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

Abnormalities in sodium metabolism, including the presence of endogenous circulating digitalis-like sodium transport inhibitors, have been implicated in the genesis of essential hypertension. Digitalis has also been reported to affect adrenal steroid output in vitro. We studied the effects of 4 days of treatment with the digitalis glycoside digoxin upon blood pressure, the renin-aldosterone axis, and pressor and steroidogenic responses to graded norepinephrine, angiotensin, and ACTH infusions in six normal men after pretreatment with dexamethasone. Digoxin produced no significant changes in blood pressure, urinary electrolyte or aldosterone excretions, PRA or aldosterone concentrations, or the incremental responses of aldosterone or cortisol to angiotensin or ACTH. However, digoxin significantly augmented pressor responsiveness to both norepinephrine and angiotensin without significantly affecting the steady state baroreceptor-heart rate reflex. These findings support the hypothesis that digitalis-like factors may have important effects upon arterial blood pressure control in man.
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PMID:Effects of digoxin on responsiveness to the pressor actions of angiotensin and norepinephrine in man. 631 64

The effects on blood pressure, the renin-angiotensin-aldosterone and the kallikrein-kinin systems were investigated in 32 patients with primary hypertension WHO stage I-II treated with captopril. Hydrochlorothiazide was added if needed to achieve a supine diastolic blood pressure of less than or equal to 90 mmHg. A placebo control group (n=8) was treated similarly. Supine mean arterial pressure fell from 133 +/- 10 on placebo to 114 +/- 12 mmHg after 4 weeks on captopril. At the same time plasma aldosterone decreased from 263 +/- 188 to 164 +/- 101 pmol . 1(-1), 24 h urinary excretion of aldosterone from 18 +/- 12 to 12 +/- 10 nmol and kallikrein from 9.0 +/- 6.7 to 6.2 +/- 4.1 nkat. Plasma angiotensin II was significantly reduced after two weeks treatment from 23.2 +/- 8.6 to 17.0 +/- 6.7 pmol . 1(-1). Before, but not during captopril, 24 h urinary kallikrein excretion correlated with plasma aldosterone levels and 24 h urinary aldosterone excretion (r=0.44 p, less than 0.05 and r=0.53, p less than 0.01, respectively). Mean arterial pressure reduction on captopril correlated with pretreatment PRA (r=0.44, p less than 0.05) but not with other measured hormone levels or changes therein. The addition of hydrochlorothiazide caused a further fall in blood pressure, but increased plasma aldosterone and 24 h urinary kallikrein excretion. Hydrochlorothiazide alone increased only 24 h urinary aldosterone excretion significantly. These findings indicate that, besides aldosterone secretion and renal arterial pressure, further mechanisms regulating the release of and activity of the renal kallikrein-kinin system exist.
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PMID:Captopril, aldosterone and urinary kallikrein in primary hypertension. 634 63

A group of 89 individuals with essential hypertension was evaluated with several measurements including the neurophysin believed to be the human oxytocin neurophysin (OT-Np), and the human vasopressin neurophysin (VP-Np). The neurophysins are proteins synthesized within cells of the supraoptic and paraventricular nuclei in conjunction with their respective hormones oxytocin and vasopressin as part of a common precursor molecule and so may reflect the simultaneous presence in plasma of their associated hormones. A poor but statistically significant correlation was noted between levels of OT-Np and renin activity in plasma (PRA) either supine (r = 0.248) or erect (r = 0.255). Levels of OT-Np averaged 1.75 ng/ml and were inversely correlated with creatinine (r = -0.252), supine blood pressure (r = -0.450), plasma volume (r = -0.327), and 24-hour urine sodium (r = -0.313). Levels of Ot-Np could be suppressed by infusion of physiologic saline. Levels of OT-Np were lower in the volume expanded state and were positively correlated with the quantity of sodium excreted into a 24-hour urine collected after the infusion (r = 0.426) and inversely correlated with the supine systolic (r = -0.379) and supine diastolic (r = -0.455) blood pressures recorded after the infusion of saline. Oestrogen, a stimulus to the secretion of OT-Np, did not account for the elevation of OT-Np observed in the study, since mean levels of oestradiol (E2) in a subset of the patients with elevated OT-Np (E2 = 36 pg/ml) were not different from levels in subjects with lower values of OT-Np (E2 = 45 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Levels of the oxytocin-associated and vasopressin-associated neurophysins in plasma and their responses in essential hypertension. 637 63

By inhibiting ACE, captopril blocks the conversion of AI or AII and augments the effects of bradykinin both in vitro and in vivo. In rats, dogs, and monkeys with 2-kidney renal hypertension, orally administered captopril rapidly and markedly reduces blood pressure; this antihypertensive effect apparently occurs via a renin-dependent mechanism; that is, the inhibition of ACE. In 1-kidney renal hypertension studies in rats and dogs, it was determined that oral doses of captopril markedly lowered blood pressure, but only after several days of dosing; the mechanism is thought to be non-renin dependent. In SHR, daily oral doses of captopril progressively lowered blood pressure; normal levels were attained by the sixth month. In all species studied, the reduction in blood pressure resulted from a reduction in total peripheral resistance; cardiac output remained unchanged or increased. In humans, captopril reduces blood pressure in patients with essential hypertension with low, normal, and high renin levels, and in patients with renovascular hypertension and hypertension associated with chronic renal failure. In hypertensive patients with high plasma renin activity, captopril apparently exerts most of its pharmacologic effects through inhibition of ACE. The means by which captopril reduces high blood pressure associated with low or normal PRA is not known, but it is clear that captopril does not act on an overactive plasma renin-angiotensin system in these cases. The antihypertensive effect of captopril is enhanced when it is given in combination with a diuretic or after salt depletion. Captopril was rapidly and well absorbed in all species tested, including man. Studies in rodents indicated that ingestion of food caused a reduction in the extent of absorption and bioavailability of captopril. Captopril and/or its metabolites were distributed extensively and rapidly throughout most tissues of normal rats; no radioactivity was detected in the brain. In vitro and in vivo, captopril formed disulfide bonds with albumin and other proteins. This binding was reversible in nature. In vitro studies in blood indicates that the disulfide dimer of captopril and mixed disulfides of captopril with L-cysteine and glutathione were formed. In intact blood cells, captopril remained in the reduced form (sulfhydryl), whereas in whole blood or plasma, captopril was converted to its disulfide dimer and other oxidative products. Biotransformation of captopril may involve both enzymatic and nonenzymatic processes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Captopril: pharmacology, metabolism and disposition. 643 80

We investigated the relation between 24-h recumbent blood pressure levels and secretory patterns of PRA, aldosterone, cortisol, and PRL in four hypertensive pesudohypoparathyroid (PsHP) males and nine age- and weight-matched males with essential hypertension. Although both groups had PRA and aldosterone circadian rhythms, the variability and concentrations of these hormones over 24 h were considerably less in PsHP patients. Plasma cortisol concentrations demonstrated a well defined circadian rhythm in both groups, with no discernable differences between the PsHP patients and the patients with essential hypertension. All patients with essential hypertension had circadian rhythms of PRL secretion, but the PsHP patients failed to demonstrate a circadian variation in PRL secretion. These results suggest that factors other than those investigated in this study are responsible for the maintenance of elevated blood pressures in PsHP patients. The absence of circadian secretion of PRL may be related to altered dopaminergic control mechanisms in PsHP patients.
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PMID:Circadian blood pressure and renin, aldosterone, cortisol, and prolactin levels in hypertensive pseudohypoparathyroid patients. 675 69

The interrelationship between PRA, urinary aldosterone excretion, and blood pressure was studied in 11 patients with essential hypertension while receiving a diuretic (1st week) and subsequently a diuretic + oxprenolol (2nd week). The diuretic reduced blood pressure and body weight but increased PRA and aldosterone. Oxprenolol reduced PRA on the 1st day but to a lesser extent on the 7th day. Blood pressure was decreased 1 day after oxprenolol administration, but to a greater extent on the 7th day. Blood pressure decrements were independent of renin suppression, but directly correlated to aldosterone changes. These data suggest that the hypotensive effect of oxprenolol in patients receiving diuretic treatment is independent of its suppression of renin. Aldosterone suppression may instead contribute to the hypotensive effect of the drug.
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PMID:The renin-angiotensin-aldosterone system and blood pressure during oxprenolol treatment in hypertensive patients pretreated with diuretics. 675 51

Hyperprolactinemia has previously been noted in patients with essential hypertension and it has been suggested that the increased PRL levels in this condition may reflect reduced central dopaminergic activity. In the present study, PRL secretion was evaluated in 17 patients with essential hypertension and in 9 normal controls as an indirect index of hypothalamic-pituitary dopaminergic activity. PRL levels were measured basally, at night, and after TRH (200 micrograms, iv), metoclopramide (10 mg, orally), and L-dopa (500 mg, orally). Basal PRL levels were similar in both groups [essential hypertension, 301.2 +/- 176.2 microunits/ml; controls, 334.2 +/- 98.8 microunits/ml (mean +/- SD)]. No differences in PRL levels were found after TRH, L-dopa, and metoclopramide or during sleep between the 2 groups. When the patients were classified according to their PRA, no differences were noticed in either basal levels or the patterns of PRL response. It is concluded that PRL secretion is normal in patients with essential hypertension, which could be indirect evidence against reduced hypothalamic-pituitary dopaminergic activity in this disease. However, minor abnormalities not detected by PRL measurements could be involved in the pathogenesis of essential hypertension.
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PMID:Dynamic evaluation of prolactin secretion in essential hypertension: evidence against hypothalamic-pituitary dopaminergic dysfunction. 680 Oct 72

Plasma and kidney renin activity (PRA, KRA) were determined in the spontaneously hypertensive (SHR) rats, the stroke-resistant and -prone substrains (SHRSR, SHRSP) from 5 to 30 weeks of age. Results were compared with those of two normotensive strains, Wistar-Kyoto (WKY) and Donryu (DON) rats. PRA in the SHRSP at 20 and 30 weeks of age were significantly increased when compared to other strains of rats (P < 0.01). In SHRSP rats at these ages, blood pressure exceeded the critical level of 220 mmHg and cerebral lesions were observed in 41% at autopsy. There were no significant differences in PRA among other hypertensive and normotensive strains. KRA in three substrains of the SHR were normal or subnormal as compared to WKY and DON rats. These results indicate that a direct role of the renin-angiotensin system in the SHR and its substrains can be excluded in the initiation and the maintenance of hypertension. However, the activated renin-angiotensin system in SHRSP rats in the course of malignant hypertension at 20 weeks of age and later, could participate in raising blood pressure above the levels of the SHR and SHRSR. Considering out data and others, there are many similarities in renin profile between the SHR and its two substrains, and human essential hypertension in which PRA can be classified as low, normal or high.
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PMID:Variation of plasma and kidney renin activities among substrains of spontaneously hypertensive rats. 699 83

The acute responsiveness of plasma catecholamine, renin (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin (PRA), and aldosterone levels to exogenous norepinephrine was studied under placebo conditions and following renin-angiotensin activation by diuretic pretreatment in 25 normal subjects and 34 patients with borderline-to-moderate essential hypertension. Norepinephrine infusion caused increases in plasma norepinephrine (PNE) that correlated with the infused norepinephrine dose (p < 0.001); this relationship was similar in normal and hypertensive subjects and unaltered by diuretic therapy. Plasma epinephrine and dopamine levels were unchanged during norepinephrine infusion. Norepinephrine infusion at pressor doses stimulated PRA (p < 0.01). The PRA responses correlated with the dose of infused norepinephrine (p < 0.0025), and norepinephrine-stimulated PRA correlated with basal PRA (p < 0.001). These norepinephrine-PRA relationships were unaltered by diuretic treatment and similar in normal and hypertensive subjects. In both groups, norepinephrine also caused a similar increase in plasma aldosterone (p < 0.05) under placebo conditions, but not following diuretic therapy. These findings demonstrate that an acute increase in the blood levels of the adrenergic neurotransmittor, norepinephrine, causes mild but distinct stimulation of plasma renin and aldosterone levels. Renin release in response to exogenous norepinephrine is not enhanced following renin-angiotensin activation by diuretic pretreatment. The responsiveness of the renin-angiotensin-aldosterone system to an acute norepinephrine input seems to be intact in essential hypertension.
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PMID:Effects of short-term norepinephrine infusion on plasma catecholamines, renin, and aldosterone in normal and hypertensive man. 699 68

After examining the most recent findings on the physiopathology of the renin-angiotensin system, techniques are analysed for the determination of renin activity (PRA). These are still inadequate and imprecise, notwithstanding radioimmunological techniques and stress is laid on the importance of their standardisation. Analysis of the various forms of arterial hypertension shows that PRA measurement has clinical value only: 1) in nephrovascular hypertension; 2) in primary hyper-reninism; 3) in primary hypercorticosuprarenalism; 4) to back up an indication for bilateral nephrectomy in terminal nephropathies with uncontrollable pressure value. At the present time, however, it would appear that PRA does not have any clinical utility for the study of essential hypertension.
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PMID:[Reninemia and its clinical value]. 700 Dec 70


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