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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of the renin-angiotensin-aldosterone system (RAAS), excretion of renal prostaglandins, renal hemodynamics, water-electrolyte balance were studied in 110 patients with chronic nephritis with arterial hypertension: 47 with hypertonic nephritis and 63 patients at the stage of renal insufficiency. Some investigations, the results of data processing, an analysis of the results of cross-group comparative studies, and the use of captopril (a drug that inhibits the activity of angiotensin-converting enzymes) confirmed the RAAS involvement in the pathogenesis of arterial hypertension in nephritides. Pathophysiological features of arterial hypertension in nephritides are the following: disturbances of physiological interrelationships between renin plasma activity and the state of water-electrolyte balance; hyperaldosteronism and depression of renal prostaglandin synthesis revealed both in unchanged and lowered renal function. The peculiarity of arterial hypertension at the stage of marked renal insufficiency is invariability of renin production resulting from structural reserves of the renal juxtaglomerular apparatus.
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PMID:[Pathophysiological features of arterial hypertension in chronic nephritis]. 332 85

The short- and long-term effects of two calcium channel blocking drugs, verapamil and nifedipine, on blood pressure, heart rate, plasma catecholamines, plasma renin activity, plasma volume and cardiac performance (echocardiography) were studied in essential hypertensive patients and in normal subjects. Verapamil, 160 mg orally, reduced blood pressure within 60 minutes in 22 hypertensive patients, but not in 12 normotensive subjects. Nifedipine, 10 mg sublingually, reduced blood pressure within 15 minutes in 19 hypertensive patients, but not in 7 normotensive subjects. Plasma noradrenaline was significantly increased both in normal subjects and in hypertensive patients only after nifedipine was administered. Verapamil (80 mg three times a day) first, and nifedipine (10 mg three times a day) thereafter, or vice versa, were given to 12 hospitalized hypertensive patients on a fixed sodium and potassium intake; the drugs produced similar blood pressure reductions, but heart rate and plasma catecholamines were increased only after nifedipine (p less than 0.05). Neither drug affected plasma volume, aldosterone or plasma renin activity. Long-term ambulatory treatment with verapamil (80 or 160 mg three times a day for 2 to 4 months) or nifedipine (10 mg three times a day for 2 months) produced changes in all variables that were similar to those observed in the hospital (controlled) study. Shortening fraction was significantly increased after nifedipine (p less than 0.05) but no change was observed after verapamil. In conclusion, blood pressure is effectively reduced by both verapamil and nifedipine; an appreciable adrenergic stimulation may be caused by nifedipine, but usually not by verapamil, and fluid retention, renin release or myocardial depression is not observed during verapamil or nifedipine treatment.
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PMID:Similarities and differences in the antihypertensive effect of two calcium antagonist drugs, verapamil and nifedipine. 351 29

Angiotensin II (ANG II) is one of the body's most powerful regulators of Na excretion, operating through extrarenal mechanisms, such as stimulation of aldosterone secretion, as well as intrarenal mechanisms. Considerable evidence suggests that the intrarenal actions of ANG II are quantitatively more important than changes in aldosterone secretion in the normal day-to-day regulation of Na balance and arterial pressure. ANG II at physiological concentrations increases proximal tubular reabsorption, but further studies are needed to determine whether ANG II also has an important effect on more distal tubular segments. ANG II also markedly constricts efferent arterioles, tending to increase Na reabsorption by altering peritubular capillary physical forces and also helping to prevent excessive decreases in glomerular filtration rate. ANG II may also decrease Na excretion and increase urine concentrating ability by reducing renal medullary blood flow. Regulation of Na excretion by ANG II is closely linked with arterial pressure control and volume homeostasis through the renal pressure natriuresis mechanism. Under many physiological conditions, such as changes in Na intake, ANG II greatly multiplies the effectiveness of the pressure natriuresis mechanism to prevent fluctuations in body fluid volume and arterial pressure. In circumstances associated with circulatory depression, such as decreased cardiac function, reductions in blood pressure and increased ANG II formation cause Na retention until arterial pressure is restored to normal. However, in pathophysiological conditions in which ANG II is inappropriately elevated, increased arterial pressure (hypertension) is required for the kidney to "escape" the potent antinatriuretic actions of ANG II and to return Na excretion to normal via the pressure natriuresis mechanism.
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PMID:Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation. 352 37

The prolonged effects (42 days) of indomethacin treatment on the renin-angiotensin-aldosterone axis, renal hemodynamics, and renal excretory function in humans were studied. Indomethacin produced a 41% sustained depression in the 24-hour excretion of prostaglandin E2 and a mild (7%) decrease in inulin clearance but did not affect the clearance of p-aminohippurate, the 24-hour excretion of sodium and potassium, or the basal values of plasma aldosterone; however, it decreased the basal values of renin and prevented the stimulated (3 hours of walking) responses of plasma renin activity and plasma aldosterone. Indomethacin also produced a decrease in both the diuretic and saluretic response to furosemide and in the renal ability to concentrate urine. The indomethacin-induced hyporeninism and hypoaldosteronism were more pronounced when the subjects were receiving a sodium-restricted diet. This finding indicates that prolonged administration of anti-inflammatory drugs induces chronic hyporeninism and hypoaldosteronism. Prolonged treatment with indomethacin also produced some of the symptoms of a syndrome of hypoprostaglandinism, such as decreased plasma renin activity, plasma aldosterone, and urinary prostaglandin E2 in association with increases in plasma potassium levels and diastolic pressure.
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PMID:Effects of long-term treatment with indomethacin on renal function. 352 4

Normal (N) rats and rats with nephrotoxic serum nephritis (NSN) were used in whole-kidney and micropuncture studies while being kept euvolemic by homologous plasma infusion and after isotonic volume expansion (VE). During euvolemia, whole kidney and single nephron (SN) glomerular filtration rate (GFR), as well as urinary sodium excretion (UNa X V), were significantly lower in NSN rats (GFR = 0.40 +/- 0.06 ml/min; SNGFR = 14.4 +/- 1.9 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min) than in controls (GFR = 1.14 +/- 0.06 ml/min; SNGFR = 32.7 +/- 2.0 nl/min; UNa X V = 0.05 +/- 0.02 microEq/min); fractional proximal and "distal" (beyond the proximal convoluted tubule) sodium reabsorption rates were significantly higher than N, further depressing urinary sodium output. Saline expansion significantly elevated GFR and decreased renal vascular resistance (RVR) in both N and NSN rats. In the latter, however, GFR remained below, and RVR above, levels observed in N rats. Urinary sodium excretion increased markedly with saline expansion in N rats, reaching 26.9 +/- 1.31 microEq/min. NSN rats exhibited a blunted natriuretic response to expansion (UNa X V = 3.85 +/- 1.02 microEq/min); however, despite a still depressed GFR and increased RVR, urinary sodium excretion in NSN rats reached levels well above euvolemic control. Fractional proximal and "distal" tubular sodium reabsorption rates were depressed by VE in both N and NSN rats. However, this depression was less evident in NSN rats, particularly in the "distal" nephron, suggesting that the stimulus for sodium reabsorption in these segments was somehow enhanced in NSN rats. Fractional potassium excretion was increased to a much greater extent in NSN than in N rats. This finding, associated with the small depression of fractional sodium reabsorption in the "distal" nephron of NSN rats, suggests a participation of elevated levels of circulating aldosterone in the sodium retention observed in this model.
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PMID:Sodium handling and renal hemodynamics in euvolemic and volume-expanded nephrotic rats. 359 9

Ten patients with hypertension and obesity were studied during a program of weight loss on an unrestricted sodium diet. The study showed that weight loss during the ten month period was accompanied by a significant decrease in urinary aldosterone, tetrahydroaldosterone -3-glucuronide and plasma renin activity values. It was also demonstrated that successful reduction in body weight was associated with a reduction in blood pressure. It is postulated that blood pressure reduction in obese patients during weight reduction may depend on decreases in aldosterone and plasma renin activity. The reduction in levels of tetrahydroaldosterone-3-glucuronide is due to an energy related depression of the glucuronidation process caused by carbohydrate deficiency. It is postulated that the lowered rate of metabolism of aldosterone as measured by the diminished formation of the metabolite tetrahydroaldosterone-3-glucuronide is an important determinant of blood pressure status during weight reduction.
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PMID:Aldosterone studies in obese patients with hypertension. 389 May 39

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.
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PMID:Drinking induced by injection of angiotensin into the rain of the rat. 432 23

A total of 132 urine specimens were obtained from 17 depressed patients and 18 controls under conditions of mild water deprivation. Mean values of milliosmoles of solute and millilitres of urine excreted per hour were obtained for each subject. The depressed patients excreted significantly less solute than the control group per unit volume of urine. There was no significant difference between the solute excretion rates of depressed patients and those who had recently recovered from depression-though the trend was towards normality. The significance of these results is discussed in relation to studies on body fluids and electrolytes and the role of ADH and aldosterone in affective disorders.
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PMID:Urine concentration in depressive illness. 555 92

Postmenopausal patients with metastatic breast cancer were treated with medroxyprogesterone acetate (MPA) (Clinovir) in dosages between 500 and 1500 mg orally per day. The relation of MPA plasma concentrations and endocrine effects were studied in a longitudinal fashion. MPA exerted suppressive effects on the basal and gonadotropin-releasing hormone (GnRH) stimulated gonadotropin secretion, cortisol, dehydroepiandrosterone (DHEA), and estradiol (E2) in a dose-dependent manner leading to a complete suppression with 1500 mg orally per day. The depression of thyroid hormones (T3 and T4) coincided with a depression of the thyroxine-binding index (TBI). MPA did not affect human growth hormone (hGH), basal and thyrotropin-releasing hormone (TRH) stimulated thyroid-stimulating hormone (TSH) and aldosterone. Basal and TRH-stimulated prolactin (PRL) secretion showed a slight but distinct elevation. From these data it is concluded that in postmenopausal patients MPA exerts its antitumor activity by an interference with the hypothalamo-pituitary adrenal axis in the sense of a selective pharmacologic hypophysectomy leading to complete suppression of adrenal steroid secretion. Additionally, MPA inhibits tumor cell growth through the progesterone receptor. A dual mechanism for the antitumor activity of high dose is postulated MPA: ablative through suppression of the hypothalamo-pituitary-adrenal axis and subsequent estrogen deprivation, and additive via the progesterone receptor directly on the tumor cell. The significance of gonadotropin suppression in the postmenopause for breast cancer growth is unclear. The depression of T3 and T4 is due to a depression of thyroid hormone-binding proteins. The elevation of PRL secretion may be explained by a slight estrogenic activity of MPA metabolites.
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PMID:Pharmacokinetic and pharmacodynamic basis for the treatment of metastatic breast cancer with high-dose medroxyprogesterone acetate. 608 20

The antihypertensive effect of a new vasodilator with betablocking properties (SK & F 92657) was investigated in 10 patients with mild to moderate essential hypertension. After a mean treatment period of 26,5 weeks (6,5-49 weeks) blood pressure was significantly reduced, from 168 +/- 22/106 +/- 6 mmHg to 144 +/- 19/94 +/- 12 mmHg (p less than 0.05 and 0.025). The mean dose was 410 mg (100-700 mg). Heart rate decreased slightly from 77 +/- 12 to 70 +/- 8 beats/min. Plasma renin activity and plasma aldosterone showed only minor changes. Nausea, heavy dreams, facial and hand flushing and mild depression were reported as side effects. In most patients the symptoms disappeared without reduction in the dose. In one patient anaemia developed after 7 weeks and treatment with prizidilol was stopped. A slight but statistically significant decrease in haemoglobin concentration of 1.1 +/- 0.6 g/dl was observed in 5 of the 10 patients (p less than 0.02). Thus, a mean dose of prizidilol of 410 +/- 242 mg/day had a mean blood pressure lowering effect of 24/12 mmHg. In 7 of the 10 patients (70%) diastolic blood pressure could be reduced to 95 mmHg or less. However, the observed haematological side-effects should be carefully monitored in further studies and may limit the clinical use of prizidilol.
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PMID:Prizidilol (SK & F 92657), a new vasodilator with beta-blocking properties in the treatment of essential hypertension. 612 80


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