulation of blood pressure in renal parenchymal disease, 57 subjects (18 normal controls, 25 patients with essential hypertension and 14 with renal parenchymal disease and hypertension) were evaluated for peripheral renin activity, 24-hour urinary kallikrein activity and whole-blood volume. Blood volumes were significantly lower in patients with essential hypertension (P less than 0.001) and those with renal disease and hypertension (P less than 0.001) than in normotensive subjects. Renin activities (measured after the subjects were standing) were also lower in patients with essential hypertension and hypertension due to renal disease (P less than 0.01 and P less than 0.02, respectively). Kallikrein activity was similar in subjects with renal disease and those with hypertension (P less than 0.05) but markedly diminished in both groups as compared with normotensive subjects (P less than 0.001 and P less than 0.01, respectively) when glomerular filtration rates were taken into account. The kallikrein-kinin system may be involved in the hypertension associated with renal parenchymal disease.
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PMID:Urinary kallikrein activity in the hypertension of renal parenchymal disease. 66 89

In 34 patients saralasin was infused after variable degrees of sodium depletion in order to differentiate between essential and renin-induced hypertension. After sodium-depletion of short duration mean arterial pressure dropped more than 10 mm Hg in 9 of 25 patients with essential and in 7 of 9 patients with renin-induced hypertension. After long-lasting sodium depletion the fall of mean arterial pressure exceeded 10 mm Hg in 11 of 16 patients with essential and in 8 of 9 patients with renin-induced hypertension. Thus saralasin did not discriminate essential and renin-induced hypertension. Also, plasma renin concentration before and after saralasin did not allow to differentiate between the two forms of hypertension. The changes of renin during infusion of saralasin was negatively correlated to the change of blood pressure. Renal vein renin ratio in patients with renovascular hypertension was not modified by saralasin. Renin and aldosterone changed inversely during saralasin infusion.
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PMID:[Saralasin-induced changes of blood pressure, renin and aldosterone in essential and renal hypertension (author's transl)]. 71 15

In patients with unilateral vascular kidney disease and hypertension, ratio of renal-vein-renin was compared with 131I-Hippuric-acid clearance and change in blood pressure during Saralasininfusion. The ratio of renal-vein-renin was positively correlated with the ratio in renal plasma flow between the kidneys in all patients studied. The ratio of renins therefore is a result of two factors: The difference in renin secretion and the difference in blood flow in the two kidneys. In patients with angiotensin independent hypertension renin-ratios up to 2.0 were found without relevance to elevated blood pressure. When the difference in renal blood flow between both kidneys was small, even a slight difference in renal vein renin indicated hypertension related to increased renin secretion. Renin-ratios in the critical range between 1.5 and 2.5 should only be interpreted in respect to a similar ratio in renal blood flow.
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PMID:[Improved interpretation of renal-vein-renin-ratio by simultaneous determination of renal 131I-hippuric-acid-clearance-ratio in patients with renovascular hypertension (author's transl)]. 75 13

The functioning canine renal allograft produces plasma renin activity (PRA) and erythropoietin (ESF) activity and can maintain normal blood pressure and normal erythropoiesis. Moreover, in response to various provocative stimuli it can: (i) increase plasma renin activity in response to low sodium intake; (ii) suppress PRA in response to high sodium intake; (iii) produce increased serum erythropoietin in response to hypoxia. The granulation activity of the juxtaglomerular apparatus correlates best with the degree of graft rejection and with the PRA in groups manipulated by changing sodium balance. This is not the case with hypoxia. Thus, the juxtaglomerular apparatus, even in the presence of vascular changes seen with the severe degree of rejection in renal allografts, can respond to stimuli that can regulate renin release. Renin production by the transplanted kidney can be dissociated from ESF secretion. Blood pressure changes in the present model were not directly associated with increased PRA or juxtaglomerular apparatus activity. In such conditions hypertension can exist in the presence of suppressed PRA and without hypergranulation of the apparatus. The majority of correlations of this study thus establish a close association of the degree of juxtaglomerular index activity with PRA levels, rather than ESF.
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PMID:The response of the juxtaglomerular apparatus to stimuli effecting renin or erythropoietin release in canine renal allografts. 76 86


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