Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several of the factors responsible for circulatory control are modified in the elderly. Loss of elasticity of the aortic wall produces a widened pulse pressure and a high incidence of systolic hypertension. Attempts to normalize this may be associated with disabling diastolic hypotension. Arterial baroreceptor sensitivity and responsiveness of the renin-angiotensin system is reduced. Further, the renal capacity to conserve sodium and water is impaired. All these increase the risks associated with antihypertensive treatment, but do not contra-indicate such treatment.
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PMID:Pathophysiology of blood pressure in the elderly. 46 75

Plasma renin activities (PRA) and aldosterone concentrations increased in parallel over a wide range of plasma volume deficits produced in unanesthetized rats by extravascular administration of polyethylene glycol (PEG) solution. When PEG-treated rats were given water to drink, their intakes were proportional to PRA; when given water and 0.5 M NaCl, PRA and the steroid concentrations diminished concurrently in association with sodium consumption. Aldosterone concentrations and NaCl intakes were markedly enhanced after PEG treatment in rats maintained on a sodium-deficient diet for 4 days. On the other hand, a clear relation between PRA and water intake, and between circulating aldosterone levels and sodium intake, was not suggested by other experiments in this series. For example, bilateral nephrectomy abolished the rise in PRA during hypovolemia yet rats drank water normally. Moreover, aldosterone concentrations were substantially elevated by PEG treatment in the nephrectomized rats yet sodium appetite was abolished. These and other findings suggest that neither angiotensin nor aldosterone plays a prominent role in stimulating water and saline intakes during hypovolemia.
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PMID:Renin and aldosterone secretions during hypovolemia in rats: relation to NaCl intake. 46 83

Endocrine and renal functions were studied in 149 patients with essential hypertension by measuring plasma electrolytes, renin activity, creatinine and aldoserone, as well as the urinary excretion of creatinine and sodium chloride, before and during treatment for hypertension. Half of the patients responded to trichlormethiazide (thiazide-responsive group) but the other half did not (thiazide-unresponsive group). Systolic and diastolic blood pressures increased progressively uith age in the thiazide-unresponsive group, but were lower and did not progress with age in the thiazide-responsive group. There was no consistent difference in plasma renin activity between the thiazide-responsive and the thiazide-unresponsive groups. The fluctuation of plasma renin activity in response to an excess of sodium chloride or to thiazide treatment was reduced progressively with age. Creatinine clearance decreased and the blood urea nitrogen level increased with age. The age-related decrease of plasma renin activity is discussed on the light of the age-related impairment in the ability of the kidney to excrete sodium and water.
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PMID:Age-related changes in endocrine and renal function in patients with essential hypertension. 46 52

In seven patients with uncomplicated essential hypertension the effects of an acute alpha-adrenergic blockade, alone and combined with a chronic beta-adrenergic blockade, on blood pressure, renal function as measured by standard clearance methods, plasma renin activity, and plasma aldosterone were evaluated. Acute alpha-adrenergic blockade with phentolamine (20 mg by intravenous infusion) significantly enhanced the antihypertensive effect of chronic beta-adrenergic blockade with slow-oxprenolol (160 mg/ day X 14 days) (- 14.5% verus - 7.4% for pulse pressure, - 12.4% versus - 6.0% for diastolic pressure, 2 alpha less than 0.05). Under combined adrenergic blockade renal plasma flow increased, glomerular filtration rate and filtration fraction decreased (2 alpha less than 0.05 each), whereas the fractional clearances of sodium, potassium, free water, and solute load remained unchanged. The activation of the renin-angiotensin-axis, elicited by alpha-adrenergic blockade alone, was suppressed by the preceding beta-adrenergic blockade. These findings demonstrate a favourable antihypertensive action of a combined blockade of alpha- und beta-adrenergic receptor sites without untoward side effects on renal function or the renin-angiotensin-axis.
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PMID:[Acute combined alpha- and beta-adrenergic blockade in essential hypertension: effects on blood pressure, renal function, renin, and aldosterone]. 47 Mar 35

Physiological levels of arginine vasopressin (AVP) were continuously infused 24 h/day into six dogs for periods ranging from 7 to 34 days. The acute and chronic responses of the mean arterial pressure (MAP), body fluid volumes, renal function indices, plasma electrolyte concentrations, plasma renin activity, and urinary electrolyte and water excretion rates were measured. MAP was unaffected acutely but rose significantly to a peak on day 9 before declining toward control. MAP was significantly and positively correlated with the plasma volume, but had a diphasic correlation with the plasma sodium concentration and the change in total body sodium. The plasma sodium concentration reached a relatively stable plateau that was maintained in spite of large changes in total body water. We conclude that AVP produces only a transient hypervolemic hypertension; that AVP is a natriuretic agent, either directly or indirectly, both acutely and chronically; and that chronically it is a more potent controller of the plasma sodium concentration than of the total body water except in extreme cases.
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PMID:Acute and chronic effects of vasopressin on blood pressure, electrolytes, and fluid volumes. 47 64

1. The mineralocorticoid 9 alpha-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an 'escape' from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the 'effective' extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. The findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.
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PMID:Studies on mineralocorticoid 'escape' in cirrhosis. 47 24

Peritoneal dialysis with 5% glucose solution was carried out in dexamethasone-pretreated rats. Dialysis brought about a severe loss of sodium and a slight loss of potassium into the peritoneal fluid. This kind of sodium depletion took place without any decrease in total body-water space, thus it evoked a severe fall in plasma sodium concentration. Plasma renin activity and the serum concentration of aldosterone increased in response to dialysis. Peak values in renin activity were attained within 60 min, whereas aldosterone concentrations exhibited a continuous rise until at least 120 min. Despite the correlation of renin and aldosterone values, neither the administration of an angiotensin I converting enzyme inhibitor (SQ 20,881) nor the reduction of plasma renin activity by indomethacin could reduce hyperaldosteronism evoked by peritoneal dialysis. Therefore, it is assumed that there is no causal relationship between renin and aldosterone in this kind of acute, severe sodium depletion.
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PMID:Hyperaldosteronism in the sodium-depleted rat: mechanism of aldosterone stimulation by peritoneal dialysis with glucose solution. 47 31

Renin activity and aldosterone concentration in plasma and excretion of sodium and potassium in urine were measured during a period of 24 hours in 12 patients undergoing hysterectomy under general anaesthesia or epidural analgesia. Analgesia extended from T4 to S5 and was effective throughout the study. The normal stress-induced increase in plasma renin activity and aldosterone was inhibited by epidural analgesia. Urinary excretion of potassium was significantly lower in the epidural group, but sodium and water retention showed no difference between groups. It is concluded that neurogenic stimuli from the surgical area are important release mechanisms of the renin-aldosterone response to surgery. The results suggest that post-operative sodium retention is caused by factors other than the mineralocorticoid system.
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PMID:Epidural analgesia inhibits the renin and aldosterone response to surgery. 48 83

Male and female albino rat pups sustained septal destruction at 10 days of age and body weight and water intakes were measured daily throughout development until 200 days of age. During development the septal and control rats received a battery of drinking tests (e.g., cellular dehydration, hypovolemia, renin). Septal rats (males and females) were hyperdipsic for daily water intakes as early as 31 days of age and the daily hyperdipsia persisted through 200 days of age. On the battery of drinking tests, septal rats consumed water at control volumes on all tests except water deprivation (following which females were hyperdipsic) and food deprivation (during which both males and females were hyperdipsic). Urine output-water intake relationships were determined, and a series of food deprivation tests were conducted during development to determine the etiology of the developmental septal hyperdipsia. All results suggest that hyperdipsia associated with septal destruction during the preweaning period is a primary condition and not secondary to altered output mechanisms, abnormal feeding-drinking patterns, or displacement behavior.
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PMID:Septal destruction in infant rats and the ontogeny of drinking behaviors. 48 93

Norepinephrine (NE) release and pressor response to sympathetic stimulation were studied in dogs under furosemide-induced acute volume depletion. The rise in blood pressure observed following carotid clamping proved similar before and after acute salt and water depletion in the first group of animals and NE rose comparably in these two conditions. Similar results were obtained in a second group of dogs that received an angiotensin II converting enzyme inhibitor (CEI). This study shows that contrary to isotonic saline loading, acute salt and water depletion cause a progressive increase in NE plasma levels. Moreover, these results clearly demonstrate that the decrease in sympatho--adrenergic response and the predominant role played by the renin--aniotensin system during chronic salt depletion are not observed in acute conditions.
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PMID:Carotid sinus reflex and norepinephrine release following acute volume depletion in dogs. 48 75


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